Patients with coronavirus disease 2019 characterized by dysregulated levels of membrane and soluble cluster of differentiation 48

Background: Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavi-rus 2 (SARS-CoV-2), can progress into a severe form of acute lung injury. The cosignaling receptor cluster of dif-ferentiation 48 (CD48) exists in membrane-bound (mCD48) and soluble (sCD48) forms and has been reported to be implicated in antiviral immunity and dysregulated in several inflammatory conditions. Therefore, CD48 dysre-gulation may be a putative feature in COVID-19-associated inflammation that deserves consideration.Objective: To analyze CD48 expression in lung autopsies and peripheral blood leukocytes and sera of patients with COVID-19. The expression of the CD48 ligand 2B4 on the membrane of peripheral blood leukocytes was also assessed.Methods: Twenty-eight lung tissue samples obtained from COVID-19 autopsies were assessed for CD48 expres-sion using gene expression profiling immunohistochemistry (HTG autoimmune panel). Peripheral whole blood was collected from 111 patients with COVID-19, and the expression of mCD48 and of membrane-bound 2B4 was analyzed by flow cytometry. Serum levels of sCD48 were assessed by enzyme-linked immunosorbent assay.Results: Lung tissue of patients with COVID-19 showed increased CD48 messenger RNA expression and infiltra-tion of CD48+ lymphocytes. In the peripheral blood, mCD48 was considerably increased on all evaluated cell types. In addition, sCD48 levels were significantly higher in patients with COVID-19, independently of disease severity.Conclusion: Considering the changes of mCD48 and sCD48, a role for CD48 in COVID-19 can be assumed and needs to be further investigated.(c) 2022 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.

Automated summary

CD48 expression in lung tissues and peripheral blood leukocytes of COVID-19 patients was found to be dysregulated, suggesting its potential involvement in disease progression and inflammation. Further investigation is needed to understand the role of CD48 in COVID-19.