Parasitic load increases and myocardial inflammation decreases in Trypanosoma cruzi-infected mice after inactivation of helper T cells

Russo, Marco; Starobinas, Nancy; Minóprio, Paola; Coutinho, António; Hontebeyrie-Joskowicz, M.

doi:10.1016/0769-2625(88)90136-5

Cited by 70 publications

(41 citation statements)

References 24 publications

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“…The requirement for CD4 ϩ T cells as critical components of a protective immune response against T. cruzi has been established by studies in mice deficient in genes encoding class II MHC or CD4 molecules and thereby lacking CD4 ϩ T cells (7,8,11,35). Mice deficient in CD4 ϩ T cells are highly susceptible to infection with T. cruzi, develop high tissue parasite burden, and die early in the acute phase of the infection with negligible inflammation (11,36).…”

Section: Discussionmentioning

confidence: 99%

Antigen-Specific Th1 But Not Th2 Cells Provide Protection from Lethal Trypanosoma cruzi Infection in Mice

Kumar

Tarleton

2001

The Journal of Immunology

105

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Infection with Trypanosoma cruzi results in the development of both type 1 and type 2 patterns of cytokine responses during acute and chronic stages of infection. To investigate the role of Th1 and Th2 subsets of CD4+ T cells in determining the outcome of T. cruzi infection in mice, we have developed T. cruzi clones that express OVA and have used OVA-specific TCR-transgenic T cells to generate OVA-specific Th1 and Th2 cells. BALB/c mice receiving 107 OVA-specific Th1 cells and then challenged with OVA-expressing T. cruzi G-OVA.GPI showed significantly lower parasitemia and increased survival in comparison to mice that received no cells. In contrast, recipients of OVA-specific Th2 cells developed higher parasitemias, exhibited higher tissue parasitism and inflammation, and had higher mortality than recipients of Th1 cells after infection with T. cruzi G-OVA.GPI. Mice receiving a mixture of both Th1 and Th2 OVA-specific cells also were not protected from lethal challenge. The protective effect of the OVA-specific Th1 cells was OVA dependent as shown by the fact that transfer of OVA-specific Th1 or Th2 cells failed to alter the course of infection or disease in mice challenged with wild-type T. cruzi. Immunohistochemical analysis of OVA-specific Th1 and Th2 cells at 4, 15, and 30 days postinfection revealed the persistence and expansion of these cells in mice challenged with T. cruzi G-OVA.GPI but not in mice infected with wild-type T. cruzi. We conclude that transfer of Ag-specific Th1 cells but not Th2 cells protect mice from a lethal infection with T. cruzi.

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Section: Discussionmentioning

confidence: 99%

Antigen-Specific Th1 But Not Th2 Cells Provide Protection from Lethal Trypanosoma cruzi Infection in Mice

Kumar

Tarleton

2001

The Journal of Immunology

105

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“…In particular, partial elimination of CD4 + or CD8 + T cells by use of monoclonal antibodies, or use of mice which lack CD4 or CD8 molecules as a result of specific genomic deletions, results in mice which are strikingly susceptible to T. cruzi infections (Araujo 1989;Rottenberg et al 1988Rottenberg et al , 1993Rottenberg et al , 1995Russo et al 1988;Tarleton 1990;Tarleton et al 1992). The role of cytokines in resistance and susceptibility of the host to infection with T. cruzi provides some understanding of these observations.…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma cruzi:Protective Immunity in Mice Immunized with Paraflagellar Rod Proteins Is Associated with a T-Helper Type 1 Response

Miller

Wrightsman

Manning

1996

Experimental Parasitology

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“…cruzi expresses trans-sialidase (TS), 4 a unique pathogen-derived surface sialidase that transfers sialic acid residues ␣2,3-linked to ␤-galactopiranose (␤Galp) on host donor molecules to mucin-like acceptor glycoproteins (6,7). In the absence of a suitable acceptor, TS displays a typical hydrolytic action similar to viral and bacterial sialidases (8).…”

mentioning

confidence: 99%

“…However, the parasite induces widespread polyclonal lymphocyte activation before the immune system mounts focused T cell responses, a condition that leads to immunopathology and represents a main obstacle for effective vaccination (3). In fact, exacerbated CD4 ϩ T cell functioning triggered by T. cruzi infection has been implicated in immunopathology (4,5).…”

mentioning

confidence: 99%

Costimulation of Host T Lymphocytes by a Trypanosomal trans-Sialidase: Involvement of CD43 Signaling

Todeschini

Nunes

Pires

et al. 2002

The Journal of Immunology

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Trans-sialidase is a membrane-bound and shed sialidase from Trypanosoma cruzi, the protozoan parasite responsible for Chagas disease. We investigated the role of soluble trans-sialidase on host CD4+ T cell activation. Trans-sialidase activated naive CD4+ T cells in vivo. Both enzymatically active and inactive recombinant trans-sialidases costimulated CD4+ T cell activation in vitro. Costimulation resulted in increased mitogen-activated protein kinase activation, proliferation, and cytokine synthesis. Furthermore, active and inactive trans-sialidases blocked activation-induced cell death in CD4+ T cells from T. cruzi-infected mice. By flow cytometry, inactive trans-sialidase bound the highly sialylated surface Ag CD43 on host CD4+ T cells. Both costimulatory and antiapoptotic effects of trans-sialidases required CD43 signaling. These results suggest that trans-sialidase family proteins are involved in exacerbated host T lymphocyte responses observed in T. cruzi infection.

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Parasitic load increases and myocardial inflammation decreases in Trypanosoma cruzi-infected mice after inactivation of helper T cells

Cited by 70 publications

References 24 publications

Antigen-Specific Th1 But Not Th2 Cells Provide Protection from Lethal Trypanosoma cruzi Infection in Mice

Antigen-Specific Th1 But Not Th2 Cells Provide Protection from Lethal Trypanosoma cruzi Infection in Mice

Trypanosoma cruzi:Protective Immunity in Mice Immunized with Paraflagellar Rod Proteins Is Associated with a T-Helper Type 1 Response

Costimulation of Host T Lymphocytes by a Trypanosomal trans-Sialidase: Involvement of CD43 Signaling

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