Acquired Cell-Mediated Immunodepression in Acute Chagas' Disease

Teixeira, Antônio R. L.; Teixeira, Glória; Macêdo, Vanize; Prata, Áluízio

doi:10.1172/jci109232

Cited by 77 publications

(34 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, studies of early activation by T. cruzi using cells from acute Chagas patients are scarce. Although classic studies have suggested a suppressive response in the early phases of human T. cruzi infection [24,25], it is clear that the immune response mounted is efficient for controlling patent parasitemia. It has been suggested that B-cell activation leading to lytic antibody production is important in parasite elimination during the acute phase [26][27][28].…”

Section: How the Early Encounter Of Trypanosoma Cruzi With Host Cellsmentioning

confidence: 99%

Current concepts in immunoregulation and pathology of human Chagas disease

Dutra¹,

Gollob

2008

Current Opinion in Infectious Diseases

113

View full text Add to dashboard Cite

Purpose of review-Chagas disease is a complex ailment caused by infection with Trypanosoma cruzi. It afflicts millions in Latin America. Years of studies have focused on the development of pathology in Chagas disease and recent studies have helped us understand the cellular mechanisms behind differential clinical evolution of Chagas disease.Recent findings-We discuss recent findings concerning the cellular immune response in human Chagas disease focusing on immunoregulation and the development of pathology. We seek to put several findings into the context of a disease that initially controls an extreme and patent infection, and later progresses to a chronic phase marked by the presence (cardiac and digestive forms), or not (indeterminate form), of associated pathology.Summary-Several theories exist to explain differential clinical evolution of Chagas disease. A coherent understanding of these theories will certainly aid in determining what combination of them approximates the true development of chagasic pathology. For achieving the goal of developing a successful therapy or intervention, it is critical that no theory be excluded at this point, but. Rather, rather that a thoughtful analysis and assimilation of the best components of each system into a central theory that best fits the reality of human Chagas disease is desirable.

show abstract

Section: How the Early Encounter Of Trypanosoma Cruzi With Host Cellsmentioning

confidence: 99%

Current concepts in immunoregulation and pathology of human Chagas disease

Dutra¹,

Gollob

2008

Current Opinion in Infectious Diseases

113

View full text Add to dashboard Cite

show abstract

“…Binding of antibodies to epimastigote forms grown in liver infusion tryptose (LIT) medium and to amastigote forms in sections of murine tissues was detected by indirect immunofluorescence assay (30,34). Epimastigote and amastigote forms of the archetype Berenice stock of T. cruzi were used as positive controls.…”

Section: Phenotypic and Genotypic Characterization Of T Cruzi-like Imentioning

confidence: 99%

“…Considering the age-specific prevalence of T. cruzi infections in adults (30) and the fact that for each acute case that is clinically identified an estimated 20 to 100 others are unrecognized (34), autochthonous human Chagas disease in the Amazon Basin may reach 7,860 to 39,300 cases. The latter figure is consistent with serologic evidence of T. cruzi infection in the Brazilian Amazon region presented in the national report on Chagas disease (65).…”

Section: Researchmentioning

confidence: 99%

Emerging Chagas Disease: Trophic Network and Cycle of Transmission ofTrypanosoma cruzifrom Palm Trees in the Amazon

Teixeira

Monteiro

Rebêlo

et al. 2001

Emerg. Infect. Dis.

View full text Add to dashboard Cite

“…Long-term persistence of the parasitic infection can lead to chronic Chagas' disease, characterized by progressive cardiomyopathy and congestive heart failure (23,51). During the acute T. cruzi infection, parasitespecific immune responses are delayed, and induction of a polyclonal B-cell response results in hypergammaglobulinemia and lymphoproliferation that occur concomitant with parasitemia and the generation of nonspecific and autoreactive antibodies (7,15,31,44,64). In the mouse model of T. cruzi infection, reduction of polyclonal B-cell responses leads to decreased disease severity (32), indicating the potential to enhance host immunity to T. cruzi through the depletion of polyclonal B-cell activation.…”

mentioning

confidence: 99%