Autoimmunity in Chagas' Disease

Cunha-Neto, Edécio; Iwai, Leo Kei; Bilate, Angelina M.; Fonseca, Simone Gonçalves; Kalil, Jorge

doi:10.1016/b978-044451271-0.50035-1

Cited by 8 publications

(7 citation statements)

References 154 publications

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“…Trypanosoma cruzi infection can lead either to induction of, or protection from, autoimmunity [33]. Mice chronically infected by T. cruzi develop cardiomiopathy, in which cardiac myosin is recognized by CD4 þ T cells [34] and molecular mimicry has been identified between the T. cruzi antigen B13 and cardiac myosin heavy chain [35].…”

Section: Discussionmentioning

confidence: 99%

Sera of patients with systemic lupus erythematosus react with plasmodial antigens and can inhibit thein vitrogrowth ofPlasmodium falciparum

et al. 2009

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The acquisition of protective immunity in malaria is a slow process during which autoantibodies are produced. The present work aimed at studying a possible interference of autoimmune responses on malaria immune protection. This was done by investigating the presence of autoantibodies in the sera of malarious patients, by searching for reactivity of autoantibodies from autoimmune patients against plasmodial antigens, and by studying the effect of such antibodies on the in vitro growth of Plasmodium falciparum. Sera from systemic lupus erythematosus (SLE) and malaria patients were tested against autologous and plasmodial antigens. Out of the 109 SLE sera tested, 48 (44%) reacted against the parasite. In addition, 26 (47%) out of 55 randomly selected sera, mainly those containing anti-DNA and antinuclear autoantibodies, were able to inhibit parasite growth to some extent. Conversely, a high frequency (81%) of sera of malaria patients exhibited reactivity against autoantigens. The results show that patients with autoimmune processes can produce antibodies that recognize plasmodial antigens in the absence of plasmodial infection, that malaria patients can produce autoantibodies, that SLE sera can inhibit plasmodial growth in vitro, and that the presence of anti-DNA and antinuclear antibodies may be important in such anti-plasmodial activity. It is concluded that autoimmune responses may have influence on the protective immunity against malaria.

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Section: Discussionmentioning

confidence: 99%

Sera of patients with systemic lupus erythematosus react with plasmodial antigens and can inhibit thein vitrogrowth ofPlasmodium falciparum

et al. 2009

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“…In T. cruzi infection many examples of molecular mimicry at the level of T cells or antibodies have been described (recently reviewed in Cunha-Neto et al 2004). However, few of these have been extensively studied and/or defined at the molecular level (see Table 3).…”

Section: Molecular Mimicrymentioning

confidence: 98%

Trypanosoma cruzi-Induced Molecular Mimicry and Chagas’ Disease

Gironès

Cuervo

Fresno

Current Topics in Microbiology and Immunology

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“…Cunha‐Neto et al . have also proposed that myosin cross‐reactive T lymphocytes infiltrating heart tissue lesions are involved in the generation of chronic chagasic pathology 59,62 . These T cells are activated by cardiac myosin heavy chain cross‐reactive T. cruzi antigen (Ag; 1).…”

Section: Autoreactive T Cellsmentioning

confidence: 99%

Role of Trypanosoma cruzi Autoreactive T Cells in the Generation of Cardiac Pathology

Gironès

Carrasco-Marı́n

Cuervo

et al. 2007

Annals of the New York Academy of Sciences

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Chagas disease, caused by Trypanosoma cruzi, affects several million people in Central and South America. About 30% of chronic patients develop cardiomyopathy probably caused by parasite persistence and/or autoimmunity. While several cross-reactive antibodies generated during mammal T. cruzi infection have been described, very few cross-reactive T cells have been identified. We performed adoptive transfer experiments of T cells isolated from chronically infected mice. The results showed the generation of cardiac pathology in the absence of parasites. We also transferred cross-reactive SAPA-specific T cells and observed unspecific alterations in heart repolarization, cardiac inflammatory infiltration, and tissue damage.

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Autoimmunity in Chagas' Disease

Cited by 8 publications

References 154 publications

Sera of patients with systemic lupus erythematosus react with plasmodial antigens and can inhibit thein vitrogrowth ofPlasmodium falciparum

Sera of patients with systemic lupus erythematosus react with plasmodial antigens and can inhibit thein vitrogrowth ofPlasmodium falciparum

Trypanosoma cruzi-Induced Molecular Mimicry and Chagas’ Disease

Role of Trypanosoma cruzi Autoreactive T Cells in the Generation of Cardiac Pathology

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