ArticleCellular & molecular immunology2026
A cholinergic checkpoint controls autoantibody selection via somatic hypermutation in lupus germinal centers.
Article in Cellular & molecular immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Systemic lupus erythematosus (SLE) pathogenesis involves the dysregulated production of mutated, high-affinity autoantibodies, a process primarily orchestrated within germinal centers (GCs). However, the precise regulatory mechanisms governing the GC-mediated generation of autoantibodies in SLE remain elusive. In lupus-prone NZM2328 mice, we observed progressive accumulation of immunoglobulin heavy chain (Igh) mutations in GC B cells during disease progression, accompanied by increased clonotype sharing between GC B cells and plasmablast/plasma cell populations. Immunophenotyping revealed that follicular helper T cells (Tfh) express high levels of choline acetyltransferase (ChAT), a key enzyme for acetylcholine (ACh) biosynthesis. Notably, ChAT expression is predominantly upregulated in Tfh cells during the induction of systemic autoimmunity. Furthermore, sustained ChAT expression in Tfh cells relies on autocrine IL-21. Conditional ablation of ChAT in CD4
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