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CD4(+)CD25(+)FoxP3(+) regulatory T cells suppress Mycobacterium tuberculosis immunity in patients with active disease.

Chen X, Zhou B, Li M, Deng Q, Wu X, Le X, Wu C, Larmonier N, Zhang W, Zhang H, Wang H, Katsanis E

Shenzhen Donghu Hospital, 2019, Buxin Road, Shenzhen 518020, China. chenxinchun@hotmail.com

CD4(+)CD25(+) regulatory T cells (Treg) play a central role in the prevention of autoimmunity and in the control of immune responses by down-regulating the function of effector CD4(+) or CD8(+) T cells. The role of Treg in Mycobacterium tuberculosis infection and persistence is inadequately documented. Therefore, the current study was designed to determine whether CD4(+)CD25(+)FoxP3(+) regulatory T cells may modulate immunity against human tuberculosis (TB). Our results indicate that the number of CD4(+)CD25(+)FoxP3(+) Treg increases in the blood or at the site of infection in active TB patients. The frequency of CD4(+)CD25(+)FoxP3(+) Treg in pleural fluid inversely correlates with local MTB-specific immunity (p<0.002). These CD4(+)CD25(+)FoxP3(+) T lymphocytes isolated from the blood and pleural fluid are capable of suppressing MTB-specific IFN-gamma and IL-10 production in TB patients. Therefore, CD4(+)CD25(+)FoxP3(+) Treg expanded in TB patients suppress M. tuberculosis immunity and may therefore contribute to the pathogenesis of human TB.

Published 19 March 2007 in Clin Immunol, 123(1): 50-9.
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