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Related Concept Videos

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Innate acting memory Th1 cells modulate heterologous diseases.

Nikolas Rakebrandt1, Nima Yassini1,2, Anna Kolz3

  • 1Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland.

Proceedings of the National Academy of Sciences of the United States of America
|June 5, 2024
PubMed
Summary
This summary is machine-generated.

Innate acting memory T (TIA) cells, originating from viral infections, mount rapid, innate-like responses. These TIA cells can protect against subsequent bacterial infections but may worsen autoimmune diseases.

Keywords:
T helper cellsadaptive immunityautoimmunityinfectioninnate

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Area of Science:

  • Immunology
  • Infectious Disease
  • Autoimmunity

Background:

  • Immune memory typically enhances responses to familiar pathogens.
  • The effect of immune memory on susceptibility to unrelated diseases remains largely unknown.
  • T helper 1 (Th1) cells are crucial for cell-mediated immunity.

Purpose of the Study:

  • To investigate the function of memory T helper 1 cells beyond specific antigen recall.
  • To identify novel subsets of memory T cells with distinct activation pathways.
  • To understand how prior infections influence susceptibility to heterologous challenges.

Main Methods:

  • Identification and characterization of a novel memory T cell subset, termed innate acting memory T (TIA) cells.
  • In vivo analysis of TIA cell activation via cytokine signaling (IL-12, IL-18, IL-33) independent of T cell receptor (TCR).
  • Assessment of TIA cell function in heterologous challenge models, including bacterial infection (*Legionella pneumophila*) and an autoimmune disease model (multiple sclerosis).

Main Results:

  • A subset of memory Th1 cells, designated TIA cells, was identified, originating from viral infections.
  • TIA cells produce interferon-gamma (IFN-γ) rapidly upon stimulation with specific cytokines (IL-12/IL-18 or IL-12/IL-33), independent of TCR signaling.
  • Rapid IFN-γ production by TIA cells conferred protection against *Legionella pneumophila* infection.
  • Antigen-independent reactivation of CD4+ TIA cells exacerbated disease in a multiple sclerosis model.

Conclusions:

  • Memory Th1 cells can develop TCR-independent, innate-like effector functions.
  • These TIA cells represent a critical link between adaptive memory and innate immunity.
  • TIA cell activity has dual effects, offering protection against certain infections while potentially promoting autoimmunity.