{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T11:52:58Z","timestamp":1792929178099,"version":"4.5.0"},"reference-count":154,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"83","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Immunol."],"published-print":{"date-parts":[[2023,5,26]]},"abstract":"<jats:p>\n            Rare immune-mediated cardiac tissue inflammation can occur after vaccination, including after SARS-CoV-2 mRNA vaccines. However, the underlying immune cellular and molecular mechanisms driving this pathology remain poorly understood. Here, we investigated a cohort of patients who developed myocarditis and\/or pericarditis with elevated troponin, B-type natriuretic peptide, and C-reactive protein levels as well as cardiac imaging abnormalities shortly after SARS-CoV-2 mRNA vaccination. Contrary to early hypotheses, patients did not demonstrate features of hypersensitivity myocarditis, nor did they have exaggerated SARS-CoV-2\u2013specific or neutralizing antibody responses consistent with a hyperimmune humoral mechanism. We additionally found no evidence of cardiac-targeted autoantibodies. Instead, unbiased systematic immune serum profiling revealed elevations in circulating interleukins (IL-1\u03b2, IL-1RA, and IL-15), chemokines (CCL4, CXCL1, and CXCL10), and matrix metalloproteases (MMP1, MMP8, MMP9, and TIMP1). Subsequent deep immune profiling using single-cell RNA and repertoire sequencing of peripheral blood mononuclear cells during acute disease revealed expansion of activated CXCR3\n            <jats:sup>+<\/jats:sup>\n            cytotoxic T cells and NK cells, both phenotypically resembling cytokine-driven killer cells. In addition, patients displayed signatures of inflammatory and profibrotic CCR2\n            <jats:sup>+<\/jats:sup>\n            CD163\n            <jats:sup>+<\/jats:sup>\n            monocytes, coupled with elevated serum-soluble CD163, that may be linked to the late gadolinium enhancement on cardiac MRI, which can persist for months after vaccination. Together, our results demonstrate up-regulation in inflammatory cytokines and corresponding lymphocytes with tissue-damaging capabilities, suggesting a cytokine-dependent pathology, which may further be accompanied by myeloid cell\u2013associated cardiac fibrosis. These findings likely rule out some previously proposed mechanisms of mRNA vaccine\u2013-associated myopericarditis and point to new ones with relevance to vaccine development and clinical care.\n          <\/jats:p>","DOI":"10.1126\/sciimmunol.adh3455","type":"journal-article","created":{"date-parts":[[2023,5,5]],"date-time":"2023-05-05T17:58:07Z","timestamp":1683309487000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":76,"title":["Cytokinopathy with aberrant cytotoxic lymphocytes and profibrotic myeloid response in SARS-CoV-2 mRNA vaccine\u2013associated myocarditis"],"prefix":"10.1126","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8259-2892","authenticated-orcid":true,"given":"Anis","family":"Barmada","sequence":"first","affiliation":[{"name":"Department of Immunobiology, Yale University School of Medicine, New Haven, CT, 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