A T cell-intrinsic function for NF-κB RelB in experimental autoimmune encephalomyelitis

Area of Science:

• Immunology
• Molecular Biology
• Neuroscience

Background:

• Nuclear factor-kappa B (NF-κB) transcription factors regulate immune responses.
• The alternative NF-κB pathway, involving RelB and NF-κB2, is linked to T cell activation, but its specific role is unclear.

Purpose of the Study:

• To investigate the role of RelB in T cell development and function, particularly in autoimmune disease models.
• To determine if RelB in T cells contributes to the pathogenesis of experimental autoimmune encephalomyelitis (EAE).

Main Methods:

• Conditional ablation of RelB in T cells of mice.
• Assessment of T cell homeostasis, activation, proliferation, and differentiation.
• Evaluation of T cell-induced autoimmune colitis and EAE severity.

Main Results:

• RelB deficiency in T cells did not affect T cell development, homeostasis, activation, or polarization.
• RelB-deficient T cells did not alter the induction of autoimmune colitis.
• Mice with RelB-deficient T cells showed reduced EAE severity, linked to decreased GM-CSF expression in the CNS.

Conclusions:

• RelB plays a specific role in the pathogenic function of T cells during EAE, not in general T cell biology.
• RelB emerges as a potential therapeutic target for multiple sclerosis (MS).