In this review, we discuss how protozoan parasites alter immature and mature B cell compartment. B1 and marginal zone (MZ) B cells, considered innate like B cells, are activated during protozoan parasite infections, and they generate short lived plasma cells providing a prompt antibody source. In addition, protozoan infections induce massive B cell response with polyclonal activation that leads to hypergammaglobulnemia with serum antibodies specific for the parasites and self and/or non related antigens. To protect themselves, the parasites have evolved unique ways to evade B cell immune responses inducing apoptosis of MZ and conventional mature B cells. As a consequence of the parasite induced-apoptosis, the early IgM response and an already establish humoral immunity are affected during the protozoan parasite infection. Moreover, some trypanosomatides trigger bone marrow immature B cell apoptosis, influencing the generation of new mature B cells. Simultaneously with their ability to release antibodies, B cells produce cytokines/quemokines that influence the characteristic of cellular immune response and consequently the progression of parasite infections.

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B-Cell Response during Protozoan Parasite Infections.

The Deadly Dance of B Cells with Trypanosomatids.

Chagas' disease in northern California: No longer an endemic diagnosis

Chagas’ disease is a widespread parasitosis affecting most Latin American countries (Carcavallo 1975; Coura 1966; Marinkelle 1975; Osimani 1972; Ponce and Zeledon 1973). The etiologic agent is a protozoan, Trypanosoma cruzi 1. This parasite is commonly transmitted to humans by hematophagous insects generically known as “triatomes,” although transmission by blood transfusion is not infrequent, and congenital infection can also occur.

Clinical and Pharmacologic Characterization and Treatment of Potentially Malignant Arrythmias of Chronic Chagasic Cardiomyopathy

Approximately one-third of people with chronic Trypanosoma cruzi infection develop Chagas cardiomyopathy, which carries a poor prognosis. Accurate prediction of which individuals will go on to develop Chagas cardiomyopathy remains elusive. We performed a systematic review of literature comparing characteristics of individuals with chronic Chagas disease with or without evidence of cardiomyopathy. Studies were not excluded on the basis of language or publication date. Our review yielded a total of 311 relevant publications. We further examined the subset of 170 studies with data regarding individual age, sex, or parasite load. A meta-analysis of 106 eligible studies indicated that male sex was associated with having Chagas cardiomyopathy (Hedge's g: 1.56, 95% CI: 1.07-2.04), and a meta-analysis of 91 eligible studies indicated that older age was associated with having Chagas cardiomyopathy (Hedge's g: 0.66, 95% CI: 0.41-0.91). A meta-analysis of four eligible studies did not find an association between parasite load and disease state. This study provides the first systematic review to assess whether age, sex, and parasite load are associated with Chagas cardiomyopathy. Our findings suggest that older and male patients with Chagas disease are more likely to have cardiomyopathy, although we are unable to identify causal relationships due to the high heterogeneity and predominantly retrospective study designs in the current literature. Prospective, multidecade studies are needed to better characterize the clinical course of Chagas disease and identify risk factors for progression to Chagas cardiomyopathy.

Risk Factors for Progression to Chronic Chagas Cardiomyopathy: A Systematic Review and Meta-Analysis.

Serum samples from 150 individuals from an area in Brazil where Chagas's disease is endemic were examined for the presence of autoantibodies (EVI and PN). Patients were divided into four groups according to the diagnostic value and prognostic significance of electrocardiographic changes. Results confirmed a close relationship between the EVI and PN antibodies and chagasic infection but their presence does not appear to relate to the severity of Chagas's heart disease.

P. Ginefra

Papers

Autoantibodies and chronic Chagas's heart disease.