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Free keywords:
SEGMENTED FILAMENTOUS BACTERIA; REGULATORY T-CELLS; ARYL-HYDROCARBON
RECEPTOR; CENTRAL-NERVOUS-SYSTEM; LACTOBACILLUS-CASEI SHIROTA;
INTESTINAL IMMUNE-RESPONSES; CD103(+) DENDRITIC CELLS; GERM-FREE MICE;
MULTIPLE-SCLEROSIS; INDUCED ARTHRITISClinical Neurology; Neurosciences; Pathology; Gut microbiota; Commensals; Multiple sclerosis; EAE; Autoimmune disease;
Abstract:
Multiple sclerosis (MS) and other chronic inflammatory autoimmune
diseases represent major public health challenges in industrialised
Western society. MS results from an autoimmune attack against myelin
structures by self-reactive lymphocytes, which are normal components of
the healthy immune repertoire. The nature of the triggers that convert
the innocuous self-reactive lymphocytes into an autoaggressive
phenotype is poorly understood. In the past, it was primarily suspected
that pathogenic infections trigger MS. However, so far, none of the
incriminated pathogenic microbes were firmly associated with the
disease. A growing body of evidence in animal models of MS implicates
the gut microbiota in the induction of central nervous system (CNS)
autoimmunity. The mammalian gut harbors a diverse population of
microbial organisms which are essential for our well being. There is an
increasing understanding that the gut microbiota not only modulates the
local immune functions but also affects the systemic immune system. We
are only just beginning to understand the nature of the interactions of
the gut microbiota with the host's immune system especially in the
context of autoimmune diseases. This review will address the influence
of intestinal microbiota on immune homeostasis and on the development
of autoimmune responses at sites distal to the intestine with a
particular emphasis placed on a discussion about CNS autoimmunity.
