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    • Keywords


      Galectin-9; immunity; inflammatory cytokines; macrophage; pulmonary tuberculosis; T-cell; Tim-3

    • Abstract


      Patients affected by pulmonary tuberculosis (PTB) manifest deficiencies in innate cellular immunity. The Tim-3/Galectin-9 axis is an important regulator of Th1 cell immunity, leading to Th1 cell apoptosis. Herein, thisstudy aims to clarify the underlying roles of the Tim-3/Galectin-9 axis in T-cell immunity in PTB. Peripheralblood mononuclear cells (PBMCs) were extracted from subjects with and without PTB to examine theexpression of CD4, CD8, CD25, and Tim-3 under the stimulation of Mycobacterium tuberculosis (MTB) andpurified protein derivative (PPD). In addition, the expression of Tim-3 and Galectin-9 in PBMCs was determined.The Tim-3/Galectin-9 axis in the PBMCs was activated or blocked to detect the secreted levels of IFN-gamma,TNF-alpha, IL-2, and IL-22. MTB stimulation increased the expression of CD4, CD8, CD25, Tim-3, andGalectin-9 in PBMCs. The blockade of Tim-3/Galectin-9 axis resulted in reduced secretion of IFN-gamma, TNF-alpha,IL-2, and IL-22 from T-cells. Moreover, Tim-3+CD4+T, Tim-3+CD8+, and Tim-3+CD25+T cells exhibited agreater ability to inhibit the replication of MTB in macrophages. Taken conjointly, the blockade of Tim-3/Galectin-9 axis inhibits the secretion of inflammatory cytokines in T-cells to regulate the T-cell immunity inPTB.

    • Author Affiliations



      1. Department of Respiratory, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China
      2. Jilin Medical University, Jilin 132013, People’s Republic of China
      3. Department of Cardiology, Jilin Province FAW General Hospital, Changchun 130011, People’s Republic of China
      4. Department of Pediatric Rheumatology, Immunology and Allergy, the First Hospital of Jilin University, Changchun 130021, People’s Republic of China
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