Immunological imprint of COVID‐19 on human peripheral blood leukocyte populations

Abstract

Background SARS‐CoV‐2 has triggered a pandemic that is now claiming many lives. Several studies have investigated cellular immune responses in COVID‐19‐infected patients during disease but little is known regarding a possible protracted impact of COVID‐19 on the adaptive and innate immune system in COVID‐19 convalescent patients. Methods We used multiparametric flow cytometry to analyze whole peripheral blood samples and determined SARS‐CoV‐2‐specific antibody levels against the S‐protein, its RBD‐subunit, and viral nucleocapsid in a cohort of COVID‐19 convalescent patients who had mild disease ~10 weeks after infection (n = 109) and healthy control subjects (n = 98). Furthermore, we correlated immunological changes with clinical and demographic parameters. Results Even ten weeks after disease COVID‐19 convalescent patients had fewer neutrophils, while their cytotoxic CD8+ T cells were activated, reflected as higher HLA‐DR and CD38 expression. Multiparametric regression analyses showed that in COVID‐19‐infected patients both CD3+CD4+ and CD3+CD8+ effector memory cells were higher, while CD25+Foxp3+ T regulatory cells were lower. In addition, both transitional B cell and plasmablast levels were significantly elevated in COVID‐19‐infected patients. Fever (duration, level) correlated with numbers of central memory CD4+ T cells and anti‐S and anti‐RBD, but not anti‐NC antibody levels. Moreover, a “young immunological age” as determined by numbers of CD3+CD45RA+CD62L+CD31+ recent thymic emigrants was associated with a loss of sense of taste and/or smell. Conclusion Acute SARS‐CoV‐2 infection leaves protracted beneficial (ie, activation of T cells) and potentially harmful (ie, reduction of neutrophils) imprints in the cellular immune system in addition to induction of specific antibody responses.

Serum levels of the IgA isotype switch factor TGF‐β1 are elevated in patients with COVID‐19

“…The study by Sterlin et al observed that elevated IgA plasmablasts shortly after the onset of symptoms of COVID-19 with the peak at the third week of the disease [23]. Plasmablast levels were also significantly elevated in COVID-19 convalescent patients [24]. Considering the TGF-b1 results together with our previous finding of serum IgA in COVID-19, the TGF-b1-IgA axis may play an important role in the pathogenesis of COVID-19.…”

The role of CD4+FoxP3+ regulatory T cells in the immunopathogenesis of COVID-19: implications for treatment

“…Although plenty of studies indicate the proportion or number of Tregs is increased in patients with COVID-19 (especially those with the milder disease), it was also reported that the number of Tregs is reduced in the patients. For example, it has been reported that Tregs (CD3 + CD4 + CD25 hi CD127 lo FoxP3 + ) in PBMCs were markedly decreased in severe COVID-19 patients [59][60][61]. The result of single-cell analysis showed that FoxP3 expression was remarkedly reduced in severe patients with COVID-19, although the expression of CD25 was higher [62].…”

How Do Inflammatory Mediators, Immune Response and Air Pollution Contribute to COVID-19 Disease Severity? A Lesson to Learn

“…It has been hypothesised that a betterpreserved immunological memory, and acquired after common cold coronavirus infection, could represent the factor highly responsible for a better prognosis, or even absence of relevant clinical symptoms, in children and young people as compared to older. Compatibly, acute SARS-CoV-2 infection leaves activated T cells and specific antibody responses [96]. Is this the first time that a coronavirus causes different symptoms in subjects of different ages?…”