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Abstract
Gut immune cells have been increasingly appreciated as important players in the central nervous system (CNS) autoimmunity in animal models of multiple sclerosis (MS). Among the gut immune cells, innate lymphoid cell type 3 (ILC3) is of special interest in MS research, as they represent the innate cell counterpart of the major pathogenic cell population in MS, i.e. T helper (Th)17 cells. Importantly, these cells have been shown to stimulate regulatory T cells (Treg) and to counteract pathogenic Th17 cells in animal models of autoimmune diseases. Besides, they are also well known for their ability to stabilize the intestinal barrier and to shape the immune response to the gut microbiota. Thus, proper maintenance of the intestinal barrier and the establishment of the regulatory milieu in the gut performed by ILC3 may prevent activation of CNS antigen-specific Th17 cells by the molecular mimicry. Recent findings on the role of ILC3 in the gut-CNS axis and their relevance for MS pathogenesis will be discussed in this paper. Possibilities of ILC3 functional modulation for the benefit of MS patients will be addressed, as well.
Highlights
One of the major open questions about multiple sclerosis (MS) pathogenesis is how the autoimmune response directed against the central nervous system (CNS) is initiated
Increased numbers of Th1/Th17 cells and decreased numbers of T regulatory cells (Treg) cells were found in the gut lamina propria, Peyer’s patches, and mesenteric lymph nodes of mice with experimental autoimmune encephalomyelitis (EAE) before the appearance of clinical symptoms, as well as at the disease peak [9]
innate lymphoid cell type 3 (ILC3) react to IL-1b produced by gut microbiota-stimulated antigen-presenting cells (DC/Mf) by secreting IL-2 which potentiates Treg activity [47], and GM-CSF which stimulates the release of IL-10 and retinoic acid (RA) from dendritic cells (DC)/Mf [56]
Summary
One of the major open questions about multiple sclerosis (MS) pathogenesis is how the autoimmune response directed against the central nervous system (CNS) is initiated. Disclosed changes in immune cells composition and accumulation within different GALT compartments in EAE animals [5,6,7,8,9,10,11,12,13] support the concept that initiation and/or regulation of autoimmune response to CNS antigens may occur in the gut.
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