*Purpose: The factors associated with severe COVID-19 disease in transplant patients are poorly understood. Despite concern that patients with weakened immune responses have increased risk of infectious complications, we hypothesized that immunosuppression might attenuate the inflammatory cascade that characterizes severe disease. We therefore evaluated whether disease severity is associated with various immune parameters.

*Methods: We characterized lymphocyte phenotypes using flow cytometry and measured cytokines by Luminex in 5 transplant recipients with the SARS-CoV2 virus. The ImmuKnow assay, which measures ATP in stimulated CD4 cells, was utilized to assess cell-mediated immunocompetence.

*Results: Higher ImmuKnow levels correlated with more severe clinical course. We found a significant linear correlation between ImmuKnow level and percentage of activated effector (CCR7-/CD69+) CD4 (p=0.042) and CD8 (p=0.003) cells in the blood as well as the CD4:CD8 ratio (p=0.001) (Table 1). In two lung secretion samples, higher ImmuKnow level correlated with a higher percentage of resident memory (CCR7-/CD69+/CD103+) CD8 T cells. Concentrations of G-CSF, IL-10, IL-6, TNF-a and MCP1 were elevated in at least 50% of our cohort and highest in the patient with the highest ImmuKnow level.

*Conclusions: Higher ImmuKnow levels correlated with more severe clinical course, higher percentages of activated effector CD4 and CD8 cells and CD4:CD8 ratio in the blood, higher percent of resident memory CD8 cells in the lung secretions, and higher levels of inflammatory cytokines. These are all factors described in patients with more severe disease, suggesting that increased immunosuppression does not increase the risk of severe COVID-19 outcomes in transplant patients.

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