2010 Fiscal Year Final Research Report
Regulation in maintenance of remission involving the prognosis of a model of Multiple Sclerosis
| Project/Area Number |
21790855
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | National Center of Neurology and Psychiatry |
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Principal Investigator |
LIN Youwei 独立行政法人国立精神・神経医療研究センター, 神経研究所免疫研究部, 併任研究員 (80392439)
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| Project Period (FY) |
2009 – 2010
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| Keywords | 神経病態免疫学 / 制御性T細胞 / 実験的自己免疫性脳脊髄炎 / ペプチド優位性 |
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| Research Abstract |
Immunization with several encephalitogenic myelin peptides causes experimental autoimmune encephalomyelitis (EAE), resembling variety types of multiple sclerosis (MS).
Noting that immunizing SJL/J mice with overlapping myelin proteolipid protein (PLP) residues 136-150 and 139-151 could induce quite different diseases ; monophasic EAE by PLP136-150 and relapsing EAE by PLP139-151, we found the non-genetic factors to maintain remission of EAE as follows : A) the hierarchy of the encephalitogenic peptide itself, which means that the more dominant peptide possessed the capacity to develop acute EAE, the less relapse and re-induction of EAE were occurred, and B) CD4^+CD25^+ regulatory T cells (Treg) induced in the lymphnodes during remission phase, which is characterized by maintenance at high level and by content of the highly potent Treg expressing both CD69 and CD103 (=DP-Treg). This DP-Treg can keep the property of Treg due to the low expression of IL-6R, nevertheless it shares some signatures with Th17, a pathogenic cause of EAE and MS, and may conduct regulatory function in situ.
Furthermore, such regulation could be observed even under non-inflammatory condition, indicating the possibility of a potent and a safe autoimmune vaccination.
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