Circulating regulatory T cells in patients with severe fever with thrombocytopenia syndrome

Abstract

We demonstrated that SFTSV infection resulted in a robust circulating Treg response in patients with SFTS. Our investigation suggested that the proportions of CD4+/total lymphocytes and CD4 + CD25+ Foxp3+/CD4 + CD25+ cells in circulating blood could serve as sensitive indices to evaluate the changes in Tregs in SFTS and predict the progression of SFTS.

Overview of the immunological mechanism underlying severe fever with thrombocytopenia syndrome (Review)

“…The proportion of cd4 + /total lymphocytes and cd4 + cd25 + /cd4 + cells noticeably declined in patients with SFTS compared with that in healthy individuals, but was higher compared with that in patients with severe disease. By contrast, the percentage of cd4 + cd25 + Foxp3 + /cd4 + cd25 + cells were markedly increased in the SFTS group but remained lower compared with that in the severe group (115). This suggests that the proportion of cd4 + /total lymphocytes, cd4 + cd25 + /cd4 + cells and cd4 + cd25 + Foxp3 + /cd4 + cd25 + cells may be an important prognostic factor for patients with SFTS.…”

“…A number of studies previously demonstrated that cd3 + , cd4 + , and cd8 + T cells are diminished in patients with SFTS (94)(95)(96)(115)(116)(117)(118)(119) and in experimental animal models (103). Sun et al (94) revealed a significant decline in CD3 + and cd4 + expression in the peripheral blood of patients with SFTS, where the average leukocyte count was 2.86±1.56x10 9 /l.…”

Single-cell landscape of peripheral immune responses to fatal SFTS

“…Generally, there is agreement in the literature that severe disease is associated with T cell dysregulation and an uncontrolled inflammatory response (Lei et al, 2015;Mendoza et al, 2019). Specifically, patients with severe or fatal disease have lower numbers of CD3 + and CD4 + T lymphocytes (Liu et al, 2017a), an increased proportion of regulatory T cells (Yi et al, 2015), enhanced myeloid-derived suppressor cell-associated T cell impairment (Li et al, 2018b), and elevated serum cytokines such as CXCL10, granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-6, MIP-1a, and MCP-1 (Liu et al, 2013;Liu et al, 2017a). In terms of B/plasmablastic cells, there is limited evidence that supports adaptive immune deficiency due to the dysregulation of B cell composition and disruption of B cellmediated humoral immunity, which can be featured as a hallmark of fatal SFTS outcome (Song et al, 2018;Suzuki et al, 2020).…”

Recent Advances in the Study of the Immune Escape Mechanism of SFTSV and Its Therapeutic Agents

“…Furthermore, during the recovery period from SFTSV infection, circulating Tregs returned to the normal range. Tregs levels correlated with various clinical parameters, which demonstrated that SFTSV infection leads to a strong response of circulating Treg in SFTS patients [54].…”