부산대학교 도서관

Over‐reactive effector responses of γδ T and αβ T cells, and their interrelation with Foxp3+Tregin pleural and other compartments. 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+Tregsin pleural and other compartments. We found that TP induced reciprocal representations of Foxp3+Tregsand 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+Tregswere not dominant, whereas striking increases in Foxp3+Tregsin 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+Tregsand 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+Tregsat 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+Tregsmight be responsive to overreactive TP but unable to influence T effector responses despite having an inverse relation with proliferating Vγ2Vδ2 T cells.