CD4 + CD25 + transforming growth factor‐β‐producing T cells are present in the lung in murine tuberculosis and may regulate the host inflammatory response *

Summary CD4 +  CD25 + regulatory T cells produce the anti‐inflammatory cytokines transforming growth factor (TGF)‐β or interleukin (IL)‐10. Regulatory T cells have been recognized to suppress autoimmunity and promote self‐tolerance. These cells may also facilitate pathogen persistence by down‐regulating the host defence response during infection with Mycobacterium tuberculosis . We evaluated TGF‐β +  and IL‐10 + lung CD4 +  CD25 + T cells in a murine model of M. tuberculosis . BALB/c mice were infected with ∼50 colony‐forming units of M. tuberculosis H37Rv intratracheally. At serial times post‐infection, lung cells were analysed for surface marker expression (CD3, CD4, CD25) and intracellular IL‐10, TGF‐β, and interferon (IFN)‐γ production (following stimulation in vitro with anti‐CD3 and anti‐CD28 antibodies). CD4 + lung lymphocytes were also selected positively after lung digestion, and stimulated in vitro for 48 h with anti‐CD3 and anti‐CD28 antibodies in the absence and presence of anti‐TGF‐β antibody, anti‐IL‐10 antibody or rmTGF‐β soluble receptor II/human Fc chimera (TGFβsrII). Supernatants were assayed for elicited IFN‐γ and IL‐2. Fluorescence activated cell sorter analyses showed that TGF‐β‐ and IL‐10‐producing CD4 +  CD25 + T cells are present in the lungs of infected mice. Neutralization of TGF‐β and IL‐10 each resulted in increases in elicited IFN‐γ, with the greatest effect seen when TGFβsrII was used. Elicited IL‐2 was not affected significantly by TGF‐β neutralization. These results confirm the presence of CD4 +  CD25 + TGF‐β + T cells in murine pulmonary tuberculosis, and support the possibility that TGF‐β may contribute to down‐regulation of the host response.