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Article: The B7 family member B7-H3 preferentially down-regulates T helper type 1-mediated immune responses

TitleThe B7 family member B7-H3 preferentially down-regulates T helper type 1-mediated immune responses
Authors
Suh, Woong KyungGajewska, Beata U.Okada, HitoshiGronski, Matthew A.Bertram, Edward M.Dawicki, WojciechDuncan, Gordon S.Bukczynski, JacobPlyte, SuzanneElia, AndrewWakeham, AndrewItie, AnnickChung, StephenDa Costa, JoanArya, SudhaHoran, TomCampbell, PaulineGaida, KevinOhashi, Pamela S.Watts, Tania H.Yoshinaga, Steven K.Bray, Mark R.Jordana, ManelMak, Tak W.
Issue Date2003
Citation
Nature Immunology, 2003, v. 4, n. 9, p. 899-906 How to Cite?
DOI: http://dx.doi.org/10.1038/ni967
AbstractWe 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.
Persistent Identifierhttp://hdl.handle.net/10722/291654
ISSN
1529-2908
2021 Impact Factor: 31.250
2020 SCImago Journal Rankings: 9.074
ISI Accession Number ID
WOS:000185002200017

 

DC FieldValueLanguage
dc.contributor.authorSuh, Woong Kyung-
dc.contributor.authorGajewska, Beata U.-
dc.contributor.authorOkada, Hitoshi-
dc.contributor.authorGronski, Matthew A.-
dc.contributor.authorBertram, Edward M.-
dc.contributor.authorDawicki, Wojciech-
dc.contributor.authorDuncan, Gordon S.-
dc.contributor.authorBukczynski, Jacob-
dc.contributor.authorPlyte, Suzanne-
dc.contributor.authorElia, Andrew-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorItie, Annick-
dc.contributor.authorChung, Stephen-
dc.contributor.authorDa Costa, Joan-
dc.contributor.authorArya, Sudha-
dc.contributor.authorHoran, Tom-
dc.contributor.authorCampbell, Pauline-
dc.contributor.authorGaida, Kevin-
dc.contributor.authorOhashi, Pamela S.-
dc.contributor.authorWatts, Tania H.-
dc.contributor.authorYoshinaga, Steven K.-
dc.contributor.authorBray, Mark R.-
dc.contributor.authorJordana, Manel-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:50Z-
dc.date.available2020-11-17T14:54:50Z-
dc.date.issued2003-
dc.identifier.citationNature Immunology, 2003, v. 4, n. 9, p. 899-906-
dc.identifier.issn1529-2908-
dc.identifier.urihttp://hdl.handle.net/10722/291654-
dc.description.abstractWe 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.-
dc.languageeng-
dc.relation.ispartofNature Immunology-
dc.titleThe B7 family member B7-H3 preferentially down-regulates T helper type 1-mediated immune responses-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/ni967-
dc.identifier.pmid12925852-
dc.identifier.scopuseid_2-s2.0-0041381300-
dc.identifier.volume4-
dc.identifier.issue9-
dc.identifier.spage899-
dc.identifier.epage906-
dc.identifier.isiWOS:000185002200017-
dc.identifier.f10001015555-
dc.identifier.issnl1529-2908-

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