MHC-II+ G-MDSC expressing CD80, CD86, or ICOSL are associated with pro-inflammatory CD4+ T cells phenotypes in the lungs of lupus-prone mice

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects various tissues of the body. One of these tissues is the lung, in which pleuropulmonary manifestations commonly occur. In these patients, homeostasis is disrupted, characterized by a decrease in T reg and an increase in T h1 and T h2 cells. Myeloid-derived suppressor cells (MDSCs) are a cell population characterized by their ability to suppress the T cell response; however, in recent years, the presence of major histocompatibility complex class II (MHC-II) molecules on MDSCs has been reported. Nevertheless, the presence of costimulatory molecules, such as CD80, CD86, and ICOSL, has not been studied yet in MDSCs expressing MHC-II in the context of SLE. In this study, we evaluated the pulmonary microenvironment in SLE mice from an immunological and histological perspective. We observed increased pro-inflammatory cytokines and cellular infiltration in lungs of SLE mice. We also observed MDSC MHC-II cells expressing CD80, CD86, and ICOSL in this tissue, along with alterations of CD4 + T cells subsets, characterized by a decrease in IL-10 frequency in SLE mice. Moreover, we observed that G-MDSCs MHC-II expressing CD80, CD86, or ICOSL correlate positively with phenotypes of CD4 + T cells that produce IL-17 and IFN-γ. For this reason, we suggest that MHC-II + G-MDSC cells may contribute to an inflammatory environment that triggers tissue damage in the lungs of SLE mice.