[Nematode infections in mice--an experimental model of immunoregulation]

There has been a substantial increase in the incidence of autoimmune and allergic diseases in Western countries in the past few decades. However, in the geographic area endemic for parasitic helminth infections, such diseases remain relatively rare. It has been hypothesized that helminths may protect against immune disorders that have been observed in urbanized area. Studies on rodents infected with nematodes Trichinella spiralis, Heligmosomoides polygyrus, Nippostrongylus brasiliensis and Trichuris muris have provided considerable information about immune mechanisms in aspects of host-parasite interaction and immunoregulation. Helminths inducing a long-lasting asymptomatic infection are regarded as major modifiers of the host immune system. Parasitic worms can establish and reproduce in mammalian hosts switching off inflammation and inducing a tolerant response to parasitic antigens. In this review we summarized recent information on the immunoregulation during nematode infection and mechanisms used by nematodes, including the induction of regulatory T cells and apoptosis in the host. The innate immune response seems to determine the different sensitivity of mice to nematode infection. In this review we also discuss results of our own studies on H. polygyrus, demonstrating that it induces different mechanisms in different strains of mice which might play important role in the modulation of immune response. In the slow responder mice apoptosis would play a key role in the outcome of immune response. Contrary to that, in fast responder mice a defensive inflammatory response is mostly down-regulated via endogenous opioids pathway. Understanding the molecular mechanisms that mediate the effects that helminths have on the immune system will provide information that can be exploited to prevent inflammatory diseases.