ArticleClinical & translational immunology2026
Adaptive immune response to the autoantigen LL-37 differentiates atherosclerotic cardiovascular disease phenotypes.
Article in Clinical & translational 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
Atherosclerosis is the common underlying pathology in atherosclerotic cardiovascular disease (ASCVD) phenotypes of myocardial infarction (MI), stroke or peripheral artery disease (PAD). Single immune cell profiling of atherosclerotic plaques demonstrates a site-specific immune profile associated with the ASCVD phenotype, and LL-37 is a reported autoantigen in atherosclerosis. Objective: To investigate whether the immune response to LL-37 would be common among different ASCVD phenotypes. Methods: Peripheral blood mononuclear cells (PBMCs) and plasma were collected from stable ASCVD patients enrolled within 12 months after MI or stroke or diagnosed with PAD. A subgroup of post-acute patients provided PBMCs at follow-up (14.7 ± 3.6 months). T-cell response to LL-37 was profiled using activation-induced markers. LL-37 IgG, immune complex (IC) levels and subclass were evaluated with ELISA. LDL is a reported binding partner of LL-37 in plasma. Therefore, cross-reactivity of LL-37 IgG-ICs with native LL-37 or LL-37 complexed with LDL (LL-37_LDL) was assessed using immune depletion. Results: LL-37 provokes increased CD4 Conclusion: LL-37 antigen specific profiling of immune response may differentiate various ASCVD phenotypes and provide mechanistic insight in pathophysiology.
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