CCR4-dependent reduction in the number and suppressor function of CD4Foxp3 cells augments IFN-γ-mediated pulmonary inflammation and aggravates tuberculosis pathogenesis.

Chronic pulmonary inflammation marked predominantly by CD4IFN-γ cells is the hallmark of tuberculosis pathogenesis in immunocompetent adults, who are substantially affected by this disease. Moreover, CD4Foxp3 cell-mediated suppression contributes to infection susceptibility. We addressed the role of CD4Foxp3 cells in tuberculosis pathogenesis, because this aspect has not been addressed during chronic infection.

CD11c(+) CD103(+) cells of Mycobacterium tuberculosis-infected C57BL/6 but not of BALB/c mice induce a high frequency of interferon-γ- or interleukin-17-producing CD4(+) cells.

The magnitude of the cellular adaptive immune response is critical for the control of Mycobacterium tuberculosis infection in the chronic phase. In addition, the genetic background is equally important for resistance or susceptibility to tuberculosis. In this study, we addressed whether lung populations of dendritic cells, obtained from genetically different hosts, would play a role in the magnitude and function of CD4(+) populations generated after M.