Myeloid Populations in Systemic Autoimmune Diseases

Abstract

Systemic autoimmune diseases (SADs) encompass a wide spectrum of clinical signs as a reflection of their complex physiopathology. A variety of mechanisms related with the innate immune system are in the origin of the loss of self-tolerance in these diseases, and for most of them, the myeloid leukocytes are key actors. Monocytes, macrophages, dendritic cells, and neutrophils are first-line immune effectors located in the interface between innate and adaptive immunity. They are crucial in the organization of the local and systemic responses to damage-associated molecular patterns (DAMPs) and determine the intensity, orientation, and duration of the local immune response through the expression of chemokines, costimulatory or protolerogenic factors. In this review, we summarize the current knowledge about the role of the main myeloid populations in the induction and maintenance of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), primary antiphospholipid antibody syndrome (PAPS), systemic sclerosis (SSc), and Sjögren's syndrome (SjS), based on the data from both mouse preclinical models and patients. According to these data, our challenge in the next few years is to better dissect the fine mechanisms underlying the pathological role of myeloid cells in these diseases in order to define specific cell subsets or proteins that can be potential targets for drug development.

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