ArticleImmunology2026
MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.
Article in Immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
Abstract
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) signalling is pivotal in the pathogenesis of MS and EAE; however, its specific contributions across various cell types in the context of these conditions remain inadequately understood. In this study, we reanalysed single-cell RNA sequencing data from MS patients and revealed significant upregulation of MYD88 in DCs and CD4
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