Chronic chagasic cardiopathy: role of CD4 T cells in the anti heart autoreactivity

Santos, Ricardo Ribeiro dos; Laus, José Luis; Mengel, José; Savino, Wilson

doi:10.1590/s0074-02761990000300015

Cited by 3 publications

(3 citation statements)

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“…There is strong evidence that autoreactivity of T cells during T. cruzi infection is limited to the CD4+ compartment. Splenic CD4+ T cells isolated from chronically infected mice mediated syngeneic heart graft rejection when injected in situ whereas CD8+ T cells and non-T cells did not [35]. In vivo depletion of CD4+ T cells with monoclonal antibodies abrogates this rejection but depletion of CD8+ T cells does not [35].…”

Section: Parasite-induced Autoimmunitymentioning

confidence: 96%

“…Splenic CD4+ T cells isolated from chronically infected mice mediated syngeneic heart graft rejection when injected in situ whereas CD8+ T cells and non-T cells did not [35]. In vivo depletion of CD4+ T cells with monoclonal antibodies abrogates this rejection but depletion of CD8+ T cells does not [35]. Further support for this observation came from in vitro studies demonstrating that CD4+ but not CD8+ T cells proliferate in response to stimulation with cardiac autoantigens and peripheral tolerance induction to a myosin-enriched heart homogenate efficiently attenuated myocardial reactivities in vitro only when mice were given concurrent anti-CD4 treatment [35].…”

Section: Parasite-induced Autoimmunitymentioning

confidence: 98%

“…In vivo depletion of CD4+ T cells with monoclonal antibodies abrogates this rejection but depletion of CD8+ T cells does not [35]. Further support for this observation came from in vitro studies demonstrating that CD4+ but not CD8+ T cells proliferate in response to stimulation with cardiac autoantigens and peripheral tolerance induction to a myosin-enriched heart homogenate efficiently attenuated myocardial reactivities in vitro only when mice were given concurrent anti-CD4 treatment [35]. There is also evidence that T. cruzi-infected mice and humans undergo less robust intrathymic negative selection resulting in a T cell repertoire containing increased numbers of potentially autoreactive cells including those of the CD4+CD8+TCRVβ5+ and CD4+CD8+TCRVβ12+ phenotypes [36].…”

Section: Parasite-induced Autoimmunitymentioning

confidence: 99%

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Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Bonney

Engman²

2008

CMM

145

137

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Chagas heart disease (CHD), caused by the protozoan parasite Trypanosoma cruzi, is the leading cause of infectious myocarditis in the world. The etiology of CHD is unclear and multiple mechanisms have been proposed to explain the pathogenesis of the disease. This review describes the proposed mechanisms of CHD pathogenesis and evaluates the historical significance and evidence supporting each. Although the majority of CHD-related pathologies are currently attributed to parasite persistence in the myocardium and autoimmunity, there is strong evidence that CHD develops as a result of additive and even synergistic effects of several distinct mechanisms rather than one factor.

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Section: Parasite-induced Autoimmunitymentioning

confidence: 96%

Section: Parasite-induced Autoimmunitymentioning

confidence: 98%

Section: Parasite-induced Autoimmunitymentioning

confidence: 99%

See 1 more Smart Citation

Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Bonney

Engman²

2008

CMM

145

137

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Role of autoreactive immunological mechanisms in chagasic carditis

Ribeiro-dos-Santos

Pirmez

Savino

1991

Research in Immunology

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Effects of severe protein restriction in levels of parasitemia and in mortality of mice accutely infected with Trypanosoma cruzi

Gomes¹,

Pereira²,

Domingues³

et al. 1994

Rev. Soc. Bras. Med. Trop.

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Adult mice were submitted to different degrees o f protein restriction fo r five weeks (4.75, 9 .5,14.25 and 19% o Clinical and epidemiological observations suggest th at m aln u tritio n , m ainly protein deprivation, plays an im portant role in the development of infections which include protozoal d iseases2 8. A lthough m ost rep o rts show enhancement of infections in malnourished patients or experimental animals, some observations have shown increased resistance to malaria infection in rats that were submitted to protein restriction3 10. Moreover, while protein deprived mice infected with Leishmania mexicana showed arrest of lesion growth during the five initial weeks of infection, with subsequent development of non-healing lesions, normally nourished mice developed progressively healing lesions9.The effects of malnutrition on the evolution of Chagas' disease has not yet been evaluated. There are few reports showing enhancement of parasitemia and more severe lesions in the heart of infected rats submitted to diets with deficient amounts of thiamine, riboflavine, pantothenate or pyridoxine16 17 1819.

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Chronic chagasic cardiopathy: role of CD4 T cells in the anti heart autoreactivity

Cited by 3 publications

References 0 publications

Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Role of autoreactive immunological mechanisms in chagasic carditis

Effects of severe protein restriction in levels of parasitemia and in mortality of mice accutely infected with Trypanosoma cruzi

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