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Abstract
T cell immunoglobulin and mucin domain 3 (TIM3) expression is associated with immunosuppression and clinical outcomes in many diseases. However, the specific mechanism of TIM3 in immune system has not been clarified. In order to illustrate the mechanism of TIM3 in immune system, we analyzed the expression, function and regulation of TIM3 in T helper (Th)1 cells, Th2 cells, Th17 cells and regulatory T cells (Treg) through flow cytometry in patients with myelodysplastic syndrom (MDS). Our data showed elevated proportion of Th2 and Treg cells, while the proportion of Th1 and Th17 cells decreased in patients with MDS (p<0.05) and the expression of TIM3 increased in Th1, Th17 and Treg cells in patients with MDS when compared with expression in control patients (p<0.05). The secretion of transforming growth factor-β in TIM3+Treg cells decreased in patients with MDS. These findings suggested that TIM3 might affect immune helper systems by regulating Treg cells and related immune cells. Therefore, studying the role of the TIM3 pathway in MDS is necessary and may help to provide a new way to explore the pathogenesis and treatments of MDS.
- Myelodysplastic syndrome
- Immune checkpoints
- T cell immunoglobulin and mucin domain 3
- T cells
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Footnotes
LL, JH and YW contributed equally.
Contributors YW analyzed the data; JH wrote the manuscript; LL designed research, and ensured correct analysis of the data, and contributed to the writing of the manuscript; JT, ZL and RF assisted in the designing of research, overseeing the collection of the data and contributed to the writing of the manuscript; HL and WZ assisted in the collection and analysis of the data.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Ethics approval This study was authorized by the Ethics Committee of Tianjin Medical University General Hospital.
Provenance and peer review Not commissioned; externally peer reviewed.
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