CD4+CD25+ T regulatory cells dampen inflammatory responses in murine mycoplasma pneumonia and are associated with promotion of IL-17 AND IFN-γ production, but not IL-10 or TGF-β. (P3055)

Abstract

Abstract Mycoplasmas cause respiratory diseases characterized by persistent infection and chronic airway inflammation. Mycoplasma lung disease is immunopathologic, with Th cells determining disease severity and resistance to infection. Th2 cell responses promote immunopathology; Th1 cells confer resistance to infection. However, little is known about the role of Treg cells in mycoplasma respiratory diseases. We hypothesized Treg cells control the severity of the inflammatory lesions and may also promote persistence of infection, as found in other diseases. To examine this, mice, given anti-CD25 antibody to deplete Treg cells, had increased disease severity due to Mycoplasma pulmonis infection. There was however no affect on mycoplasma numbers recovered from the lungs. Treg cells promote the secretion of IFN-γ and IL-17 mycoplasma-specific CD4+ T cell responses in vitro. We were unable to detect significant changes in IL-10 and TGF-β production. In addition, Treg cell depletion increased Th2 (IL-13) responses. Populations of Treg cells from lymph nodes had increased expression of IFN-γ or IL-17 after infection. Thus, Treg cells play an important role in controlling damaging immune responses in mycoplasma respiratory infection but do not influence the level of mycoplasma infection. It appears that Treg cells dampen mycoplama inflammatory disease through a novel mechanism mediated production of IFN-γ and IL-17.