PD-1 deficiency in mice leads to autoimmune dilated cardiomyopathy, suggesting PD-1 is a crucial factor in preventing autoimmune heart disease.
Alerts to possible cardiotoxicity of PD-1 inhibitors; leaves open translation to human autoimmune cardiomyopathy.
Dilated cardiomyopathy is a severe pathology of the heart with poorly understood etiology. Disruption of the gene encoding the negative immunoregulatory receptor PD-1 in BALB/c mice, but not in BALB/c RAG-2-/- mice, caused dilated cardiomyopathy with severely impaired contraction and sudden death by congestive heart failure. Affected hearts showed diffuse deposition of immunoglobulin G (IgG) on the surface of cardiomyocytes. All of the affected PD-1-/- mice exhibited high-titer circulating IgG autoantibodies reactive to a 33-kilodalton protein expressed specifically on the surface of cardiomyocytes. These results indicate that PD-1 may be an important factor contributing to the prevention of autoimmune diseases.
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Nishimura et al. (2001) studied this question.
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