Pathogenesis of Chagas disease: time to move on.
Trypanosoma cruzi is the etiologic agent of Chagas disease. The contributions of parasite and immune system for disease pathogenesis remain unresolved and controversial. The possibility that Chagas disease was an autoimmune progression triggered by T. cruzi infection led some to question the benefit of treating chronically T. cruzi-infected persons with drugs. Furthermore, it provided the rationale for not investing in research aimed at a vaccine which might carry a risk of inducing autoimmunity or exacerbating inflammation. This viewpoint was adopted by cash-strapped health systems in the developing economies where the disease is endemic and has been repeatedly challenged by researchers and clinicians in recent years and there is now a considerable body of evidence and broad consensus that parasite persistence is requisite for pathogenesis and that antiparasitic immunity can be protective against T. cruzi pathogenesis without eliciting autoimmune pathology. Thus, treatment of chronically infected patients is likely to yield positive outcomes and efforts to understand immunity and vaccine development should be recognized as a priority area of research for Chagas disease.
Department of Biochemistry and Immunology, Institute of Biological Sciences, Belo Horizonte, Brazil.
Fabiana S
FS
Machado
Kevin M
KM
Tyler
Fatima
F
Brant
Lisia
L
Esper
Mauro M
MM
Teixeira
Herbert B
HB
Tanowitz
D000818:Animals; D000917:Antibody Formation; D015551:Autoimmunity; D014355:Chagas Disease / Q000276:immunology / Q000473:pathology*; D018925:Chemokines / Q000502:physiology; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D007111:Immunity, Cellular; D051379:Mice; D051193:Toll-Like Receptors / Q000502:physiology
D018925:Chemokines; D016207:Cytokines; D051193:Toll-Like Receptors