학술논문
The B7 family member B7-H3 preferentially down-regulates T helper type 1-mediated immune responses.
Document Type
Article
Author
Suh, Woong-kyung; Gajewska, Beata U.; Hitoshi Okada; Gronski, Matthew A.; Bertram, Edward M.; Dawicki, Wojciech; Duncan, Gordon S.; Jacob Bukczynski; Plyte, Suzanne; Elia, Andrew; Wakeham, Andrew; Itie, Annick; Stephen Chung; da Costa, Joan; Arya, Sudha; Horan, Tom; Campbell, Pauline; Gaida, Kevin; Ohashi, Pamela S.; Watts, Tania H.
Source
Subject
*GENE targeting
*T cells
*CELL proliferation
*IMMUNE response
*INTERLEUKINS
*INTERFERONS
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Language
ISSN
1529-2908
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 (TH1) rather than type 2 (TH2). B7-H3 expression was consistently enhanced by interferon-? 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 TH1 responses. [ABSTRACT FROM AUTHOR]