Helminth-induced regulation of T-cell transfer colitis requires intact and regulated T cell Stat6 signaling in mice.
Eur J Immunol
; 51(2): 433-444, 2021 02.
Article
em En
| MEDLINE
| ID: mdl-33067820
ABSTRACT
Infection with parasitic worms (helminths) alters host immune responses and can inhibit pathogenic inflammation. Helminth infection promotes a strong Th2 and T regulatory response while suppressing Th1 and Th17 function. Th2 responses are largely dependent on transcriptional programs directed by Stat6-signaling. We examined the importance of intact T cell Stat6 signaling on helminth-induced suppression of murine colitis that results from T cell transfer into immune-deficient mice. Colonization with the intestinal nematode Heligmosomoides polygyrus bakeri resolves WT T cell transfer colitis. However, if the transferred T cells lack intact Stat6 then helminth exposure failed to attenuate colitis or suppress MLN T cell IFN-γ or IL17 production. Loss of Stat6 signaling resulted in decreased IL10 and increased IFN-γ co-expression by IL-17+ T cells. We also transferred T cells from mice with constitutive T cell expression of activated Stat6 (Stat6VT). These mice developed a severe eosinophilic colitis that also was not attenuated by helminth infection. These results show that T cell expression of intact but regulated Stat6 signaling is required for helminth infection-associated regulation of pathogenic intestinal inflammation.
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Base de dados:
MEDLINE
Assunto principal:
Nematospiroides dubius
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Transdução de Sinais
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Infecções por Strongylida
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Linfócitos T Reguladores
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Colite
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Fator de Transcrição STAT6
Limite:
Animals
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article