Nature immunology · 2003
The B7 family member B7-H3 preferentially down-regulates T helper type 1-mediated immune responses.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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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
Аннотация
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.
Предметные рубрики MeSH
AnimalsAutoantibodiesB7 AntigensB7-1 AntigenDendritic CellsDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryInterferon-gammaInterleukin-4Lymphocyte ActivationLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, KnockoutOrthomyxoviridaeReceptors, Antigen, T-CellTh1 CellsVesicular stomatitis Indiana virus