Innate acting memory Th1 cells modulate heterologous diseases.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 38838013.
- Also identified by DOI 10.1073/pnas.2312837121 and PMC identifier 11181110.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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 (T<sub>IA</sub>) cells that originate from a viral infection and produce IFN-γ with innate kinetics upon heterologous challenge in vivo. Activation of memory T<sub>IA</sub> 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 T<sub>IA</sub> cells is protective in subsequent heterologous challenge with the bacterial pathogen <i>Legionella pneumophila</i>. In contrast, antigen-independent reactivation of CD4<sup>+</sup> memory T<sub>IA</sub> 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.
Medical subject headings
- Th1 Cells
- Immunologic Memory
- Immunity, Innate
- Interferon-gamma