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Trypanosoma cruzi: The immunological consequences of infection
Author(s) -
Hudson Leslie
Publication year - 1983
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240210406
Subject(s) - trypanosoma cruzi , immune system , parasite hosting , chagas disease , biology , immunology , antigen , immunopathology , disease , intracellular parasite , virology , microbiology and biotechnology , medicine , pathology , computer science , world wide web
Trypanosoma cruzi, the causative agent of Chagas' disease, infects an estimated 12 million people in Latin America and may induce cardiopathy and megaformation of the oesophagus and colon. During the early, acute stage of the infection, parasite‐induced inflammatory infiltrates may cause transitory disease which terminates with the emergence of an immune response sufficient to reduce the parasite to insignificant levels. Even so, severe disease may develop many years after the original infection. It has been suggested that this might result from an autoimmune process triggered by the parasite and mediated either (1) by the adsorption of parasite antigens to host cells, thus rendering these cells susceptible to the host's own antiparasite immune response, or (2) via cross‐reactive antigens shared by the host and parasite. In common with many parasitic diseases, there is an urgent need for studies on the T‐cell response to T cruzi infection, as this might not only hold the key to the immunopathology but also serve as a means of clearing this lifelong infection which survives by sequestering into an intracellular site.