CCR6 regulates EAE pathogenesis by controlling regulatory CD4+ T-cell recruitment to target tissues. Export

@article{citeulike:4828377, abstract = {The T-cell subsets, characterized by their cytokine production profiles and immune regulatory functions, depend on correct in vivo location to interact with accessory or target cells for effective immune responses. Differentiation of naive CD4(+) T cells into effectors is accompanied by sequentially regulated expression of the chemokine receptors responsible for cell recruitment to specific tissues. We studied CCR6 function in EAE, a CD4(+) T-cell-mediated CNS disease characterized by mononuclear infiltration and demyelination. CCR6(-/-) mice showed an altered time course of EAE development, with delayed onset, a higher clinical score, and more persistent symptoms than in controls. An imbalanced cytokine profile and reduced Foxp3(+) cell frequency characterized CNS tissues from CCR6(-/-) compared with CCR6(+/+) mice during the disease effector phase. Transfer of CCR6(+/+) Treg to CCR6(-/-) mice the day before EAE induction reduced the clinical score associated with an increased in infiltrating Foxp3(+) cells and recovery of the cytokine balance in CCR6(-/-) mouse CNS. Competitive assays between CCR6(+/+) and CCR6(-/-) Treg adoptively transferred to CCR6(-/-) mice showed impaired ability of CCR6(-/-) Treg to infiltrate CNS tissues in EAE-affected mice. Our data indicate a CCR6 requirement by CD4(+) Treg to downregulate the CNS inflammatory process and neurological signs associated with EAE.}, author = {Villares, R. and Cadenas, V. and Lozano, M. and Almonacid, L. and Zaballos, A. and Mart\'{\i}nez-A, C. and Varona, R.}, citeulike-article-id = {4828377}, citeulike-linkout-0 = {http://dx.doi.org/10.1002/eji.200839123}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19499521}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19499521}, doi = {10.1002/eji.200839123}, issn = {1521-4141}, journal = {European journal of immunology}, keywords = {autoimmune\_diseases, ccr6, chemokine, eae, immune\_regulation, t\_cells, treg\_cells}, month = {June}, number = {6}, pages = {1671--1681}, posted-at = {2009-06-12 18:23:09}, priority = {2}, title = {CCR6 regulates EAE pathogenesis by controlling regulatory CD4+ T-cell recruitment to target tissues.}, url = {http://dx.doi.org/10.1002/eji.200839123}, volume = {39}, year = {2009} }

TY - JOUR ID - citeulike:4828377 L3 - citeulike-article-id:4828377 N2 - The T-cell subsets, characterized by their cytokine production profiles and immune regulatory functions, depend on correct in vivo location to interact with accessory or target cells for effective immune responses. Differentiation of naive CD4(+) T cells into effectors is accompanied by sequentially regulated expression of the chemokine receptors responsible for cell recruitment to specific tissues. We studied CCR6 function in EAE, a CD4(+) T-cell-mediated CNS disease characterized by mononuclear infiltration and demyelination. CCR6(-/-) mice showed an altered time course of EAE development, with delayed onset, a higher clinical score, and more persistent symptoms than in controls. An imbalanced cytokine profile and reduced Foxp3(+) cell frequency characterized CNS tissues from CCR6(-/-) compared with CCR6(+/+) mice during the disease effector phase. Transfer of CCR6(+/+) Treg to CCR6(-/-) mice the day before EAE induction reduced the clinical score associated with an increased in infiltrating Foxp3(+) cells and recovery of the cytokine balance in CCR6(-/-) mouse CNS. Competitive assays between CCR6(+/+) and CCR6(-/-) Treg adoptively transferred to CCR6(-/-) mice showed impaired ability of CCR6(-/-) Treg to infiltrate CNS tissues in EAE-affected mice. Our data indicate a CCR6 requirement by CD4(+) Treg to downregulate the CNS inflammatory process and neurological signs associated with EAE. IS - 6 JF - European journal of immunology SN - 1521-4141 EP - 1681 TI - CCR6 regulates EAE pathogenesis by controlling regulatory CD4+ T-cell recruitment to target tissues. VL - 39 SP - 1671 KW - autoimmune_diseases KW - ccr6 KW - chemokine KW - eae KW - immune_regulation KW - t_cells KW - treg_cells AU - Villares, R AU - Cadenas, V AU - Lozano, M AU - Almonacid, L AU - Zaballos, A AU - Martínez-A, C AU - Varona, R PY - 2009/06// UR - http://dx.doi.org/10.1002/eji.200839123 ER -