Please use this identifier to cite or link to this item: https://ninho.inca.gov.br/jspui/handle/123456789/12118
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dc.contributor.authorViola, Joao Paulo de Biaso-
dc.contributor.authorKiani, Alexander-
dc.contributor.authorViola, Patricia Torres Bozza-
dc.contributor.authorRao, Anjana-
dc.date.accessioned2022-12-28T16:55:56Z-
dc.date.available2022-12-28T16:55:56Z-
dc.date.issued1998-04-
dc.identifier.issn1528-0020-
dc.identifier.urihttps://ninho.inca.gov.br/jspui/handle/123456789/12118-
dc.description.abstractTranscription factors of the NFAT (nuclear factor of activated T cells) family regulate the expression of many genes encoding immunoregulatory cytokines and cell surface proteins during the immune response. The NFAT protein NFAT1 (NFATp) is expressed and functional in T cells, B cells, mast cells, and natural killer cells. Here we report a detailed analysis of the enhanced eosinophil responses of NFAT1-deficient mice, observed in an in vivo model of allergic inflammation. In addition to the pleural eosinophilia described previously, NFAT1-/- mice that have been sensitized with antigen display a significant increase, relative to wild-type mice, in the numbers of eosinophils in bone marrow and peripheral blood. After restimulation with antigen in vitro, antigen-responsive T cells from the draining lymph nodes of NFAT1-/- mice show increased expression of mRNA encoding the Th2 cytokines interleukin-4 (IL-4), IL-5, and IL-13. Consistent with this finding, there is a pronounced increase in the levels of IL-5 and IL-13 in the pleural cavities of sensitized NFAT1-/- mice after allergen challenge in vivo. Furthermore, development of eosinophilia depends on overexpression of IL-4 and IL-5, because it is strongly inhibited by administration of neutralizing antibodies to either of these cytokines. These results indicate that NFAT1-deficient mice are prone to develop a classically allergic phenotype characterized by eosinophilia and increased production of Th2 cytokines. Thus, the presence of NFAT1 might inhibit the allergic response, perhaps by interfering with the development of Th2 immune responses, and the lack or dysfunction of NFAT1 could potentially underlie certain cases of atopic disease.pt_BR
dc.subjectEosinófilospt_BR
dc.subjectEosinophilspt_BR
dc.subjectFatores de Transcrição NFATCpt_BR
dc.subjectNFATC Transcription Factorspt_BR
dc.subjectInterleucina-4pt_BR
dc.subjectInterleukin-4pt_BR
dc.subjectInterleucina-5pt_BR
dc.subjectInterleukin-5pt_BR
dc.subjectCitocinaspt_BR
dc.subjectCytokinespt_BR
dc.subjectArginasept_BR
dc.titleRegulation of allergic inflammation and eosinophil recruitment in mice lacking the transcription factor NFAT1: role of interleukin-4 (IL-4) and IL-5pt_BR
dc.TypeArticlept_BR
Appears in Collections:Artigos de Periódicos da Pesquisa Experimental e Translacional

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