2017 Fiscal Year Final Research Report
A role of anti-inflammatory T cell subset on LUBAC-deficient autoinflammatory diseases
| Project/Area Number |
16K19106
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Experimental pathology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | 炎症 / T細胞 / Treg / 細胞死 / 自己免疫 / 自己炎症 / LUBAC / cpdm |
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| Outline of Final Research Achievements |
The linear ubiquitin chain assembly complex (LUBAC), which is one of ubiquitin ligase family, has critical roles to sufficient activation of canonical NF-κB signaling and regulation of cell death upon TNFR signaling activation. Spontaneous LUBAC-defective mice, called chronic proliferative dermatitis (cpdm) mice, show enhanced TNFα-induced cell death of the epithelial keratinocytes that induces chronic autoinflammation including severe dermatitis, in which innate immune cells have been recognized to dominantly involve in the inflammatory processes. In this study, we focused on the pathological roles of T cells, which have been ignored because they were rarely detected on the skin lesions. As a result, we concluded that T cells drive progression of the skin cell death and chronic inflammatory environment through a novel mechanism.
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| Free Research Field |
免疫学
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