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Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • CD4+ conventional T cells (Tconv) are key players in cancer and autoimmunity.
  • The NF-κB signaling pathway is involved in Tconv biology, but subunit-specific roles are unclear.

Purpose of the Study:

  • To investigate the distinct roles of NF-κB subunits RelA and c-Rel in Tconv function.
  • To determine the impact of these subunits in autoimmune and cancer contexts.

Main Methods:

  • Utilized mouse models with targeted gene deletion of RelA and c-Rel in Tconv.
  • Analyzed Tconv activation, cytokine production, and lineage polarization (TH17).
  • Assessed disease outcomes in models of multiple sclerosis and cancer, including response to PD-1 blockade therapy.

Main Results:

  • RelA deficiency protected mice from neuroinflammation, linked to defective TH17 cell differentiation.
  • c-Rel deficiency in Tconv impaired anti-tumor immunity and response to PD-1 blockade.
  • RelA regulates Tconv activation and cytokine production, while c-Rel is critical for anti-tumor responses.

Conclusions:

  • Canonical NF-κB subunits RelA and c-Rel have distinct, context-dependent functions in Tconv.
  • RelA is important for Tconv-mediated autoimmunity, whereas c-Rel is crucial for anti-tumor immunity.
  • Findings support the development of subunit-targeted immunotherapies for cancer and autoimmune diseases.