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Article: Generation and characterization of B7-H4/B7S1/B7x-deficient mice

TitleGeneration and characterization of B7-H4/B7S1/B7x-deficient mice
Authors
Issue Date2006
Citation
Molecular and Cellular Biology, 2006, v. 26, n. 17, p. 6403-6411 How to Cite?
AbstractMembers of the B7 family of cosignaling molecules regulate T-cell proliferation and effector functions by engaging cognate receptors on T cells. In vitro and in vivo blockade experiments indicated that B7-H4 (also known as B7S1 or B7x) inhibits proliferation, cytokine production, and cytotoxicity of T cells. B7-H4 binds to an unknown receptor(s) that is expressed on activated T cells. However, whether B7-H4 plays nonredundant immune regulatory roles in vivo has not been tested. We generated B7-H4-deficient mice to investigate the roles of B7-H4 during various immune reactions. Consistent with its inhibitory function in vitro, B7-H4-deficient mice mounted mildly augmented T-helper 1 (Th1) responses and displayed slightly lowered parasite burdens upon Leishmania major infection compared to the wild-type mice. However, the lack of B7-H4 did not affect hypersensitive inflammatory responses in the airway or skin that are induced by either Th1 or Th2 cells. Likewise, B7-H4-deficient mice developed normal cytotoxic T-lymphocyte reactions against viral infection. Thus, B7-H4 plays a negative regulatory role in vivo but the impact of B7-H4 deficiency is minimal. These results suggest that B7-H4 is one of multiple negative cosignaling molecules that collectively provide a fine-tuning mechanism for T-cell-mediated immune responses. Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/292583
ISSN
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 1.452
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSuh, Woong Kyung-
dc.contributor.authorWang, Seng-
dc.contributor.authorDuncan, Gordon S.-
dc.contributor.authorMiyazaki, Yoshiyuki-
dc.contributor.authorCates, Elizabeth-
dc.contributor.authorWalker, Tina-
dc.contributor.authorGajewska, Beata U.-
dc.contributor.authorDeenick, Elissa-
dc.contributor.authorDawicki, Wojciech-
dc.contributor.authorOkada, Hitoshi-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorItie, Annick-
dc.contributor.authorWatts, Tania H.-
dc.contributor.authorOhashi, Pamela S.-
dc.contributor.authorJordana, Manel-
dc.contributor.authorYoshida, Hiroki-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:56:47Z-
dc.date.available2020-11-17T14:56:47Z-
dc.date.issued2006-
dc.identifier.citationMolecular and Cellular Biology, 2006, v. 26, n. 17, p. 6403-6411-
dc.identifier.issn0270-7306-
dc.identifier.urihttp://hdl.handle.net/10722/292583-
dc.description.abstractMembers of the B7 family of cosignaling molecules regulate T-cell proliferation and effector functions by engaging cognate receptors on T cells. In vitro and in vivo blockade experiments indicated that B7-H4 (also known as B7S1 or B7x) inhibits proliferation, cytokine production, and cytotoxicity of T cells. B7-H4 binds to an unknown receptor(s) that is expressed on activated T cells. However, whether B7-H4 plays nonredundant immune regulatory roles in vivo has not been tested. We generated B7-H4-deficient mice to investigate the roles of B7-H4 during various immune reactions. Consistent with its inhibitory function in vitro, B7-H4-deficient mice mounted mildly augmented T-helper 1 (Th1) responses and displayed slightly lowered parasite burdens upon Leishmania major infection compared to the wild-type mice. However, the lack of B7-H4 did not affect hypersensitive inflammatory responses in the airway or skin that are induced by either Th1 or Th2 cells. Likewise, B7-H4-deficient mice developed normal cytotoxic T-lymphocyte reactions against viral infection. Thus, B7-H4 plays a negative regulatory role in vivo but the impact of B7-H4 deficiency is minimal. These results suggest that B7-H4 is one of multiple negative cosignaling molecules that collectively provide a fine-tuning mechanism for T-cell-mediated immune responses. Copyright © 2006, American Society for Microbiology. All Rights Reserved.-
dc.languageeng-
dc.relation.ispartofMolecular and Cellular Biology-
dc.titleGeneration and characterization of B7-H4/B7S1/B7x-deficient mice-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/MCB.00755-06-
dc.identifier.pmid16914726-
dc.identifier.pmcidPMC1592821-
dc.identifier.scopuseid_2-s2.0-33747786345-
dc.identifier.volume26-
dc.identifier.issue17-
dc.identifier.spage6403-
dc.identifier.epage6411-
dc.identifier.isiWOS:000239848800008-
dc.identifier.issnl0270-7306-

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