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Pathological consequences of host response to parasite

par Hontebeyrie, Mireille;Truyens, Carine ;Brenière, Simone Frédérique Rédérique S.F.
Référence American Trypanosomiasis: Chagas Disease One Hundred Years of Research, Elsevier, page (669-690)
Publication Publié, 2010-09

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Résumé :

Since more than 30 years, the hypothesis of autoimmunity is considered for chronic Chagas disease, especially for the most severe manifestation: the chronic Chagas heart disease. Actually, many studies were performed to sustain this hypothesis and successful outcomes reached to demonstrate molecular mimicry and presence of autoreactive T and B cells with potential pathological impact. The most severe pathology induced by Trypanosoma cruzi concerns the heart disease that affects 20-30% of the infected patients and leads to sudden death. Only 5-10% suffer from megaesophagus, megacolon, or peripheral neuropathies. The pathophysiology of Chagas heart disease is still not totally understood and two main mechanisms have been proposed; one is parasite-dependent myocardial damage and the other is impaired immunological responses associated to molecular mimicry. If the clinical features were well known since the beginning of the twentieth century, it remains to explore the mechanisms underlying the development of this chronic disease. Moreover, the recent researches have mostly focused on mechanisms of protection mediated by CD8+T cells and definition of candidates for vaccination. Due to the restrictive rules of ethical approaches in humans, this chapter discusses the validity of the mouse model to learn about the pathological consequences of host-immune response to T. cruzi.