Abstract
Chagas disease (CD) is a chronic systemic vector-borne infection caused by the protozoan Trypanosoma cruzi. It has spread from Latin America through migration, becoming a global issue (Perez-Molina and Molina, 2018). Its prevalence is ∼7 million people worldwide, of whom 30-40% will develop severe chronic complications such as cardiomyopathy or megaviscerae, with a considerable impact on morbimortality (WHO, 2020; WHO, 2021). The parasite is transmitted after metacyclic trypomastigotes in the feces of a triatomine insect enter the host through the bite wound. They penetrate cells and transform into amastigotes, where they multiply by binary fission and differentiate again into circulating trypomastigotes after rupture of the host cell. The triatomine vector ingests them from an infected individual and they replicate in its intestine in the form of epimastigotes. The cycle closes after the epimastigotes differentiate again into metacyclic trypomastigotes (Perez-Molina and Molina, 2018). Chronic clinical manifestations in CD have been associated with a disproportionate inflammation compared to the parasitic burden (Cunha-Neto et al., 2011), driven by direct parasitic invasiveness (Bonney and Engman, 2008; Epting et al., 2010), damage to bystander cells (De Bona et al., 2018), cellular injury due to non-specific immune responses (Bellotti et al., 1996; Zhang and Tarleton, 1999; Bonney and Engman, 2015; De Bona et al., 2018), autoimmunity (Leon et al., 2001; Engman and Leon, 2002; Bonney and Engman, 2015; De Bona et al., 2018), and vasculitis (Roffe et al., 2016; Weaver et al., 2019). Herein, we review the autoimmune mechanisms behind chronic CD and, particularly, the knowledge gaps in the immunopathogenesis of vasculitis developed in patients with CD.
Highlights
Chagas disease (CD) is a chronic systemic vector-borne infection caused by the protozoan Trypanosoma cruzi
Inflammatory responses mediated both by T CD4+ and CD8+ cells (Tarleton, 2001; Cunha-Neto et al, 2011), antibodydependent cell-mediated cytotoxicity (ADCC) (Bonney and Engman, 2008) and complement activation with formation of the membrane attack complex (MAC) (Aiello et al, 2002) are proposed factors for autoimmune-induced cell damage
One study found that cutaneous vasculitis in patients with systemic lupus erythematosus (SLE) was significantly associated with the presence of anti-ribosomal P protein antibodies (Shinjo and Bonfá, 2011), a commonly found autoantibody in patients with chronic CD (Mesri et al, 1990; Bonfa et al, 1993; Kaplan et al, 1997; Abraham and Derk, 2015). This is the only common autoantibody in vasculitis and CD, which makes us hypothesize about its implications in the pathogeny of vasculitis associated with chronic infection by T. cruzi, especially after immunoglobulin deposits have been found in the vascular walls of affected patients
Summary
Chagas disease (CD) is a chronic systemic vector-borne infection caused by the protozoan Trypanosoma cruzi. It has spread from Latin America through migration, becoming a global issue (Pérez-Molina and Molina, 2018). The parasite is transmitted after metacyclic trypomastigotes in the feces of a triatomine insect enter the host through the bite wound. They penetrate cells and transform into amastigotes, where they multiply by binary fission and differentiate again into circulating trypomastigotes after rupture of the host cell. We review the autoimmune mechanisms behind chronic CD and, the knowledge gaps in the immunopathogenesis of vasculitis developed in patients with CD
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