期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 115, 期 3, 页码 711-717出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200522982
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资金
- NICHD NIH HHS [R01 HD037104] Funding Source: Medline
- NIDDK NIH HHS [R01 DK058897] Funding Source: Medline
Herpesvirus entry mediator (HVEM), a TNF receptor superfamily member, has been previously described as a T cell costimulatory receptor. Surprisingly, HVEM-/- T cells showed enhanced responses to in vitro concanavalin A (ConA) stimulation when compared with WT T cells. Consistent with these findings, HVEM-/- mice exhibited increased morbidity and mortality as compared with WT mice in a model of ConA-mediated T cell-dependent autoimmune hepatitis. HVEM-/- mice produced higher levels of multiple cytokines, which were dependent on the presence of CD4(+)T cells. Furthermore, HVEM-/- mice were more susceptible to MOG peptide-induced experimental autoimmune encephalopathy, and they showed increased T cell proliferation and cytokine production in response to antigen-specific challenge. Taken together, our data revealed an unexpected regulatory role of HVEM in T cell-mediated immune responses and autoimmune diseases.
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