Interleukins Produced in Response to Infection by Parasitic Worms Protect the Body from Autoimmune Attack

A recent paper discussed the molecular basis for the lower incidence of type I diabetes in developing countries caused by intestinal worm infections.

Chronic intestinal worm infections are known to blunt the effect of the self-aggressive T-cells that cause diabetes and other autoimmune diseases. To determine which molecular signals trigger this loss of autoimmune activity investigators at the University of Medicine and Dentistry of New Jersey (Newark, USA) infected nonobese diabetic (NOD) mice with the strictly enteric nematode parasite, Heligmosomoides polygyrus and then evaluated the types of cytokines produced by these animals.

They reported in the July 18, 2012, online edition of the journal Mucosal Immunology that two weeks of infection with H. polygyrus (which was then cured using oral drugs) induced T-cells to produce the cytokines interleukin (IL)-4 and IL-10, which acted independently to block T-cell autoimmune activity and provide lasting protection against development of type I diabetes. Blockade of IL-10 signaling in some mice during this short interval eliminated the protective effects of the worm infection and resulted in pancreatic beta-cell destruction and ultimately type I diabetes.

These results outline potential mechanisms to explain the potency of parasite-induced control of inflammatory diseases. Follow-up clinical studies are using eggs from another parasitic worm, Trichuris suis, to treat patients with Crohn’s disease and multiple sclerosis.

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University of Medicine and Dentistry of New Jersey