| Literature DB >> 12925852 |
Woong-Kyung Suh1, Beata U Gajewska, Hitoshi Okada, Matthew A Gronski, Edward M Bertram, Wojciech Dawicki, Gordon S Duncan, Jacob Bukczynski, Suzanne Plyte, Andrew Elia, Andrew Wakeham, Annick Itie, Stephen Chung, Joan Da Costa, Sudha Arya, Tom Horan, Pauline Campbell, Kevin Gaida, Pamela S Ohashi, Tania H Watts, Steven K Yoshinaga, Mark R Bray, Manel Jordana, Tak W Mak.
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.Entities:
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Year: 2003 PMID： 12925852 DOI： 10.1038/ni967
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606