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SARS-CoV-2-Associated T-Cell Responses in the Presence of Humoral Immunodeficiency

Authors
  • Gupta, Sudhir
  • Su, Houfen
  • Narsai, Tejal
  • Agrawal, Sudhanshu
Type
Published Article
Journal
International Archives of Allergy and Immunology
Publisher
S. Karger AG
Publication Date
Jan 22, 2021
Volume
182
Issue
3
Pages
195–209
Identifiers
DOI: 10.1159/000514193
PMID: 33486489
Source
Karger
Keywords
License
Green
External links

Abstract

We report perhaps the most comprehensive study of subsets of CD4+ and CD8+ and subsets of B cells in a mild symptomatic SARS-CoV-2+ immunocompetent patient and a common variable immunodeficiency disease (CVID) patient who had normal absolute lymphocyte counts and remained negative for SARS-CoV-2 IgG antibodies. Naïve (T<sub>N</sub>), central memory (T<sub>CM</sub>), effector memory (T<sub>EM</sub>), and terminally differentiated effector memory (T<sub>EMRA</sub>) subsets of CD4+ and CD8+ T cells, subsets of T follicular helper cells (cT<sub>FH</sub>, T<sub>FH</sub>1, T<sub>FH</sub>2, T<sub>FH</sub>17, T<sub>FH</sub>1/T<sub>FH</sub>17, and T<sub>FR</sub>), CD4 Treg, CD8 Treg, mature B cells, transitional B cells, marginal zone B cells, germinal center (GC) B cells, CD21<sup>low</sup> B cells, antibody-secreting cells (plasmablasts), and Breg cells were examined in patients and age-matched controls with appropriate monoclonal antibodies and isotype controls using multicolor flow cytometry. Different patterns of abnormalities (often contrasting) were observed in the subsets of CD4+ T, CD8+ T, B-cell subsets, and regulatory lymphocytes among the immunocompetent patient and CVID patient as compared to corresponding healthy controls. Furthermore, when data were analyzed between the 2 patients, the immunocompetent patient demonstrated greater changes in various subsets as compared to the CVID patient. These data demonstrate different immunological responses to SARS-CoV-2 infection in an immunocompetent patient and the CVID patient. A marked decrease in GC B cells and plasmablasts may be responsible for failure to make SARS-CoV-2 antibodies. The lack of SARS-CoV-2 antibodies with mild clinical disease suggests an important role of T-cell response in defense against SARS-CoV-2 infection.

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