CiteULike: AlfonsoVicenteSuarez's library [180 articles] http://www.citeulike.org/user/AlfonsoVicenteSuarez CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2800416 <i>J. Cell Biol., Vol. 112, No. 5. (1 March 1991), pp. 965-979.</i><br /><br />10.1083/jcb.112.5.965 Overexpression of the cellular retinoic acid binding protein-I (CRABP- I) results in a reduction in differentiation-specific gene expression in F9 teratocarcinoma cells JF Boylan LJ Gudas doi:10.1083/jcb.112.5.965 J. Cell Biol., Vol. 112, No. 5. (1 March 1991), pp. 965-979. 2008-05-15T00:59:11-00:00 J. Cell Biol. 112 5 965 979 crabp ra http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2705497 <i>Int. Immunol., Vol. 19 (October 2007), pp. 1145-1155.</i><br /><br />Monocyte-derived dendritic cells (mDCs) and NK cells are reciprocally activate via cytokines and cellcell contact. Although seven human NKG2D ligands (NKG2DLs), UL16-binding proteins (ULBP) 1, 2, 3 and 4, retinoic acid early transcript 1G (RAET1G) and MHC class I-related chains A and B, have been reported, the differential distribution and roles of these ligands in the maturation of human mDCs have not been elucidated. In the present study, we produced polyclonal antibodies (pAbs) directed against human ULBP1, 2 and 3. All these ULBPs were detected on human mDCs when probed by the pAbs, although their expression profiles were different. We next investigated what kinds of Toll-like receptor agonists and RNA viruses [influenza virus, human respiratory syncytial virus (RSV), measles virus and hepatitis C virus (HCV)] induced the expression of NKG2DLs on mDCs. ULBP1 was up-regulated on mDCs in response to LPS or infection with RSV. The expression of ULBP2 was induced by LPS and poly I:C, indicating that the TIR-containing adapter molecule-1 (TIR domain-containing adaptor-inducing IFN) pathway is associated with ULBP2 induction. Although infection with HCV did not cause up-regulation of NKG2DLs, other RNA virus infections and poly I:C promoted expression of ULBP2 and RAET1G in an IFN-alpha/beta-independent manner. Finally, the over-expression of ULBP1 and 2 on mDCs facilitated NK cell proliferation and IFN-gamma production through a mDCNK cell interaction in the presence of IL-2. Hence, the results reflect the important role of NKG2DLs on human mDCs in mDC-mediated NK cell activation. Induction of NKG2D ligands on human dendritic cells by TLR ligand stimulation and RNA virus infection Takashi Ebihara Hisayo Masuda Takashi Akazawa Masashi Shingai Hideaki Kikuta Tadashi Ariga Misako Matsumoto Tsukasa Seya doi:10.1093/intimm/dxm073 Int. Immunol., Vol. 19 (October 2007), pp. 1145-1155. 2008-04-23T04:48:21-00:00 Int. Immunol. 19 1145 1155 ra http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2255493 <i>Nature Immunology, Vol. 9, No. 2., pp. 119-120.</i> Stress gets under your skin Daniel Andrews Mark Smyth doi:10.1038/ni0208-119 Nature Immunology, Vol. 9, No. 2., pp. 119-120. 2008-01-19T06:11:56-00:00 Nature Immunology 1529-2908 9 2 119 120 Nature Publishing Group ra rae-1 http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/329642 <i>Nature Immunology, Vol. 6, No. 10. (04 September 2005), pp. 1011-1019.</i> Interaction between conventional dendritic cells and natural killer cells is integral to the activation of effective antiviral immunity Christopher Andoniou Serani van Dommelen Valentina Voigt Daniel Andrews Geraldine Brizard Carine Asselin-Paturel Thomas Delale Katryn Stacey Giorgio Trinchieri Mariapia Degli-Esposti doi:10.1038/ni1244 Nature Immunology, Vol. 6, No. 10. (04 September 2005), pp. 1011-1019. 2005-09-22T05:54:07-00:00 Nature Immunology 1529-2908 6 10 1011 1019 Nature Publishing Group ra rae-1 http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2782017 <i>Proceedings of the National Academy of Sciences, Vol. 102, No. 31. (2 August 2005), pp. 10846-10851.</i><br /><br />The interaction of NKG2D, a stimulatory receptor expressed on natural killer (NK) cells and activated CD8+ T cells, and its ligands mediates stimulatory and costimulatory signals to these cells. Here, we demonstrate that DNA-based vaccines, encoding syngeneic or allogeneic NKG2D ligands together with tumor antigens such as survivin or carcinoembryonic antigen, markedly activate both innate and adaptive antitumor immunity. Such vaccines result in highly effective, NK- and CD8+ T cell-mediated protection against either breast or colon carcinoma cells in prophylactic and therapeutic settings. Notably, this protection was irrespective of the NKG2D ligand expression level of the tumor cells. Hence, this strategy has the potential to lead to widely applicable and possibly clinically useful DNA-based cancer vaccines. 10.1073/pnas.0502208102 DNA-based vaccines activate innate and adaptive antitumor immunity by engaging the NKG2D receptor He Zhou Yunping Luo Jeng-Fan Lo Charles Kaplan Masato Mizutani Noriko Mizutani Jiing-Dwan Lee James Primus Jurgen Becker Rong Xiang Ralph Reisfeld doi:10.1073/pnas.0502208102 Proceedings of the National Academy of Sciences, Vol. 102, No. 31. (2 August 2005), pp. 10846-10851. 2008-05-09T23:48:55-00:00 Proceedings of the National Academy of Sciences 102 31 10846 10851 ra rae-1 http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2781997 <i>Cancer Res, Vol. 65, No. 14. (15 July 2005), pp. 6409-6417.</i><br /><br />BCR/ABL fusion gene, encoding a paradigmatic tyrosine kinase involved in chronic myelogenous leukemia (CML), can modulate the expression of genes involved in natural killer (NK) cell target recognition. Recent reports outline the role of allogeneic antileukemic NK effectors in the graft-versus-leukemia effect but the regulation of NK cell activation in the setting of graft-versus-leukemia effect remains unknown. Here we show that dendritic cells derived from monocytes of CML patients are selectively endowed with NK cell stimulatory capacity in vitro. We further show, using a gene transfer approach in mouse bone marrow progenitors, that ABL/ABL is necessary to promote dendritic cell-mediated NK cell activation. The dendritic cell/NK cell cross-talk in ABL/ABL-induced CML seems unique because JunB or IFN consensus sequence binding protein loss of functions, associated with other myeloproliferative disorders, do not promote dendritic cell-mediated NK cell activation. NK cell activation by leukemic dendritic cells involves NKG2D activating receptors and is blocked by imatinib mesylate. Indeed, ABL/ABL translocation enhances the expression levels of the NKG2D ligands on dendritic cells, which is counteracted by imatinib mesylate. Altogether, the clonal ABL/ABL dendritic cells display the unique and selective ability to activate NK cells and may participate in the NK cell control of CML. This study also highlights the deleterious role of imatinib mesylate at the dendritic cell level for NK cell activation. 10.1158/0008-5472.CAN-04-2675 BCR/ABL Promotes Dendritic Cell-Mediated Natural Killer Cell Activation Magali Terme Christophe Borg Francois Guilhot Carole Masurier Caroline Flament Erwin Wagner Sophie Caillat-Zucman Alain Bernheim Ali Turhan Anne Caignard Laurence Zitvogel doi:10.1158/0008-5472.CAN-04-2675 Cancer Res, Vol. 65, No. 14. (15 July 2005), pp. 6409-6417. 2008-05-09T23:33:06-00:00 Cancer Res 65 14 6409 6417 ra rae-1 http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1452955 <i>Immunity, Vol. 12, No. 6. (June 2000), pp. 721-727.</i><br /><br />Here we describe a family of GPI-anchored cell surface proteins that function as ligands for the mouse activating NKG2D receptor. These molecules are encoded by the retinoic acid early inducible (RAE-1) and H60 minor histocompatibility antigen genes on mouse chromosome 10 and show weak homology with MHC class I. Expression of the NKG2D ligands is low or absent on normal, adult tissues; however, they are constitutively expressed on some tumors and upregulated by retinoic acid. Ectopic expression of RAE-1 and H60 confers target susceptibility to NK cell attack. These studies identify a family of ligands for the activating NKG2D receptor on NK and T cells, which may play an important role in innate and adaptive immunity. Retinoic acid early inducible genes define a ligand family for the activating NKG2D receptor in mice. A Cerwenka AB Bakker T McClanahan J Wagner J Wu JH Phillips LL Lanier Immunity, Vol. 12, No. 6. (June 2000), pp. 721-727. 2007-07-12T20:32:30-00:00 Immunity 1074-7613 12 6 721 727 ra rae-1 http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2320046 <i>Nat Rev Immunol, Vol. 4, No. 6. (June 2004), pp. 478-485.</i> Interactions between commensal intestinal bacteria and the immune system. AJ Macpherson NL Harris doi:10.1038/nri1373 Nat Rev Immunol, Vol. 4, No. 6. (June 2004), pp. 478-485. 2008-02-01T16:58:22-00:00 Nat Rev Immunol 1474-1733 4 6 478 485 anatomy-immune http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2319977 <i>J. Exp. Med., Vol. 203, No. 3. (20 March 2006), pp. 497-500.</i><br /><br />The surface of the intestinal mucosa is constantly assaulted by food antigens and enormous numbers of commensal microbes and their products, which are sampled by dendritic cells (DCs). Recent work shows that the mesenteric lymph nodes (MLNs) are the key site for tolerance induction to food proteins and that they also act as a firewall to prevent live commensal intestinal bacteria from penetrating the systemic immune system. 10.1084/jem.20060227 Mesenteric lymph nodes at the center of immune anatomy Andrew Macpherson Karen Smith doi:10.1084/jem.20060227 J. Exp. Med., Vol. 203, No. 3. (20 March 2006), pp. 497-500. 2008-02-01T16:30:17-00:00 J. Exp. Med. 203 3 497 500 anatomy-immune http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/271197 <i>Nature Reviews Immunology, Vol. 5, No. 8. (01 August 2005), pp. 606-616.</i> Structure and function of the spleen Reina Mebius Georg Kraal doi:10.1038/nri1669 Nature Reviews Immunology, Vol. 5, No. 8. (01 August 2005), pp. 606-616. 2005-08-01T21:28:57-00:00 Nature Reviews Immunology 1474-1733 5 8 606 616 Nature Publishing Group anatomy-immune http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1794608 <i>Nature Immunology, Vol. 8, No. 11. (19 October 2007), pp. 1153-1157.</i> Dynamics of host defense: the view at the front lines Peter Velázquez Janelle Waite Michael Dustin doi:10.1038/ni1520 Nature Immunology, Vol. 8, No. 11. (19 October 2007), pp. 1153-1157. 2007-10-20T17:08:48-00:00 Nature Immunology 1529-2908 8 11 1153 1157 Nature Publishing Group anatomy-immune http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2319930 <i>Nat Rev Immunol, Vol. 3, No. 4. (April 2003), pp. 331-341.</i><br /><br />The intestinal immune system has to discriminate between harmful and beneficial antigens. Although strong protective immunity is essential to prevent invasion by pathogens, equivalent responses against dietary proteins or commensal bacteria can lead to chronic disease. These responses are normally prevented by a complex interplay of regulatory mechanisms. This article reviews the unique aspects of the local microenvironment of the intestinal immune system and discuss how these promote the development of regulatory responses that ensure the maintenance of homeostasis in the gut. Anatomical basis of tolerance and immunity to intestinal antigens. AM Mowat doi:10.1038/nri1057 Nat Rev Immunol, Vol. 3, No. 4. (April 2003), pp. 331-341. 2008-02-01T16:13:07-00:00 Nat Rev Immunol 1474-1733 3 4 331 341 anatomy-immune http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2319904 <i>Nat Rev Immunol, Vol. 3, No. 11. (November 2003), pp. 867-878.</i> Homing and cellular traffic in lymph nodes. UH von Andrian TR Mempel doi:10.1038/nri1222 Nat Rev Immunol, Vol. 3, No. 11. (November 2003), pp. 867-878. 2008-02-01T16:04:22-00:00 Nat Rev Immunol 1474-1733 3 11 867 878 anatomy-immune http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/2319701 <i></i> Starting at the Beginning: New Perspectives on the Biology of Mucosal T Cells - Annual Review of Immunology, 22(1):217 - Abstract Hilde Cheroutre 2008-02-01T15:03:47-00:00 mucosal-immunology http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1903975 <i>J. Exp. Med., Vol. 185, No. 4. (17 February 1997), pp. 695-706.</i><br /><br />The genetic origins of CD8+ T cell-recognized unique antigens to which mice respond when immunized with syngeneic tumor cells are unknown. The ultraviolet light-induced murine tumor 8101 expresses an H-2Kb-restricted immunodominant antigen, A, that induces cytolytic CD8+ T cells in vivo A+ 8101 cells are rejected by naive mice while A[-] 8101 tumor cells grow. To identify the antigen H-2Kb molecules were immunoprecipitated from A+ 8101 cells and peptides were eluted by acid. The sensitizing peptide was isolated by sequential reverse-phase HPLC and sequenced using microcapillary HPLC-triple quadruple mass spectrometry. The peptide, SNFVFAGI, matched the sequence of the DEAD box protein p68 RNA helicase except for a single amino acid substitution, caused by a single nucleotide change. This mutation was somatic since fibroblasts from the mouse of tumor origin expressed the wild-type sequence. The amino acid substitution created an anchor for binding of the mutant peptide to H-2Kb. Our results are consistent with mutant p68 being responsible for rejection of the tumor. Several functions of p68, which include nucleolar assembly and inhibition of DNA unwinding, may be mediated through its IQ domain, which was altered by the mutation. This is the first description of a somatic tumor-specific mutation in the coding region of a nucleic acid helicase. 10.1084/jem.185.4.695 The Immunodominant Antigen of an Ultraviolet-induced Regressor Tumor Is Generated by a Somatic Point Mutation in the DEAD Box Helicase p68 Purnima Dubey Ronald Hendrickson Stephen Meredith Christopher Siegel Jeffrey Shabanowitz Jonathan Skipper Victor Engelhard Donald Hunt Hans Schreiber doi:10.1084/jem.185.4.695 J. Exp. Med., Vol. 185, No. 4. (17 February 1997), pp. 695-706. 2007-11-12T20:25:31-00:00 J. Exp. Med. 185 4 695 706 tumor-rejection http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1903969 <i>J. Exp. Med., Vol. 153, No. 5. (1 May 1981), pp. 1344-1359.</i><br /><br />We have shown that both regressor and progressor clones can be isolated from a UV regressor tumor, RD-1024. Although the daughter clones are characterized by differences in tumorigenic potential in normal transplant hosts, they nevertheless seem to express the same major tumor rejection antigens, because immunization with either the regressor parent tumor, RD-1024, or with regressor Cl 8 protects against subsequent challenge with progressor C1 4 or Cl 9. Consistent with the in vivo-generated data is the evidence that draining lymph node cells with functional specificity for regressor Cl 8 are capable of cross-reactive cytotoxicity in an in vitro chromium release assay.We have demonstrated an indirect interaction occurring in vivo between regressor and progressor cells, in that Cl 8 cells have the ability to influence the outcome of simultaneous or sequential challenge with Cl 4 or Cl 9 cells. Because 500 rad of gamma irradiation has been shown to compromise the ability of mice to respond to a primary challenge with tumor, an immunological mechanism is implicated in the ultimate rejection of progressor tumor in a doubly challenged host.The importance of these results lies in the knowledge that these interacting subpopulations have been isolated directly from a tumor growing in vivo and that no selection pressure has been exerted on the cells greater than the short in vitro culture period necessary for the isolation and expansion of individual clones. The apparent immunoregulatory potential in a tumor-bearing animal is thus seen to be modified in accordance with the phenotypic heterogeneity of the cells within that tumor. 10.1084/jem.153.5.1344 Heterogeneity of tumorigenicity phenotype in murine tumors. I. Characterization of regressor and progressor clones isolated from a nonmutagenized ultraviolet regressor tumor M Schmitt Ra Daynes doi:10.1084/jem.153.5.1344 J. Exp. Med., Vol. 153, No. 5. (1 May 1981), pp. 1344-1359. 2007-11-12T20:24:27-00:00 J. Exp. Med. 153 5 1344 1359 tumor-rejection http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1903171 <i>Cancer Res, Vol. 66, No. 14. (15 July 2006), pp. 7301-7309.</i><br /><br />Although regulatory T cells (Tregs) have been detected in clinically apparent and experimentally induced tumors, the significance of their presence is obscured because past studies examined late-stage tumors that had formed in immunocompetent hosts and thus had evolved mechanisms to escape immunologic recognition and/or elimination. Herein, we report the first comparative analysis of the antitumor response to 3'-methylcholanthrene-induced tumors, which either grow progressively (progressor tumors) or are rejected by the immune system (regressor tumors). Surprisingly, we found that both progressor and regressor tumors harbored proliferating (i.e., activated) Foxp3+CD25+Tregs. However, progressor tumors contained a higher percentage of Tregs in the lymphocyte subset versus regressor tumors. The Tregs in progressor tumors were derived from peripheral CD25+ natural Tregs, accumulated early after tumor challenge and were actively proliferating, suggesting that progressor tumors recruited and/or activated endogenous Tregs as a mechanism of escaping immune destruction. To explore whether Tregs directly contributed to the progressive growth phenotype of progressor tumors, we monitored tumor outgrowth in naive wild-type recipients pretreated with either a control monoclonal antibody (mAb) or a depleting CD25-specific mAb. In mice predepleted of CD25+ cells, the tumors that subsequently developed displayed an increased accumulation of proliferating CD8+ T cells and were rejected. These results show that, although Tregs are activated in both regressor and progressor tumors, the ratio of regulatory to effector T cells is critical in determining whether the host successfully rejects the tumor or eventually succumbs to tumor outgrowth. (Cancer Res 2006; 66(14): 7301-9) 10.1158/0008-5472.CAN-06-0556 Comparative Analysis of Regulatory and Effector T Cells in Progressively Growing versus Rejecting Tumors of Similar Origins Jack Bui Ravindra Uppaluri Chyi-Song Hsieh Robert Schreiber doi:10.1158/0008-5472.CAN-06-0556 Cancer Res, Vol. 66, No. 14. (15 July 2006), pp. 7301-7309. 2007-11-12T16:10:28-00:00 Cancer Res 66 14 7301 7309 tumor-rejection http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1891503 <i></i> Spontaneous tumor rejection by cbl-b-deficient CD8+ T cells -- Loeser et al. 204 (4): 879 -- The Journal of Experimental Medicine 2007-11-09T22:51:37-00:00 tumor-rejection http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1891501 <i></i> Spontaneous tumor rejection by cbl-b-deficient CD8+ T cells -- Loeser et al. 204 (4): 879 -- The Journal of Experimental Medicine 2007-11-09T22:50:13-00:00 tumor-rejection http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1852444 <i></i> Immunity -- Martin and Chan 2007-11-01T19:52:49-00:00 bcells-autoimmunity http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1781484 <i></i> The family of five: TIR-domain-containing adaptors in Toll-like receptor signalling : Article : Nature Reviews Immunology 2007-10-17T21:33:35-00:00 tlr-signaling http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1781374 <i></i> Bacterial CpG-DNA and lipopolysaccharides activate Toll-like receptors at distinct cellular compartments 2007-10-17T20:39:38-00:00 tlr-signaling http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1777711 <i></i> REGULATION OF TH2 DIFFERENTIATION AND Il4 LOCUS ACCESSIBILITY - Annual Review of Immunology, 24(1):607 - Full Text 2007-10-17T03:40:24-00:00 th-differentiation http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1776829 <i></i> Intravenous injection of soluble antigen induces thymic and peripheral T-cell apoptosis -- Liblau et al. 93 (7): 3031 -- Proceedings of the National Academy of Sciences 2007-10-16T22:22:12-00:00 tolerance-models http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1776680 <i></i><br /><br />Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein. T Cell Deletion in High Antigen Dose Therapy of Autoimmune Encephalomyelitis Jeffrey Critchfield Michael Racke Juan Zúñiga-Pflücker Barbara Cannella Cedric Raine Joan Goverman Michael Lenardo 2007-10-16T21:27:37-00:00 tolerance-models http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1776643 <i></i> Aqueous antigens induce in vivo tolerance selectively in IL-2- and IFN- gamma-producing (Th1) cells -- Burstein et al. 148 (12): 3687 -- The Journal of Immunology 2007-10-16T21:14:35-00:00 tolerance-models http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1776592 <i></i> Antigen-specific tolerance strategies for the prevention and treatment of autoimmune disease : Article : Nature Reviews Immunology 2007-10-16T20:58:41-00:00 tolerance-models http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1772049 <i></i> MACROPHAGE RECEPTORS AND IMMUNE RECOGNITION - Annual Review of Immunology, 23(1):901 - Full Text 2007-10-16T03:02:58-00:00 macrophages-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1772032 <i>Cell, Vol. 124, No. 2. (27 January 2006), pp. 263-266.</i><br /><br />Macrophages within the tumor microenvironment facilitate angiogenesis and extracellular-matrix breakdown and remodeling and promote tumor cell motility. Recent studies reveal that direct communication between macrophages and tumor cells leads to invasion and egress of tumor cells into the blood vessels (intravasation). Thus, macrophages are at the center of the invasion microenvironment and are an important drug target for cancer therapy. Macrophages: Obligate Partners for Tumor Cell Migration, Invasion, and Metastasis John Condeelis Jeffrey Pollard doi:10.1016/j.cell.2006.01.007 Cell, Vol. 124, No. 2. (27 January 2006), pp. 263-266. 2007-10-16T02:56:18-00:00 Cell 124 2 263 266 macrophages-tumor http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1772024 <i></i> Autocrine Production of IL-10 Mediates Defective IL-12 Production and NF-kappaB Activation in Tumor-Associated Macrophages -- Sica et al. 164 (2): 762 -- The Journal of Immunology 2007-10-16T02:54:19-00:00 macrophages-tumor http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1770382 <i></i> DOES THE IMMUNE SYSTEM SEE TUMORS AS FOREIGN OR SELF? - Annual Review of Immunology, 21(1):807 - Full Text Dm Pardoll 2007-10-15T14:15:33-00:00 basic-tumor http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1767947 <i></i> ANTIGEN PRESENTATION AND T CELL STIMULATION BY DENDRITIC CELLS - Annual Review of Immunology, 20(1):621 - Full Text 2007-10-14T20:28:07-00:00 basic-dcs http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1751306 <i>Current Opinion in Immunology, Vol. 18, No. 4. (August 2006), pp. 503-511.</i><br /><br />Tissue-resident dendritic cells (DCs) that migrate from peripheral sites to lymphoid organs are essential in the initiation of adaptive immune responses and for the maintenance of peripheral tolerance, and have been extensively studied. By contrast, blood-borne DCs represent a heterogeneous population, the origin, destination and function of which are still unclear. Recent studies have shown that circulating DCs capture blood-borne antigen and transport it into the extra-vascular space of lymphoid tissues for processing and presentation. Other findings suggest that a fraction of tissue-resident DCs might enter the blood after having acquired antigen in the periphery. Together, these studies imply that circulating DCs might modulate immune responses by translocating antigenic material from its point of origin to remote target tissues. Generation, migration and function of circulating dendritic cells Roberto Bonasio Ulrich von Andrian doi:10.1016/j.coi.2006.05.011 Current Opinion in Immunology, Vol. 18, No. 4. (August 2006), pp. 503-511. 2007-10-10T16:32:27-00:00 Current Opinion in Immunology 18 4 503 511 migration-dcs http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1688016 <i>J. Exp. Med., Vol. 196, No. 4. (19 August 2002), pp. 541-549.</i><br /><br />Progressing tumors in man and mouse are often infiltrated by dendritic cells (DCs). Deficient antitumor immunity could be related to a lack of tumor-associated antigen (TAA) presentation by tumor-infiltrating DCs (TIDCs) or to a functional defect of TIDCs. Here we investigated the phenotype and function of TIDCs in transplantable and transgenic mouse tumor models. Although TIDCs could encompass various known DC subsets, most had an immature phenotype. We observed that TIDCs were able to present TAA in the context of major histocompatibility complex class I but that they were refractory to stimulation with the combination of lipopolysaccharide, interferon gamma, and anti-CD40 antibody. We could revert TIDC paralysis, however, by in vitro or in vivo stimulation with the combination of a CpG immunostimulatory sequence and an anti-interleukin 10 receptor (IL-10R) antibody. CpG or anti-IL-10R alone were inactive in TIDCs, whereas CpG triggered activation in normal DCs. In particular, CpG plus anti-IL-10R enhanced the TAA-specific immune response and triggered de novo IL-12 production. Subsequently, CpG plus anti-IL-10R treatment showed robust antitumor therapeutic activity exceeding by far that of CpG alone, and elicited antitumor immune memory. 10.1084/jem.20020732 Reversal of Tumor-induced Dendritic Cell Paralysis by CpG Immunostimulatory Oligonucleotide and Anti-Interleukin 10 Receptor Antibody Alain Vicari Claudia Chiodoni Celine Vaure Smina Ait-Yahia Christophe Dercamp Fabien Matsos Olivier Reynard Catherine Taverne Philippe Merle Mario Colombo Anne O'Garra Giorgio Trinchieri Christophe Caux doi:10.1084/jem.20020732 J. Exp. Med., Vol. 196, No. 4. (19 August 2002), pp. 541-549. 2007-09-23T22:45:31-00:00 J. Exp. Med. 196 4 541 549 tolerogenic-dcs tumor-dcs http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1642454 <i>Biochemical and Biophysical Research Communications, Vol. 355, No. 1. (30 March 2007), pp. 280-285.</i><br /><br />Bacterial flagellin is recognized by Toll-like receptor (TLR5) and activates NF-[kappa]B which leads to the induction of proinflammatory gene expression. Salmonella expresses two flagellin proteins, FliC and FljB. We purified FliC and FljB and examined the ability of the Salmonella flagellins to activate the NF-[kappa]B transcription factor in human embryonic kidney cells. We found that FliC and FljB as purified proteins possessed a comparable specific activity for activation of NF-[kappa]B-dependent gene expression in HEK293 cells. We also determined the ability of UV-inactivated bacteria, both wild-type and fliC and fljB mutant strains, to activate NF-[kappa]B. Wild-type fliC+/fljB+ Salmonella and the fliC+/fljB- mutant strain were robust activators, whereas the fliC-/fljB+ and flhC- mutant strains were very poor activators. The NF-[kappa]B activation capacity of bacterial strains correlated with their flagellin expression level. Finally, Salmonella cell wall-associated polymeric flagellin displayed greatly reduced ability to activate NF-[kappa]B compared to purified monomeric flagellin. Activation of NF-[kappa]B-dependent gene expression by Salmonella flagellins FliC and FljB Raphael Simon Charles Samuel doi:10.1016/j.bbrc.2007.01.148 Biochemical and Biophysical Research Communications, Vol. 355, No. 1. (30 March 2007), pp. 280-285. 2007-09-10T16:00:02-00:00 Biochemical and Biophysical Research Communications 355 1 280 285 flagellin-biphasic http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1642416 <i>J. Clin. Invest., Vol. 107, No. 1. (1 January 2001), pp. 99-109.</i><br /><br />This study investigated whether soluble paracrine factors mediated Salmonella-induced IL-8 expression in polarized model intestinal epithelia. We found that the basolateral media of model epithelia that had been apically infected with Salmonella typhimurium for a short period (10 minutes) could activate IL-8 secretion in virgin model epithelia, demonstrating that a proinflammatory factor (PIF) was indeed present. Initial characterization found that PIF was a heat-stable protein with a molecular mass of about 50 kDa that acts on the basolateral, but not apical, surface of model intestinal epithelia to elicit IL-8 secretion. PIF was not present in the media of model epithelia stimulated with other inducers of IL-8 secretion (TNF-alpha or carbachol) but was present in S. typhimurium supernatants, indicating PIF is of bacterial origin. PIF was purified from bacterial culture supernatants by anion/cation exchange chromatography and SDS-PAGE and found by using microsequencing to be the protein flagellin. In support of this finding, flagellin-deficient S. typhimurium mutants did not secrete detectable levels of PIF (i.e., a bioactivity that induced IL-8 secretion when placed basolaterally on model epithelia). Furthermore, viable flagellin-deficient mutant organisms (fliC/fljB and flhD) failed to elicit IL-8 secretion when added apically to model intestinal epithelia. These findings indicate that translocation of flagellin across epithelia, subsequent to apical epithelial-S. typhimurium interaction, is likely a major means of activating a mucosal inflammatory response. Salmonella typhimurium translocates flagellin across intestinal epithelia, inducing a proinflammatory response Andrew Gewirtz Peter Simon Clare Schmitt Laura Taylor Curt Hagedorn Alison O'Brien Andrew Neish James Madara J. Clin. Invest., Vol. 107, No. 1. (1 January 2001), pp. 99-109. 2007-09-10T15:29:36-00:00 J. Clin. Invest. 107 1 99 109 flagellin-biphasic http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1908 <i>Nature Reviews Immunology, Vol. 4, No. 12. (01 December 2004), pp. 965-977.</i> A BAF-centred view of the immune system Tian Chi doi:10.1038/nri1501 Nature Reviews Immunology, Vol. 4, No. 12. (01 December 2004), pp. 965-977. 2004-12-06T02:32:05-00:00 Nature Reviews Immunology 4 12 965 977 chromatin structure http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1582905 <i>J. Exp. Med., Vol. 193, No. 2. (16 January 2001), pp. 5F-10.</i><br /><br />10.1084/jem.193.2.F5 Differentiation of T Regulatory Cells by Immature Dendritic Cells Maria-Grazia Roncarolo Megan Levings Catia Traversari doi:10.1084/jem.193.2.F5 J. Exp. Med., Vol. 193, No. 2. (16 January 2001), pp. 5F-10. 2007-08-22T13:46:30-00:00 J. Exp. Med. 193 2 5F 10 tolerogenic-dcs http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1572795 <i></i> CD40/CD154 Interactions at the Interface of Tolerance and Immunity - Annual Review of Immunology, 22(1):307 - Abstract 2007-08-17T18:43:50-00:00 randy-noelle http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1570869 <i>Clin Cancer Res, Vol. 13, No. 2. (15 January 2007), pp. 733s-740.</i><br /><br />In patients with progressive malignancy, the natural balance between proinflammatory (Yang) and inhibitory (regulatory or Yin) immune pathways is disrupted and favors cancer-specific immune suppression. Therapy with interleukin 2 (IL-2) can mobilize immune effector cells that recognize and destroy cancer. High-dose IL-2 is the only therapy that has consistently induced complete durable remissions in patients with metastatic renal cell carcinoma (RCC) but only in a few of them. The lack of benefit in most metastatic RCC patients is likely due to the ineffective manipulation of other immune circuits critical in regulating tumor cytotoxic pathways. The limited clinical activity of IL-2, RCC vaccines, and other immune therapies to date leads us to postulate that effective clinical treatment strategies will need to simultaneously enhance proinflammatory pathways and disrupt regulatory pathways. We present preliminary studies in RCC patients to highlight the complexity of the regulatory pathways and our approach to shifting the balance of proinflammatory and regulatory immune pathways using dendritic cell-tumor lysate vaccine followed by cytokine therapy. 10.1158/1078-0432.CCR-06-2064 Developing a Rational Tumor Vaccine Therapy for Renal Cell Carcinoma: Immune Yin and Yang Marc Ernstoff Todd Crocenzi John Seigne Nancy Crosby Bernard Cole Jan Fisher Jill Uhlenhake Diane Mellinger Cathy Foster Conrad Farnham Kathleen Mackay Zbigniew Szczepiorkowski Susan Webber Alan Schned Robert Harris Richard Barth John Heaney Randolph Noelle doi:10.1158/1078-0432.CCR-06-2064 Clin Cancer Res, Vol. 13, No. 2. (15 January 2007), pp. 733s-740. 2007-08-16T20:44:54-00:00 Clin Cancer Res 13 2 733s 740 randy-noelle http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/808729 <i>Nature, Vol. 442, No. 7106. (20 August 2006), pp. 997-1002.</i> Mast cells are essential intermediaries in regulatory T-cell tolerance Li-Fan Lu Evan Lind David Gondek Kathy Bennett Michael Gleeson Karina Pino-Lagos Zachary Scott Anthony Coyle Jennifer Reed Jacques Van Snick Terry Strom Xin Zheng Randolph Noelle doi:10.1038/nature05010 Nature, Vol. 442, No. 7106. (20 August 2006), pp. 997-1002. 2006-08-20T19:12:35-00:00 Nature 0028-0836 442 7106 997 1002 Nature Publishing Group randy-noelle http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1570867 <i>J Exp Med, Vol. 204, No. 8. (6 August 2007), pp. 1765-1774.</i><br /><br />We demonstrate that all-trans retinoic acid (RA) induces FoxP3(+) adaptive T regulatory cells (A-Tregs) to acquire a gut-homing phenotype (alpha4beta7(+) CC chemokine receptor 9(+)) and the capacity to home to the lamina propria of the small intestine. Under conditions that favor the differentiation of A-Tregs (transforming growth factor-beta1 and interleukin 2) in vitro, the inclusion of RA induces nearly all activated CD4(+) T cells to express FoxP3 and greatly increases the accumulation of these cells. In the absence of RA, A-Treg differentiation is abruptly impaired by proficient antigen presenting cells or through direct co-stimulation. In the presence of RA, A-Treg generation occurs even in the presence of high levels of co-stimulation, with RA attenuating co-stimulation from interfering from FoxP3 induction. The recognition that RA induces gut imprinting, together with our finding that it enhances A-Treg conversion, differentiation, and expansion, indicates that RA production in vivo may drive both the imprinting and A-Treg development in the face of overt inflammation. All-trans retinoic acid mediates enhanced T reg cell growth, differentiation, and gut homing in the face of high levels of co-stimulation. MJ Benson K Pino-Lagos M Rosemblatt RJ Noelle doi:10.1084/jem.20070719 J Exp Med, Vol. 204, No. 8. (6 August 2007), pp. 1765-1774. 2007-08-16T20:41:59-00:00 J Exp Med 0022-1007 204 8 1765 1774 randy-noelle http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1558868 <i>J Immunol, Vol. 176, No. 5. (1 March 2006), pp. 3181-3188.</i><br /><br />Group B streptococcus (GBS) is the major cause of sepsis in newborn infants. In vitro, inactivated GBS stimulates macrophages to produce inflammatory proteins via the TLR adapter protein MyD88. Furthermore, inflammatory cytokine release in response to GBS greatly exceeds that following stimulation with pneumococci. In this study, we attempted to unravel signaling events that are involved in GBS-, but not Streptococcus pneumoniae-stimulated phagocytes to identify molecular targets for adjunctive sepsis therapy. We found that inactivated GBS and S. pneumoniae differed in the activation of the MAPK JNK, but not IkappaB kinase. Furthermore, JNK was essential for the transcriptional activation of inflammatory cytokine genes in response to GBS. Inhibition of JNK by the anthrapyrazolone SP600125 abrogated GBS-induced cytokine formation via an AP-1- and NF-kappaB-dependent mechanism without impairing antibacterial properties such as phagocytosis of GBS and the formation of intracellular oxidative species. In contrast, inhibition of the MAPK p38 impaired both antibacterial processes. In a neonatal mouse model of GBS sepsis SP600125 inhibited the inflammatory response and improved survival. In conclusion, JNK plays a major role in the inflammatory, but not in the direct antibacterial response to inactivated GBS, and may thus serve as a rational target for an adjunctive GBS sepsis therapy. c-Jun Kinase Is a Critical Signaling Molecule in a Neonatal Model of Group B Streptococcal Sepsis Sybille Kenzel Guiseppe Mancuso Richard Malley Guiseppe Teti Douglas Golenbock Philipp Henneke J Immunol, Vol. 176, No. 5. (1 March 2006), pp. 3181-3188. 2007-08-13T21:06:26-00:00 J Immunol 176 5 3181 3188 tlrs-mapks http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1558814 <i>Nat Cell Biol, Vol. 4, No. 5. (May 2002), pp. E131-E136.</i> AP-1 as a regulator of cell life and death Eitan Shaulian Michael Karin doi:10.1038/ncb0502-e131 Nat Cell Biol, Vol. 4, No. 5. (May 2002), pp. E131-E136. 2007-08-13T20:33:26-00:00 Nat Cell Biol 4 5 E131 E136 tlrs-mapks http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/472747 <i>Cell Death and Differentiation, Vol. aop, No. current.</i> TLR signaling T Kawai S Akira doi:10.1038/sj.cdd.4401850 Cell Death and Differentiation, Vol. aop, No. current. 2006-01-20T16:53:40-00:00 Cell Death and Differentiation 1350-9047 aop current Nature Publishing Group tlr-signaling http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1558552 <i></i> Recognition and Signaling by Toll-Like Receptors - Annual Review of Cell and Developmental Biology, 22(1):409 - Full Text 2007-08-13T18:46:46-00:00 tlr-signaling http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1531229 <i>J Immunol, Vol. 174, No. 11. (1 June 2005), pp. 7433-7439.</i><br /><br />Ex vivo treatment of bone marrow-derived dendritic cells (DCs) with TNF-alpha has been previously shown to induce partial maturation of DCs that are able to suppress autoimmunity. In this study, we demonstrate that i.v. administration of TNF-alpha-treated, semimature DCs pulsed with thyrogloblin (Tg), but not with OVA Ag, inhibits the subsequent development of Tg-induced experimental autoimmune thyroiditis (EAT) in CBA/J mice. This protocol activates CD4+CD25+ T cells in vivo, which secrete IL-10 upon specific recognition of Tg in vitro and express regulatory T cell (Treg)-associated markers such as glucocorticoid-induced TNFR, CTLA-4, and Foxp3. These CD4+CD25+ Treg cells suppressed the proliferation and cytokine release of Tg-specific, CD4+CD25- effector cells in vitro, in an IL-10-independent, cell contact-dependent manner. Prior adoptive transfer of the same CD4+CD25+ Treg cells into CBA/J hosts suppressed Tg-induced EAT. These results demonstrate that the tolerogenic potential of Tg-pulsed, semimature DCs in EAT is likely to be mediated through the selective activation of Tg-specific CD4+CD25+ Treg cells and provide new insights for the study of Ag-specific immunoregulation of autoimmune diseases. Tolerogenic Semimature Dendritic Cells Suppress Experimental Autoimmune Thyroiditis by Activation of Thyroglobulin-Specific CD4+CD25+ T Cells Panayotis Verginis Haiyan Li George Carayanniotis J Immunol, Vol. 174, No. 11. (1 June 2005), pp. 7433-7439. 2007-08-02T20:02:14-00:00 J Immunol 174 11 7433 7439 tolerogenic-dcs http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1531225 <i>Trends in Immunology, Vol. 23, No. 9. (1 September 2002), pp. 445-449.</i><br /><br />Dendritic cells (DCs) are currently divided into tolerogenic immature and immunogenic mature differentiation stages. However, recent findings challenge this model by reporting mature DCs as inducers of regulatory CD4+ T cells in vivo. This implies that decisive tolerogenic and immunogenic maturation signals for DCs might exist. Closer inspection reveals that tolerance is observed when partial- or semi-maturation of DCs occurs, whereas only full DC maturation is immunogenic. The decisive immunogenic signal seems to be the release of proinflammatory cytokines from the DCs. Moreover, the semi-mature DC phenotype is comparable to steady-state migratory veiled DCs within the lymphatics, which seem to continuously tolerize lymph node T cells against tissue-derived self-antigens or apoptotic cells. Immature, semi-mature and fully mature dendritic cells: which signals induce tolerance or immunity? Manfred Lutz Gerold Schuler doi:10.1016/S1471-4906(02)02281-0 Trends in Immunology, Vol. 23, No. 9. (1 September 2002), pp. 445-449. 2007-08-02T19:56:21-00:00 Trends in Immunology 23 9 445 449 tolerogenic-dcs http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1531102 <i>J Immunol, Vol. 179, No. 2. (15 July 2007), pp. 1147-1154.</i><br /><br />Flagellin is a key component of the flagella of many pathogens, including Pseudomonas aeruginosa. Flagellin is an attractive vaccine candidate because it is readily produced and manipulated as a recombinant protein and has intrinsic adjuvant activity mediated through TLR5. Although DNA vaccines encoding native Pseudomonas B-type (FliC) or A-type (FlaA) flagellin are strongly immunogenic, the resultant Ab response interferes with the interaction of homologous flagellin with TLR5. This reduces the ability of the host to clear homologous, but not heterologous, flagellin-expressing P. aeruginosa. To circumvent this problem, a DNA vaccine encoding a mutant FliC R90A flagellin was developed. The mutant Ag encoded by this vaccine was highly immunogenic, but its ability to interact with TLR5 was reduced by >100-fold. Vaccination with this flagellin mutant DNA vaccine induced cross-reactive Abs against both FliC and FlaA, but few Abs capable of interfering with TLR5 activation. The flagellin mutant DNA vaccine provided excellent protection against both FliC- and FlaA-expressing P. aeruginosa. These findings suggest that vaccines against flagellated pathogens should avoid inducing Abs against TLR5 and raise the possibility that flagellated bacteria evade host elimination by facilitating the production of Abs that reduce the host's ability to mount an innate immune response. Blocking of the TLR5 Activation Domain Hampers Protective Potential of Flagellin DNA Vaccine Sukumar Saha Fumihiko Takeshita Tomoko Matsuda Nao Jounai Kouji Kobiyama Tetsuya Matsumoto Shin Sasaki Atsushi Yoshida Ke-Qin Xin Dennis Klinman Satoshi Uematsu Ken Ishii Shizuo Akira Kenji Okuda J Immunol, Vol. 179, No. 2. (15 July 2007), pp. 1147-1154. 2007-08-02T18:42:58-00:00 J Immunol 179 2 1147 1154 flagellin-tumor tlr5-flagellin http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1530987 <i>J Immunol, Vol. 176, No. 11. (1 June 2006), pp. 6624-6630.</i><br /><br />Flagellin, the structural protein subunit of the bacterial flagellum, is specifically recognized by TLR-5 and has potent immunomodulatory effects. The antitumor effects of purified Salmonella typhimurium flagellin were evaluated in mice transplanted s.c. with a weakly immunogenic murine tumor or with its variant stably transfected to express the highly antigenic human HER-2 oncoprotein. Peritumoral administration of flagellin 8-10 days after tumor implantation did not affect the growth rate of the weakly immunogenic tumor but significantly inhibited growth of the antigenic variant tumor. In contrast, flagellin administered at the time of implantation of the antigenic tumor led to accelerated tumor growth. These contrasting effects of flagellin on tumor growth correlated with the type of immune response induced; i.e., late flagellin administration was associated with an increased IFN-gamma:IL-4 ratio and the decreased frequency of CD4+CD25+ T regulatory cells, whereas flagellin treatment at the time of tumor implantation decreased the IFN-gamma:IL-4 ratio and increased CD4+CD25+ T cell frequency. When the early flagellin treatment was combined with administration of CpG-containing oligodeoxynucleotides, tumor growth was completely suppressed, indicating synergy between flagellin and CpG-containing oligodeoxynucleotides. Together, these data provide evidence that flagellin can have contrasting effects on tumor growth. Antitumor Activity of the TLR-5 Ligand Flagellin in Mouse Models of Cancer Lucia Sfondrini Anna Rossini Dario Besusso Andrea Merlo Elda Tagliabue Sylvie Menard Andrea Balsari J Immunol, Vol. 176, No. 11. (1 June 2006), pp. 6624-6630. 2007-08-02T16:40:40-00:00 J Immunol 176 11 6624 6630 flagellin-tumor