Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 711-717 |
| Number of pages | 7 |
| Journal | Journal of Clinical Investigation |
| Volume | 115 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 1 2005 |
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- Medicine(all)
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The role of herpesvirus entry mediator as a negative regulator of T cell-mediated responses. / Wang, Yang; Subudhi, Sumit K.; Anders, Robert A.; Lo, James; Sun, Yonglian; Blink, Sarah; Wang, Yugang; Wang, Jing; Liu, Xiaojuan; Mink, Karin; Degrandi, Daniel; Pfeffer, Klaus; Fu, Yang Xin.
In: Journal of Clinical Investigation, Vol. 115, No. 3, 01.03.2005, p. 711-717.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The role of herpesvirus entry mediator as a negative regulator of T cell-mediated responses
AU - Wang, Yang
AU - Subudhi, Sumit K.
AU - Anders, Robert A.
AU - Lo, James
AU - Sun, Yonglian
AU - Blink, Sarah
AU - Wang, Yugang
AU - Wang, Jing
AU - Liu, Xiaojuan
AU - Mink, Karin
AU - Degrandi, Daniel
AU - Pfeffer, Klaus
AU - Fu, Yang Xin
PY - 2005/3/1
Y1 - 2005/3/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=20044389839&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=20044389839&partnerID=8YFLogxK
U2 - 10.1172/JCI200522982
DO - 10.1172/JCI200522982
M3 - Article
C2 - 15696194
AN - SCOPUS:20044389839
VL - 115
SP - 711
EP - 717
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
SN - 0021-9738
IS - 3
ER -