Abstract
Myeloid-derived suppressor cells (MDSCs) are identified as a heterogeneous population of cells with the function to suppress innate as well as adaptive immune responses. The initial studies of MDSCs were primarily focused on the field of animal tumor models or cancer patients. In cancer, MDSCs play the deleterious role to inhibit tumor immunity and to promote tumor development. Over the past few years, an increasing number of studies have investigated the role of MDSCs in autoimmune diseases. The beneficial effects of MDSCs in autoimmunity have been reported by some studies, and thus, immunosuppressive MDSCs may be a novel therapeutic target in autoimmune diseases. There are some controversial findings as well. Many questions such as the activation, differentiation, and suppressive functions of MDSCs and their roles in autoimmune diseases remain unclear. In this review, we have discussed the current understanding of MDSCs in autoimmune diseases.
Highlights
Myeloid-derived suppressor cells (MDSCs) started to be described more than three decades ago mainly in cancer [1, 2]
MDSCs serve as the negative regulator of immune responses, and they are likely to play a protective role in autoimmune diseases by inhibiting T cell-mediated immune responses
A growing body of evidence has suggested that MDSCs may be actively participating in the development of autoimmune diseases, such as multiple sclerosis (MS) [8, 25, 45], systemic lupus erythematosus (SLE) [11, 46], type 1diabetes (T1D) [47], inflammatory bowel disease (IBD) [9, 48], and rheumatoid arthritis (RA) [49]
Summary
Myeloid-derived suppressor cells (MDSCs) started to be described more than three decades ago mainly in cancer [1, 2]. MDSCs are suggested to be an important cell component for creating tumor immunosuppressive microenvironment [3,4,5,6,7]. In recent years, it has been reported about the involvement of MDSCs in a variety of inflammatory disorders, including autoimmune diseases [8,9,10,11,12]. MDSCs can suppress the immune response through a variety of different mechanisms, including close cell-cell contact and soluble mediators, of which the predominant factors are arginase-1 (Arg-1) and inducible nitric oxide synthase (iNOS) [33]. The relationship between MDSCs and B cells remains to be further studied
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