期刊
JOURNAL OF IMMUNOLOGY
卷 191, 期 11, 页码 5489-5500出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1301235
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类别
资金
- European Research Council [261079NEUROTRAFFICKING]
- National Multiple Sclerosis Society
- Fondazione Italiana Sclerosi Multipla
- Associazione Italiana per la Ricerca sul Cancro [IG 8690]
- Ministry of Education and Research
- Fondazione Cariverona
- Harry Weaver Neuroscience Scholar of the National Multiple Sclerosis Society [2144A2/1]
- Fondazione Italiana Sclerosi Multipla [2009/R/33]
Regulatory T cells (Tregs) maintain tolerance toward self-antigens and suppress autoimmune diseases, although the underlying molecular mechanisms are unclear. In this study, we show that mice deficient for P-selectin glycoprotein ligand-1 (PSGL-1) develop a more severe form of experimental autoimmune encephalomyelitis than wild type animals do, suggesting that PSGL-1 has a role in the negative regulation of autoimmunity. We found that Tregs lacking PSGL-1 were unable to suppress experimental autoimmune encephalomyelitis and failed to inhibit T cell proliferation in vivo in the lymph nodes. Using two-photon laser-scanning microscopy in the lymph node, we found that PSGL-1 expression on Tregs had no role in the suppression of early T cell priming after immunization with Ag. Instead, PSGL-1-deficient Tregs lost the ability to modulate T cell movement and failed to inhibit the T cell-dendritic cell contacts and T cell clustering essential for sustained T cell activation during the late phase of the immune response. Notably, PSGL-1 expression on myelin-specific effector T cells had no role in T cell locomotion in the lymph node. Our data show that PSGL-1 represents a previously unknown, phase-specific mechanism for Treg-mediated suppression of the persistence of immune responses and autoimmunity induction.
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