Activity: Talk/lecture or presentation › Presentation
Description
Dendritic cells (DCs) play a central role in both the development and maintenance of adaptive immunity by their ability to prime and regulate T cell function. These interactions between DCs and T cells are crucial to the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Myeloid differentiation primary response protein 88 (MyD88) signaling is pivotal in the pathogenesis of MS and EAE. We found significant upregulation of MYD88 in DCs and CD4+ T cells isolated from PBMCs of patients with MS. Notably, the absence of Myd88 in DCs resulted in significantly reduced interactions with T cell clusters. Mechanistically, MyD88-/- DCs exhibited impaired maturation and a reduced production of pro-inflammatory cytokines, which are essential for promoting Th1 and Th17 cell differentiation. Importantly, the absence of MyD88 in DCs ameliorated EAE symptom by modulating peripheral T cell responses. Our findings suggest that MyD88 is essential for the priming of inflammatory T cells and the activation of DCs, and their interactions with T cells, underscoring its role in neuroinflammation.
Period
14 Nov 2025
Held at
Department of Infectious Diseases and Public Health