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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
Issue Date2003
Citation
Nature Immunology, 2003, v. 4, n. 9, p. 899-906 How to Cite?
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
2023 Impact Factor: 27.7
2023 SCImago Journal Rankings: 11.274
ISI Accession Number ID

 

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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