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Zeng J.-C.,Guangdong Medical College | Zeng J.-C.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Lin D.-Z.,Dongguan Hospital for Prophylaxis and Treatment of Chronic Disease | Yi L.-L.,Dongguan Hospital for Prophylaxis and Treatment of Chronic Disease | And 14 more authors.
American Journal of Translational Research | Year: 2014

Despite past extensive studies, the role of B and T lymphocyte attenuator (BTLA) in αβ T cells in patients with active pulmonary tuberculosis (ATB) remains poorly understood. Here we demonstrate that BTLA expression on αβ T cells is decreased in patients with M. tuberculosis (Mtb) infection. Particularly, BTLA expression levels are likely critical for αβ T cells to manifest and maintain an active central memory phenotype with high capacity for secretion of IFN-γ and perforin, which are important for immune memory against TB infection. BTLAhigh αβ T cells also exhibited higher capacity in response to Mtb peptide stimulation. In contrast to the role of BTLA played for negative regulation of immune responses, our data in the current studies suggest that BTLA expression on αβ T cells is likely associated with protective immune memory against Mtb infection in the setting of patients with active pulmonary tuberculosis. This previous unappreciated role for BTLA may have implications for prevention and treatment of patients with Mtb infection. © 2014, E-Century Publishing Corporation. All rights reserved.


Zeng J.,Chinese Institute of Clinical Medicine | Zeng J.,Guangdong Medical College | Song Z.,Guangdong Medical College | Cai X.,Guangdong Medical College | And 18 more authors.
Journal of Leukocyte Biology | Year: 2015

Although tuberculous pleurisy (TP) presumably involves a hypersensitivity reaction, there is limited evidence indicating overreactive effector responses of γδ T cells and αβ T cells and their interrelation with Foxp3+ Tregs in pleural and other compartments. We found that TP induced reciprocal representations of Foxp3+Tregs and Mtb phosphoantigen-specific Vγ2Vδ2 T cells in different anatomic compartments. Patients with TP exhibited appreciable numbers of “proliferating” Ki-67+ Vγ2Vδ2 T cells in the airway where Foxp3+ Tregs were not dominant, whereas striking increases in Foxp3+ Tregs in the blood and pleural compartments coincided with low frequencies of Vγ2Vδ2 T cells. Interestingly, anti-tuberculosis chemotherapy control of Mtb infection in patients with TP reversed reciprocal representations of Foxp3+ Tregs and proliferating Vγ2Vδ2 T cells. Surprisingly, despite high-level Foxp3+ Tregs, TP appeared to drive overreactive responses of IFN-γ-producing Vγ2Vδ2, CD4+CD25+, and CD8+CD25+ T effector subpopulations, whereas IL-22-producing Vγ2Vδ2 T cells increased subtly. Th1 effector responses were sustained despite remarkable declines in Foxp3+ Tregs at 1 mo after the treatment. Overreactive T effector responses of Mtb-reactive γδ T cells, αβ CD25+CD4+, and CD25+CD8+ T cell subpopulations appear to be immune features for TP. Increased Foxp3+ Tregs might be responsive to overreactive TP but unable to influence T effector responses despite having an inverse relation with proliferating Vγ2Vδ2 T cells. © Society for Leukocyte Biology.

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