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The B7 family member B7-H3 preferentially down-regulates T helper type 1-mediated immune responses |
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| Authors: | Suh Woong-Kyung Gajewska Beata U Okada Hitoshi Gronski Matthew A Bertram Edward M Dawicki Wojciech Duncan Gordon S Bukczynski Jacob Plyte Suzanne Elia Andrew Wakeham Andrew Itie Annick Chung Stephen Da Costa Joan Arya Sudha Horan Tom Campbell Pauline Gaida Kevin Ohashi Pamela S Watts Tania H Yoshinaga Steven K Bray Mark R Jordana Manel Mak Tak W |
| Affiliation: | Advanced Medical Discovery Institute, Ontario Cancer Institute, and Department of Medical Biophysics, University of Toronto, 620 University Avenue, Toronto, Ontario M5G 2C1, Canada. wsuh@uhnres.utoronto.ca |
| Abstract: | We investigated the in vivo function of the B7 family member B7-H3 (also known as B7RP-2) by gene targeting. B7-H3 inhibited T cell proliferation mediated by antibody to T cell receptor or allogeneic antigen-presenting cells. B7-H3-deficient mice developed more severe airway inflammation than did wild-type mice in conditions in which T helper cells differentiated toward type 1 (T(H)1) rather than type 2 (T(H)2). B7-H3 expression was consistently enhanced by interferon-gamma but suppressed by interleukin 4 in dendritic cells. B7-H3-deficient mice developed experimental autoimmune encephalomyelitis several days earlier than their wild-type littermates, and accumulated higher concentrations of autoantibodies to DNA. Thus, B7-H3 is a negative regulator that preferentially affects T(H)1 responses. |
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