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PMID:12925852
Citation |
Suh, WK, Gajewska, BU, Okada, H, Gronski, MA, Bertram, EM, Dawicki, W, Duncan, GS, Bukczynski, J, Plyte, S, Elia, A, Wakeham, A, Itie, A, Chung, S, Da Costa, J, Arya, S, Horan, T, Campbell, P, Gaida, K, Ohashi, PS, Watts, TH, Yoshinaga, SK, Bray, MR, Jordana, M and Mak, TW (2003) The B7 family member B7-H3 preferentially down-regulates T helper type 1-mediated immune responses. Nat. Immunol. 4:899-906 |
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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. |
Links |
PubMed Online version:10.1038/ni967 |
Keywords |
Animals; Antigens, CD80/biosynthesis; Antigens, CD80/immunology; Autoantibodies/immunology; Autoantibodies/metabolism; B7 Antigens; Dendritic Cells/immunology; Dendritic Cells/metabolism; Down-Regulation/immunology; Encephalomyelitis, Autoimmune, Experimental/immunology; Encephalomyelitis, Autoimmune, Experimental/pathology; Flow Cytometry; Interferon-gamma/immunology; Interleukin-4/immunology; Lymphocyte Activation/immunology; Lymphocytic choriomeningitis virus/immunology; Mice; Mice, Inbred C57BL; Mice, Knockout; Orthomyxoviridae/immunology; Receptors, Antigen, T-Cell/immunology; Th1 Cells/immunology; Vesicular stomatitis Indiana virus/immunology |
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Significance
Annotations
Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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