The B7 family member B7-H3 preferentially down-regulates T helper type 1–mediated immune responses
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- 17 August 2003
- journal article
- research article
- Published by Springer Nature in Nature Immunology
- Vol. 4 (9) , 899-906
- https://doi.org/10.1038/ni967
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-γ 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.Keywords
This publication has 46 references indexed in Scilit:
- BTLA is a lymphocyte inhibitory receptor with similarities to CTLA-4 and PD-1Nature Immunology, 2003
- The B7 Family of Ligands and Its Receptors: New Pathways for Costimulation and Inhibition of Immune ResponsesAnnual Review of Immunology, 2002
- PD-1:PD-L inhibitory pathway affects both CD4+ and CD8+ T cells and is overcome by IL-2European Journal of Immunology, 2002
- The B7–CD28 superfamilyNature Reviews Immunology, 2002
- Autoimmune Dilated Cardiomyopathy in PD-1 Receptor-Deficient MiceScience, 2001
- Duration of TCR Stimulation Determines Costimulatory Requirement of T CellsImmunity, 1996
- CD28/B7 SYSTEM OF T CELL COSTIMULATIONAnnual Review of Immunology, 1996
- Lymphoproliferative Disorders with Early Lethality in Mice Deficient in Ctla-4Science, 1995
- Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan tissue destruction, revealing a critical negative regulatory role of CTLA-4Immunity, 1995
- Generation of large numbers of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor.The Journal of Experimental Medicine, 1992