Parasite-induced TH1 cells and intestinal dysbiosis cooperate in IFN-γ-dependent elimination of Paneth cells.
Nat Immunol
; 14(2): 136-42, 2013 Feb.
Article
em En
| MEDLINE
| ID: mdl-23263554
ABSTRACT
Activation of Toll-like receptors (TLRs) by pathogens triggers cytokine production and T cell activation, immune defense mechanisms that are linked to immunopathology. Here we show that IFN-γ production by CD4(+) T(H)1 cells during mucosal responses to the protozoan parasite Toxoplasma gondii resulted in dysbiosis and the elimination of Paneth cells. Paneth cell death led to loss of antimicrobial peptides and occurred in conjunction with uncontrolled expansion of the Enterobacteriaceae family of Gram-negative bacteria. The expanded intestinal bacteria were required for the parasite-induced intestinal pathology. The investigation of cell type-specific factors regulating T(H)1 polarization during T. gondii infection identified the T cell-intrinsic TLR pathway as a major regulator of IFN-γ production in CD4(+) T cells responsible for Paneth cell death, dysbiosis and intestinal immunopathology.
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Base de dados:
MEDLINE
Assunto principal:
Toxoplasma
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Transdução de Sinais
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Toxoplasmose Animal
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Células Th1
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Celulas de Paneth
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Enterobacteriaceae
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Infecções por Enterobacteriaceae
Idioma:
En
Ano de publicação:
2013
Tipo de documento:
Article