ArticleMedicine2026
Genetically proxied circulating PD-1/PD-L1 levels and broadly defined myocarditis: A bidirectional Mendelian randomization study with exploratory lipidomic analyses.
Article in Medicine, 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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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.
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2 authors.
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Abstract
Myocarditis is an inflammatory myocardial disease with potentially severe outcomes. Programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) regulate immune tolerance, but the association between lifelong genetically proxied circulating PD-1/PD-L1 levels and broadly defined myocarditis remains uncertain. We investigated these associations and explored related plasma lipid species. We conducted bidirectional 2-sample Mendelian randomization using proteomic genome-wide association data from the UK Biobank Pharma Proteomics Project and INTERVAL. FinnGen Release 10 was the primary broadly defined myocarditis outcome, and an independent myocarditis genome-wide association study (GCST90018882) provided outcome-level validation. Complementary estimators, heterogeneity and pleiotropy diagnostics, influence analyses, MR-RAPS, and supportive meta-analyses were performed. Associations with 179 plasma lipid species were examined in exploratory analyses. Higher genetically proxied circulating PD-L1 was inversely associated with broadly defined myocarditis in UKB-PPP (odds ratio [OR] 0.834, 95% confidence interval [CI] 0.698-0.995; P = .0441), and the independent INTERVAL analysis yielded a concordant inverse estimate (OR 0.619, 95% CI: 0.434-0.883; P = .0083); no clear association was observed for PD-1. The MR-RAPS estimate retained the inverse direction; estimates against the independent broadly defined myocarditis dataset were also inverse, and supportive meta-analyses across protein and outcome sources yielded inverse pooled estimates. Reverse MR did not support effects of broadly defined myocarditis liability on circulating PD-1 or PD-L1. Exploratory lipid analyses identified nominal associations requiring confirmation. Higher genetically proxied circulating PD-L1 may be associated with a lower risk of broadly defined myocarditis, supporting further investigation of PD-L1-related immune regulation. These findings do not directly estimate the effects of pharmacologic PD-1/PD-L1 blockade. The lipid findings are hypothesis-generating.
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