Innate acting memory Th1 cells modulate heterologous diseases.
Proc Natl Acad Sci U S A
; 121(24): e2312837121, 2024 Jun 11.
Article
en En
| MEDLINE
| ID: mdl-38838013
ABSTRACT
Through immune memory, infections have a lasting effect on the host. While memory cells enable accelerated and enhanced responses upon rechallenge with the same pathogen, their impact on susceptibility to unrelated diseases is unclear. We identify a subset of memory T helper 1 (Th1) cells termed innate acting memory T (TIA) cells that originate from a viral infection and produce IFN-γ with innate kinetics upon heterologous challenge in vivo. Activation of memory TIA cells is induced in response to IL-12 in combination with IL-18 or IL-33 but is TCR independent. Rapid IFN-γ production by memory TIA cells is protective in subsequent heterologous challenge with the bacterial pathogen Legionella pneumophila. In contrast, antigen-independent reactivation of CD4+ memory TIA cells accelerates disease onset in an autoimmune model of multiple sclerosis. Our findings demonstrate that memory Th1 cells can acquire additional TCR-independent functionality to mount rapid, innate-like responses that modulate susceptibility to heterologous challenges.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Interferón gamma
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Células TH1
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Inmunidad Innata
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Memoria Inmunológica
Límite:
Animals
Idioma:
En
Año:
2024
Tipo del documento:
Article