Acute respiratory distress syndrome/acute lung injury (ALI) was described in 1967. The uncontrolled inflammation is a central issue of the syndrome. The regulatory T cells (Tregs), formerly known as suppressor T cells, are a subpopulation of T cells. Tregs indirectly limits immune inflammation-inflicted tissue damage by employing multiple mechanisms and creating the appropriate immune environment for successful tissue repair. And it plays a central role in the resolution of ALI. Accordingly, for this review, we will focus on Treg populations which are critical for inflammatory immunity of ALI, and the effect of interaction between Treg subsets and cytokines on ALI. And then explore the possibility of cytokines as beneficial factors in inflammation resolution of ALI.

Postinfluenza pneumococcal pneumonia is a common cause of death in humans. However, the role of IL-27 in the pathogenesis of secondary pneumococcal pneumonia after influenza is unknown. We now report that influenza infection induced pulmonary IL-27 production in a type I IFN-α/β receptor (IFNAR) signalling-dependent manner, which sensitized mice to secondary pneumococcal infection downstream of IFNAR pathway. Mice deficient in IL-27 receptor were resistant to secondary pneumococcal infection and generated more IL-17A-producing γδ T cells but not αβ T cells, thereby leading to enhanced neutrophil response during the early phase of host defence. IL-27 treatment could suppress the development of IL-17A-producing γδ T cells activated by Streptococcus pneumoniae and dendritic cells. This suppressive activity of IL-27 on γδ T cells was dependent on transcription factor STAT1. Finally, neutralization of IL-27 or administration of IL-17A restored the role of γδ T cells in combating secondary pneumococcal infection. Our study defines what we believe to be a novel role of IL-27 in impairing host innate immunity against pneumococcal infection.

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These findings suggest that IL-38 attenuates sepsis by decreasing inflammation and increasing bacterial clearance, thus providing a novel tool for antisepsis therapy.

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