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In this study, we found that a subpopulation of CD4 + CD25 +  (85% Foxp3 + ) cells from persons with latent tuberculosis infection (LTBI) inhibits growth of  M. tuberculosis  ( M. tb ) in human monocyte-derived macrophages (MDMs). A soluble factor, Rho GDP dissociation inhibitor (D4GDI), produced by apoptotic CD4 + CD25 +  (85% Foxp3 + ) cells is responsible for this inhibition of  M. tb  growth in human macrophages and in mice.  M. tb -expanded CD4 + CD25 + Foxp3 + D4GDI +  cells do not produce IL-10, TGF-β and IFN-γ. D4GDI inhibited growth of  M. tb  in MDMs by enhancing production of IL-1β, TNF-α and ROS, and by increasing apoptosis of  M. tb -infected MDMs. D4GDI was concentrated at the site of disease in tuberculosis patients, with higher levels detected in pleural fluid than in serum. However, in response to  M. tb , PBMC from tuberculosis patients produced less D4GDI than PBMC from persons with LTBI.  M. tb -expanded CD4 + CD25 +  (85% Foxp3 + ) cells and D4GDI induced intracellular  M. tb  to express the dormancy survival regulator DosR and DosR-dependent genes, suggesting that D4GDI induces a non-replicating state in the pathogen. Our study provides the first evidence that a subpopulation of CD4 + CD25 +  (85% Foxp3 + ) cells enhances immunity to  M. tb , and that production of D4GDI by this subpopulation inhibits  M. tb  growth.

A Rho GDP Dissociation Inhibitor Produced by Apoptotic T-Cells Inhibits Growth of Mycobacterium tuberculosis