Targeting the CXCL9/CXCL10-CXCR3+ CD8+ T Cell Axis: Unraveling Anti-PD-1 Antibody-Associated Cardiotoxicity in Pressure Overload Heart Failure

MedXY Editorial Team•Sep 6, 2026•Cardiology

Anti-PD-1 antibody treatment and specific deletion of Pdcd1 in CD8+ T cells worsens pressure overload-induced cardiac remodeling and heart failure (HF) in murine models.
Increased myocardial infiltration of CXCR3+ CD8+ T cells under PD-1 inhibition leads to granzyme B and perforin-mediated mitochondrial complex I dysfunction in cardiomyocytes.
Cardiac fibroblast-derived chemokines CXCL9 and CXCL10 mediate chemotaxis of CXCR3+ CD8+ T cells, amplifying myocardial injury in pressure overload settings.
Targeting the CXCL9/CXCL10-CXCR3 axis or granzyme B pharmacologically or genetically rescues cardiac function, representing potential therapeutic strategies against anti-PD-1-associated cardiotoxicity.

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This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Anti-PD-1 antibody treatment and specific deletion of Pdcd1 in CD8+ T cells worsens pressure overload-induced cardiac remodeling and heart failure (HF) in murine models.
Increased myocardial infiltration of CXCR3+ CD8+ T cells under PD-1 inhibition leads to granzyme B and perforin-mediated mitochondrial complex I dysfunction in cardiomyocytes.
Cardiac fibroblast-derived chemokines CXCL9 and CXCL10 mediate chemotaxis of CXCR3+ CD8+ T cells, amplifying myocardial injury in pressure overload settings.
Targeting the CXCL9/CXCL10-CXCR3 axis or granzyme B pharmacologically or genetically rescues cardiac function, representing potential therapeutic strategies against anti-PD-1-associated cardiotoxicity.