2017 Fiscal Year Final Research Report
The role of phosphatase regulatory subunit G5PR in the differentiation of autoantibody producing cells from B1 cells
| Project/Area Number |
15K09532
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Nara Medical University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 自己抗体 / G5PR / JNK / 形質細胞分化 / 胚中心 |
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| Outline of Final Research Achievements |
Self-reactive IgG autoantibodies are hallmark of autoimmune diseases, and often cause tissue damage. Although B1 cells, which naturally produce self-reactive IgM, are thought to be the precursor cells of IgG autoantibody-secreting cells in autoimmune diseases, the underlying mechanisms of differentiation process remain poorly understood. Here, we showed that activated B1 cells from autoimmune-prone mice migrated into germinal center of secondary lymphoid organ and then underwent a process of class switch recombination to IgG and differentiation into antibody-producing plasma cells. In addition, stimulation of TLR ligand and various cytokines in the germinal center like environment induced G5PR expression in B1 cells, leading to JNK suppression and plasma cell differentiation. These results suggest that regulation of G5PR/JNK pathway might be a potential therapeutic target for autoimmune diseases.
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| Free Research Field |
免疫学
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