A new study entitled “Intestinal Barrier Dysfunction Develops at the Onset of Experimental Autoimmune Encephalomyelitis, and Can Be Induced by Adoptive Transfer of Auto-Reactive T Cells” published in September issue of PloS One, reports that disruption of intestinal homeostasis supports Experimental Autoimmune Encephalomyelitis, the prototypic mouse model of human Multiple sclerosis.
Multiple sclerosis (MS) is an inflammatory autoimmune disorder characterized by targeted destruction of myelin — a major component of the central nervous system — by self-reactive inflammatory T cells. Recent observations suggest an association between MS and inflammatory bowel disease (IBD), with increased incidence of Crohn’s disease (CD) and ulcerative colitis (UC), the two most common types of IBD, among MS patients. IBD is characterized by a chronic inflammation of the gastrointestinal tract, leading to disruption of the intestinal epithelial barrier, a phenomenon known as “leaky gut.” This loss of epithelial barrier function may allow luminal antigens to abnormally activate the host-immune response leading to a systemic autoimmune response. In the present study, the authors evaluated if Experimental Autoimmune Encephalomyelitis (EAE), a model for human MS in rodents, is accompanied by loss of mucosal immune homeostasis.
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