Autoimmune islet destruction in spontaneous type 1 diabetes is not beta-cell exclusive Export

@article{Winer2003, abstract = {Pancreatic islets of Langerhans are enveloped by peri-islet Schwann cells (pSC), which express glial fibrillary acidic protein (GFAP) and S100beta. pSC-autoreactive T- and B-cell responses arise in 3- to 4-week-old diabetes-prone non-obese diabetic (NOD) mice, followed by progressive pSC destruction before detectable beta-cell death. Humans with probable prediabetes generate similar autoreactivities, and autoantibodies in islet-cell autoantibody (lCA) -positive sera co-localize to pSC. Moreover, GFAP-specific NOD T-cell lines transferred pathogenic peri-insulitis to NOD/severe combined immunodeficient (NOD/SCID) mice, and immunotherapy with GFAP or S100beta prevented diabetes. pSC survived in rat insulin promoter Iymphocytic choriomeningitis virus (rip-LCMV) glycoprotein/CD8+ T-cell receptor(gp) double-transgenic mice with virus-induced diabetes, suggesting that pSC death is not an obligate consequence of local inflammation and beta-cell destruction. However, pSC were deleted in spontaneously diabetic NOD mice carrying the CD8+/8.3 T-cell receptor transgene, a T cell receptor commonly expressed in earliest islet infiltrates. Autoimmune targeting of pancreatic nervous system tissue elements seems to be an integral, early part of natural type 1 diabetes.}, author = {Winer, S. and Tsui, H. and Lau, A. and Song, A. and Li, X. and Cheung, R. K. and Sampson, A. and Afifiyan, F. and Elford, A. and Jackowski, G. and Becker, D. J. and Santamaria, P. and Ohashi, P. and Dosch, H. M.}, citeulike-article-id = {168243}, journal = {Nat Med}, keywords = {bibtex-import, diabetes, islet}, number = {2}, pages = {198--205}, posted-at = {2005-04-23 06:42:40}, priority = {0}, title = {Autoimmune islet destruction in spontaneous type 1 diabetes is not beta-cell exclusive}, volume = {9}, year = {2003} }

TY - JOUR ID - Winer2003 L3 - citeulike-article-id:168243 N2 - Pancreatic islets of Langerhans are enveloped by peri-islet Schwann cells (pSC), which express glial fibrillary acidic protein (GFAP) and S100beta. pSC-autoreactive T- and B-cell responses arise in 3- to 4-week-old diabetes-prone non-obese diabetic (NOD) mice, followed by progressive pSC destruction before detectable beta-cell death. Humans with probable prediabetes generate similar autoreactivities, and autoantibodies in islet-cell autoantibody (lCA) -positive sera co-localize to pSC. Moreover, GFAP-specific NOD T-cell lines transferred pathogenic peri-insulitis to NOD/severe combined immunodeficient (NOD/SCID) mice, and immunotherapy with GFAP or S100beta prevented diabetes. pSC survived in rat insulin promoter Iymphocytic choriomeningitis virus (rip-LCMV) glycoprotein/CD8+ T-cell receptor(gp) double-transgenic mice with virus-induced diabetes, suggesting that pSC death is not an obligate consequence of local inflammation and beta-cell destruction. However, pSC were deleted in spontaneously diabetic NOD mice carrying the CD8+/8.3 T-cell receptor transgene, a T cell receptor commonly expressed in earliest islet infiltrates. Autoimmune targeting of pancreatic nervous system tissue elements seems to be an integral, early part of natural type 1 diabetes. IS - 2 JF - Nat Med EP - 205 TI - Autoimmune islet destruction in spontaneous type 1 diabetes is not beta-cell exclusive VL - 9 SP - 198 KW - bibtex-import KW - diabetes KW - islet AU - Winer, S AU - Tsui, H AU - Lau, A AU - Song, A AU - Li, X AU - Cheung, RK AU - Sampson, A AU - Afifiyan, F AU - Elford, A AU - Jackowski, G AU - Becker, DJ AU - Santamaria, P AU - Ohashi, P AU - Dosch, HM PY - 2003/// ER -