A Novel Pathway of Platelet Activation in ACS Mediated by LL-37 Immunoglobulin G Autoantibody Immune Complexes.
Dimayuga. Paul C PC; Chyu. Kuang-Yuh KY; Zhao. Xiaoning X; Zhou. Jianchang J; Lio. Nicole Wai Man NWM; Chernomordik. Fernando F; Berman. Daniel D; Shah. Prediman K PK; Cercek. Bojan B
Key Findings
- LL‑37 IgG antibodies did not correlate with coronary calcium scores
- People who later suffered a myocardial infarction had higher baseline LL‑37 IgG levels
- During acute coronary syndrome, lower LL‑37 IgG was tied to more LL‑37 immune complexes that activated platelets via FcγRIIa
Practical Outcomes
- For biohackers, this research suggests LL‑37 antibody levels might serve as a future biomarker for heart risk, but there are no current protocols or supplements to modify it. Monitoring LL‑37 isn’t actionable yet, and no dosage or intervention guidance is provided.
Summary
The study found that a protein called LL‑37, which can trigger immune reactions, shows different antibody patterns in people who later have heart attacks versus those with acute coronary events. Higher LL‑37 antibodies were seen before a heart attack, while lower levels during an acute event were linked to more immune complexes that can activate platelets, potentially worsening clotting.
Abstract
The cathelicidin antimicrobial peptide LL-37 is a self-antigen in neutrophil extracellular traps that provokes autoantibody responses in autoimmune/autoinflammatory conditions. LL-37 immunoglobulin (Ig) G autoantibody levels were measured in subjects with and without atherosclerotic cardiovascular disease assessed using the coronary artery calcium score, in patients who had a future myocardial infarction and in a cohort of acute coronary syndrome (ACS) patients. LL-37 IgG levels were not associated with coronary artery calcium score, but future myocardial infarction patients had significantly higher LL-37 IgG at baseline. Reduced LL-37 IgG in ACS was associated with increased LL-37 IgG-immune complex. ACS plasma increased activated CD62P+ platelets from healthy donors mediated in part by LL-37 IgG-immune complexes and platelet Fc gamma receptor 2a.
Study Information
pubmed
2024
2024-07-22T00:00:00.000Z
10.1016/j.jacbts.2024.04.012
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