Dataset Information

Activin a suppresses peripheral CD8⁺ T lymphocyte activity in acute-phase Kawasaki disease.

ABSTRACT:

Background

Kawasaki disease is an autoimmune disease characterized by systemic vasculitis of unknown aetiology and most commonly occurs in children under 5?years old. Previous studies have found that the over-activation of lymphocytes is an important mechanism of Kawasaki disease. Activin A, also known as immunosuppressive factor P, is a multifunctional growth and transforming factor. However, whether activin A is involved in the regulation of peripheral lymphocytes activity in Kawasaki disease is unclear. Thus, we aimed to investigate the effect of activin A on the activity of peripheral lymphocytes in acute-phase Kawasaki disease.

Methods

Seven patients with Kawasaki disease and seven healthy controls were studied. Peripheral blood lymphocytes were isolated by Ficoll density gradient centrifugation. The activation of CD4⁺ and CD8⁺ T cells and CD19⁺ B cells was investigated by flow cytometry. The expression of activin type IIA receptors was investigated by flow cytometry.

Results

Immune imbalance in CD4 and CD8 lymphocytes were detected in acute-phase Kawasaki disease. The expression of activin type IIA receptors on CD8⁺ T cells and CD19⁺ B cells was increased in acute-phase Kawasaki disease and decreased following treatment with activin A. Activin A suppressed the expression of CD25 and CD69 on CD8⁺ T cells and the expression of CD69 on CD19⁺ B cells.

Conclusions

The expression of activin type IIA receptor was increased on CD8⁺ T cells and CD19⁺ B cells in Kawasaki disease. Activin A suppressed the expression of CD25, CD69 and activin type IIA receptors on peripheral CD8⁺ T lymphocyte. Activin A plays different roles in different lymphocyte subsets and suppresses peripheral CD8⁺ T lymphocyte activity in acute-phase Kawasaki disease.

SUBMITTER: Wu Q

PROVIDER: S-EPMC7903692 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

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Publications

Activin a suppresses peripheral CD8<sup>+</sup> T lymphocyte activity in acute-phase Kawasaki disease.

Wu Qian Q Weng Ruohang R Xu Yongbin Y Wang Linlin L Huang Yanyan Y Yang Jun J

BMC immunology 20210223 1

<h4>Background</h4>Kawasaki disease is an autoimmune disease characterized by systemic vasculitis of unknown aetiology and most commonly occurs in children under 5 years old. Previous studies have found that the over-activation of lymphocytes is an important mechanism of Kawasaki disease. Activin A, also known as immunosuppressive factor P, is a multifunctional growth and transforming factor. However, whether activin A is involved in the regulation of peripheral lymphocytes activity in Kawasaki ...[more]

PMID: 33622252

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Project description:BackgroundTuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) is a clinical aggravation of TB symptoms observed among a fraction of HIV coinfected patients shortly after the start of antiretroviral therapy (ART). Of note, TB-IRIS is characterized by exacerbated inflammation and tissue damage that occurs in response to the elevated production of CD4+ T cell-derived IFN-γ. Nevertheless, the possible participation of CD8+ T cells in TB-IRIS development remains unclear.MethodsWe performed a comprehensive assessment of the composition of CD8+ T cell memory subsets and their association with circulating inflammation-related molecules in TB-HIV coinfected patients initiating ART.ResultsWe found that TB-IRIS individuals display higher frequencies of Antigen-experienced CD8+ T cells during the onset of IRIS and that the levels of these cells positively correlate with baseline mycobacterial smear grade. TB-IRIS individuals exhibited higher frequencies of effector memory and lower percentages of naïve CD8+ T cells than their Non-IRIS counterparts. In both TB-IRIS and Non-IRIS patients, ART commencement was associated with fewer significant correlations among memory CD8+ T cells and cells from other immune compartments. Networks analysis revealed distinct patterns of correlation between each memory subset with inflammatory cytokines suggesting different dynamics of CD8+ T cell memory subsets reconstitution. TB-IRIS patients displayed lower levels of memory cells positive for CXCR3 (a chemokine receptor that plays a role in trafficking activated CD8+ T cells to the tissues) than Non-IRIS individuals before and after ART. Furthermore, we found that CXCR3+ naïve CD8+ T cells were inversely associated with the risk of TB-IRIS development. On the other hand, we noticed that the frequencies of CXCR3+ effector CD8+ T cells were positively associated with the probability of TB-IRIS development.ConclusionOur data suggest that TB-IRIS individuals display a distinct profile of memory CD8+ T cell subsets reconstitution after ART initiation. Moreover, our data point to a differential association between the frequencies of CXCR3+ CD8+ T cells and the risk of TB-IRIS development. Collectively, our findings lend insights into the potential role of memory CD8+ T cells in TB-IRIS pathophysiology.

Dataset Information

Activin a suppresses peripheral CD8⁺ T lymphocyte activity in acute-phase Kawasaki disease.

Background

Methods

Results

Conclusions

Publications

Activin a suppresses peripheral CD8<sup>+</sup> T lymphocyte activity in acute-phase Kawasaki disease.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Activin a suppresses peripheral CD8+ T lymphocyte activity in acute-phase Kawasaki disease.

Background

Methods

Results

Conclusions

Publications

Activin a suppresses peripheral CD8<sup>+</sup> T lymphocyte activity in acute-phase Kawasaki disease.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Activin a suppresses peripheral CD8⁺ T lymphocyte activity in acute-phase Kawasaki disease.