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Article: Normal thymic selection, superantigen-induced deletion and Fas-mediated apoptosis of T cells in IL-2 receptor beta chain-deficient mice

TitleNormal thymic selection, superantigen-induced deletion and Fas-mediated apoptosis of T cells in IL-2 receptor beta chain-deficient mice
Authors
KeywordsFas-mediated apoptosis
Cytokine secretion
IL-2
Programmed cell death
Thymocyte selection
Issue Date1997
Citation
International Immunology, 1997, v. 9, n. 9, p. 1367-1374 How to Cite?
AbstractMice lacking the IL-2 receptor β chain (IL-PRβ) exhibit an autoimmune reaction characterized by generalized T cell activation, production of autoantibodies, myeloproliferation and severe anemia. T cells of IL-2Rβ(-/-) mice were examined to elucidate the mechanism responsible for their abnormal activation and to determine how such abnormal activation might affect other cell lineages. Elevated levels of IgG, IgE and autoantibodies in IL-PRβ(-/-) mice were found to be associated with activated CD4+ T cells which secreted elevated levels of IL-4. Thymocytes in IL-PRβ(-/-) mice showed normal negative and positive selection patterns when analyzed in transgenic mice bearing a TCR specific for HY antigen, suggesting that neither IL-2 nor IL-15 is essential for thymic selection. Peripheral T cells in IL-PRβ-deficient mice underwent normal programmed cell death in response to staphylococcal enterotoxin B superantigen, in contrast to cells from mice deficient for either IL-2 or IL-2Rα. Activated T cells in IL-SRβ-deficient mice expressed normal levels of Fas antigen and underwent normal apoptosis in response to induction with anti-Fas mAb. Thus, the accumulation of activated T cells in IL-2Rβ(-/-) mice does not appear to be derived from abnormalities in either thymic selection or Fas-mediated apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/291407
ISSN
2023 Impact Factor: 4.8
2023 SCImago Journal Rankings: 1.427
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSuzuki, Haruhiko-
dc.contributor.authorHayakawa, Akemi-
dc.contributor.authorBouchard, Denis-
dc.contributor.authorNakashima, Izumi-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:18Z-
dc.date.available2020-11-17T14:54:18Z-
dc.date.issued1997-
dc.identifier.citationInternational Immunology, 1997, v. 9, n. 9, p. 1367-1374-
dc.identifier.issn0953-8178-
dc.identifier.urihttp://hdl.handle.net/10722/291407-
dc.description.abstractMice lacking the IL-2 receptor β chain (IL-PRβ) exhibit an autoimmune reaction characterized by generalized T cell activation, production of autoantibodies, myeloproliferation and severe anemia. T cells of IL-2Rβ(-/-) mice were examined to elucidate the mechanism responsible for their abnormal activation and to determine how such abnormal activation might affect other cell lineages. Elevated levels of IgG, IgE and autoantibodies in IL-PRβ(-/-) mice were found to be associated with activated CD4+ T cells which secreted elevated levels of IL-4. Thymocytes in IL-PRβ(-/-) mice showed normal negative and positive selection patterns when analyzed in transgenic mice bearing a TCR specific for HY antigen, suggesting that neither IL-2 nor IL-15 is essential for thymic selection. Peripheral T cells in IL-PRβ-deficient mice underwent normal programmed cell death in response to staphylococcal enterotoxin B superantigen, in contrast to cells from mice deficient for either IL-2 or IL-2Rα. Activated T cells in IL-SRβ-deficient mice expressed normal levels of Fas antigen and underwent normal apoptosis in response to induction with anti-Fas mAb. Thus, the accumulation of activated T cells in IL-2Rβ(-/-) mice does not appear to be derived from abnormalities in either thymic selection or Fas-mediated apoptosis.-
dc.languageeng-
dc.relation.ispartofInternational Immunology-
dc.subjectFas-mediated apoptosis-
dc.subjectCytokine secretion-
dc.subjectIL-2-
dc.subjectProgrammed cell death-
dc.subjectThymocyte selection-
dc.titleNormal thymic selection, superantigen-induced deletion and Fas-mediated apoptosis of T cells in IL-2 receptor beta chain-deficient mice-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/intimm/9.9.1367-
dc.identifier.pmid9310840-
dc.identifier.scopuseid_2-s2.0-0030861424-
dc.identifier.volume9-
dc.identifier.issue9-
dc.identifier.spage1367-
dc.identifier.epage1374-
dc.identifier.isiWOS:A1997XX03500016-
dc.identifier.issnl0953-8178-

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