In a recent study published in the Journal of Hepatology, researchers reported that the coronavirus disease 2019 (COVID-19) vaccination could elicit a distinct T cell-dominant immune-mediated hepatitis.
Vaccination against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is critical to combat the COVID-19 pandemic. Recently, several reports have surfaced indicating autoimmune hepatitis (AIH)-like conditions post-COVID-19 vaccination, not observed during clinical trials. Liver injury has been observed with both vector- and messenger ribonucleic acid (mRNA)-based vaccines with a varying period of vaccination-to-symptom onset.
Autoimmune serological tests revealed mild hyperglobulinemia, antinuclear antibodies (ANA), and borderline positivity for anti-mitochondrial M2 antibody (AMA-M2) and anti-smooth muscle antibodies, while anti-liver kidney microsomal (LKM) antibody tests were negative. The liver biopsy revealed interface hepatitis with moderate lymphoplasmacytic infiltrate and lobular necrotic and apoptotic foci. These clinical findings were consistent with a probable AIH, and the treatment was 9 mg of budesonide/day. In the ensuing weeks, levels of liver enzymes dropped, and another relapse occurred after 39 days of therapy initiation, controlled by systemic steroids and ursodeoxycholic acid.
The researchers noted a slight increase in peripheral immunoglobulins and intrahepatic enrichment of plasma and B cells. Strikingly, cytotoxic CD8 T cells (CD38-expressing) were the most enriched to the extent that they were the most abundant immune cells in the liver.
These observations implicated T cells as the pathogenic cell type associated with the vaccination-related immune hepatitis as the novel AIH subtype. These findings indicated that vaccination with BNT162b2 might cause immune-mediated hepatitis by vaccine-elicited cellular immunity mechanisms.