Expression of HLA-DR and KLRG1 enhances the cytotoxic potential and cytokine secretion capacity of CD3 T cells in tuberculosis patients.

Int Immunopharmacol

Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang 310014, China. Electronic address:

Published: May 2024

Background: Human T cells play an important role in immunity against tuberculosis (TB) infection. Activating receptor HLA-DR and inhibitory receptor KLRG1 are critical regulators of T cell function during viral infection and tumorigenesis, but they have been less studied in TB infection.

Methods: In this study, we explored the relationship between CD3 T cell expression of HLA-DR and KLRG1 receptors and function against TB infection. Flow cytometry was conducted to assess the immunomodulatory effects of HLA-DR and KLRG1 receptors on CD3 T cells in patients with different TB infection status.

Results: We found activating receptors HLA-DR, NKG2C, CD57 and NKP46, and inhibitory receptors KLRG1 and KIR on CD3 T cells in different TB infection status showed different distribution patterns; the cytotoxic potential and cytokine secretion capacity of CD3 T cells after Mtb-specific antigen stimulation were significantly enhanced in TB infection groups. Further studies revealed HLA-DR T and KLRG1 T cells expressed higher activating and inhibitory receptors than the negative population. In addition, the expression of cytotoxic potential and cytokine secretion capacity of HLA-DR T and KLRG1 T cells was significantly higher than that of HLA-DR T and KLRG1 T cells.

Conclusions: Expression of HLA-DR and KLRG1 enhances the cytotoxic potential and cytokine secretion capacity of CD3 T cells in TB patients, suggesting CD3 T cells expressing HLA-DR and KLRG1 are important effector cell phenotypes involved in the host anti-TB infection. HLA-DR and KLRG1 expressed by CD3 T cells may be potential predictive markers of TB disease progression and clinical immune assessment.

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http://dx.doi.org/10.1016/j.intimp.2024.112115DOI Listing

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