Cutting Edge: Characterization of Human Tissue-Resident Memory T Cells at Different Infection Sites in Patients with Tuberculosis

Tissue-resident memory T cells (TRMs) have a key role in mediating the host defense against tuberculosis (TB) in mice, but their human counterparts have not been well characterized. In this article, we recruited patients with TB and determined TRM frequency, trafficking, activation marker expression...

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Published in:The Journal of immunology (1950) 2020-05, Vol.204 (9), p.2331-2336
Main Authors: Yang, Qianting, Zhang, Mingxia, Chen, Qi, Chen, Weixin, Wei, Cailin, Qiao, Kun, Ye, Taosheng, Deng, Guofang, Li, Jin, Zhu, Jialou, Cai, Yi, Chen, Xinchun, Ma, Li
Format: Article
Language:English
Subjects:
Adult
Biomarkers - blood
Bronchoalveolar Lavage Fluid - immunology
Cells, Cultured
Cutting Edge
Female
Humans
Immunologic Memory - immunology
Interferon-gamma - immunology
Interleukin-2 - immunology
Lung - immunology
Lung - microbiology
Macrophages - immunology
Macrophages - microbiology
Male
Mycobacterium tuberculosis - immunology
Phenotype
T-Lymphocytes - immunology
T-Lymphocytes - microbiology
Tuberculosis - blood
Tuberculosis - immunology
Tuberculosis - microbiology
Tumor Necrosis Factor-alpha - immunology
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Summary:Tissue-resident memory T cells (TRMs) have a key role in mediating the host defense against tuberculosis (TB) in mice, but their human counterparts have not been well characterized. In this article, we recruited patients with TB and determined TRM frequency, trafficking, activation marker expression, and cytokine production by flow or mass cytometry at different infection sites, including peripheral blood, pleural fluid, bronchoalveolar lavage fluid, and lung. We found a high frequency of TRMs at all infection sites apart from the peripheral blood. These TRMs exhibited a memory phenotype, were highly activated (based on CD38 and HLA-DR expression), and expressed high levels of trafficking (CCR5 and CXCR6) and exhaustion (PD-1) markers. When stimulated with , TRMs secreted cytokines, including IFN-γ, TNF-α, and IL-2, and exhibited a multifunctional phenotype. TRMs limited intracellular replication in macrophages. These data inform our current understanding of immunosurveillance at different infection sites in patients with TB.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1901326