| Autor: |
Rakebrandt, Nikolas, Yassini, Nima, Kolz, Anna, Schorer, Michelle, Lambert, Katharina, Goljat, Eva, Brull, Anna Estrada, Rauld, Celine, Balazs, Zsolt, Krauthammer, Michael, Carballido, José M., Peters, Anneli, Joller, Nicole |
| Předmět: |
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| Zdroj: |
Proceedings of the National Academy of Sciences of the United States of America; 6/11/2024, Vol. 121 Issue 24, p1-11, 22p |
| Abstrakt: |
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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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