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Mycoplasmas cause respiratory diseases characterized by persistent infection and chronic airway inflammation. Mycoplasma lung disease is immunopathologic, with CD4 +  Th cells determining both disease severity and resistance to infection. Th2 cell responses promote immunopathology, while Th1 cells confer resistance to infection. However, regulatory CD4 +  T cells may also have a role in the pathogenesis of mycoplasma respiratory diseases. We hypothesized Treg cells control the severity of the inflammatory lesions and may also promote persistence of infection. To examine this, BALB/c mice were depleted of CD25 +  cells, and had increased disease severity due to  Mycoplasma pulmonis  infection. Increases in mycoplasma antibody responses and lymphocyte infiltration into lungs also occurred after CD25 +  cell depletion. CD4 + CD25 +  regulatory T cells promoted IFN-γ and IL-17 mycoplasma-specific CD4 +  T cell responses  in vitro  and  in vivo , while dampening IL-13 +  Th responses. Neither IL-10 nor TGF-ß expression was detected in CD4 + CD25 +  T cells from lymph nodes. Thus, a regulatory T cell population plays an important role in controlling damaging immune responses in mycoplasma respiratory disease but does not contribute to persistence of infection. It appears that a regulatory T cell population preferentially dampens Th2 cell-mediated inflammatory responses to mycoplasma through a mechanism independent of IL-10 or TGF-ß characteristic of “classic” Treg cells.

Regulatory CD4+CD25+ T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses