Anti-Ia treatment modulates specific and polyclonal antibody responses in Trypanosoma cruzi-infected mice

Spinella, Sylviane; Liegeard, Pascale; Guilbert, B; Hontebeyrie-Joskowicz, M.

doi:10.1016/0896-8411(89)90005-x

Cited by 12 publications

(4 citation statements)

References 32 publications

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“…Ten days after injection, mice were killed and spleen cells were assessed for PFC by reverse plaque assay, as described above. Anti-mouse isotypes were previously described [33]: rabbit anti-mouse IgG3 or IgGl isotypes were kindly provided by A. Coutinho (Pasteur Institute), rabbit anti-mouse IgG2, or IgG*t, were purchased from Miles and Zymed Labs. (San Francisco, CA), respectively.…”

Section: Assessment Of In Vivo Polyclonal B Cell Responsesmentioning

confidence: 99%

A CD4⁺ T_H2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG₂ polyclonal response in vivo

Spinella¹,

Milon²,

Hontebeyrie-Joskowicz³

1990

Eur J Immunol

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In our study we describe further characteristics of a CD4+ T cell line (G-05) isolated from lymph nodes of C3H/HeJ mice chronically infected with Trypanosoma cruzi. This T cell line secreted lymphokines such as interleukin (IL) 4 and IL 5 and could be defined as a TH2 type of helper T cells. By passive transfer into naive mice, the G-05 line was able to induce a polyclonal B cell activation in the spleen. This splenic B cell activation was quite similar to that seen in chronically T. cruzi-infected animals, where the isotypic pattern presents a large increase of IgG2a and IgG2b isotypes. Moreover, it was possible to reproduce this kind of polyclonal B cell activation in vivo, with the supernatant of G-05 T cells cultured in the presence of T. cruzi extract, accessory cells and exogenous IL 2. Analysis of this supernatant showed the presence of large amounts of IL 4, IL 5, IL 3 and IL 6 but not of interferon-gamma, and residual IL 2 activity was not significant. These results suggest that the G-05 T cells considered as TH2 cells on the basis of their lymphokine production are involved in the development of the in vivo polyclonal B cell activation in T. cruzi infection.

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Section: Assessment Of In Vivo Polyclonal B Cell Responsesmentioning

confidence: 99%

A CD4⁺ T_H2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG₂ polyclonal response in vivo

Spinella¹,

Milon²,

Hontebeyrie-Joskowicz³

1990

Eur J Immunol

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“…During T. cruzi acute experimental infection, all compartments of the immune system are disturbed as illustrated by T and B cell polyclonal activation, cytokine production, thymic atrophy, immunosuppression, and high autoantibody production [2–5]. The majority of the antibodies triggered by the infection are nonspecific and fail to bind parasite antigens [6].…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma cruzimitochondrial malate dehydrogenase triggers polyclonal B-cell activation

Montes

Zúñiga

Vázquez

et al. 2002

Clinical and Experimental Immunology

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SUMMARYIt has been proposed that Trypanosoma cruzi, the aetiologic agent of Chagas' disease, produces mitogenic substances responsible for the polyclonal B-cell activation observed during the acute phase of the infection. Isolation and characterization of the molecules involved in the induction of polyclonal activation observed during infectious diseases have posed a great challenge for the immunologist over the last decade. In this work we report that a 33 kD protein obtained from an alkaline fraction of T. cruzi epimastigotes (FI) stimulates proliferation and promotes differentiation into antibody-secreting cells of normal murine B cells in a T-cell independent manner. By flow cytometry we also found that the 33 kDa protein induces an increase in the expression of MHC class II and B7.2 but not B7.1 molecules on the B-cell surface. Sequencing by mass spectrometry identified the T. cruzi 33 kD protein as hypothetical oxidoreductase, a member of the aldo/ketoreductase family. In this report we demonstrate that this protein is also present in the infective bloodstream trypomastigote form of the parasite and was identified as T. cruzi mitochondrial malate dehydrogenase (mMDH) by enzyme activity and by Western blotting using a specific mMDH polyclonal antiserum. The biologic relevance of mMDH-induced polyclonal activation concerning T. cruzi infection is discussed.

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“…Estudos posteriores mostraram que a leucocitose é decorrente da ativação policlonal de células B (KIERZENBAUM & HAYES, 1980) do tipo B1 (Ly-1 + -CD5 + ) e B2 (MINOPRIO et al, 1986;MINOPRIO et al, 1989), mobilizadas do omento e medula óssea, respectivamente (MARCONDES et al, 2000). A ativação de células B leva sua diferenciação a plasmócitos secretores de anticorpos, causando hipergamaglobulinemia, com predomínio de isotipos IgM, IgG2a e IgG2b (ORTIZ-ORTIZ et al, 1980;TARLENTON & KUHN, 1983;MINOPRIO et al, 1986;SPINELLA et al, 1989). A análise da reatividade dos anticorpos policlonais indicou a presença de anticorpos parasito-específicos (TARLENTON & KUHN, 1983), apesar de outros estudos mostrarem que a maioria destes anticorpos não possui especificidade para parasita e apresentariam reatividade para uma variedade de antígenos, inclusive antígenos próprios (MINOPRIO et al, 1986;MINOPRIO et al, 1989b).…”

Section: A Resposta Imune E T Cruziunclassified

“…No entanto, comparativamente, ocorreria uma ativação preferencial de células CD8 + (KIERZENBAUM & HAYES, 1980;MINOPRIO et al, 1986b). As causas da ativação policlonal em linfócitos é um fenômeno que estaria associado principalmente aos ativadores policlonais (Ag) do parasita (HERNANDEZ-MUNAIN et al, 1992;MONTES et al, 1996;DA SILVA et al, 1998;MONTES et al, 1999;BILATE et al, 2000), estimulando diretamente os linfócitos ou ativando as células para secreção de citocinas como células T CD4 + (MINOPRIO et al, 1987;SPINELLA et al, 1989) e CD11b + (MONTES et al, 2006).…”

Section: A Resposta Imune E T Cruziunclassified

Papel dos leucotrienos durante a infecção experimental de camundongos com 'Trypanosoma cruzi'

Canavaci¹

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No presente trabalho verificamos o papel dos Leucotrienos na modulação da resposta imune durante a fase aguda da infecção experimental pelo Trypanosoma cruzi, usando como modelo camundongos deficientes da enzima 5-lipoxigenase (5-LOko). Os nossos dados demonstram que camundongos infectados pelo T. cruzi produzem metabólitos do ácido aracdônico como PGE 2 , LTB 4 e LTC 4. Comparados aos animais controles, os animais 5-LOko apresenta parasitemia mais tardia e menor, tem menor parasitismo tissular, menor infiltrado de células inflamatórias no coração e musculatura esquelética e apresenta menor taxa de mortalidade durante a fase aguda, indicando que animais deficientes de leucotrienos são mais resistentes a infecção pelo parasito. Animais 5-LOko está relacionado com a manutenção de números elevados de células F4/80 + e redução de células CD11b + durante a infecção e menor número de células T ativadas expressando os marcadores CD4 + CD69 + , CD4 + CD25 + , CD4 + CD44 + e CD8 + CD69 + , números inalterados de células T regulatórias CD4 + CD25 + GITR + e menor produção de anticorpos parasito-específicos do isotipo IgG2a. O controle eficiente de parasitas por animais 5-LOko está associado ao aumento de células Gr-1 + e CD11c + GR-1 + , produção aumentada IL-12, IFN-γ, e produzirem menos PGE 2 , IL-10, ao contrario, animais controles, incapazes de controlar parasitas circulantes, produzem mais PGE 2 e IL-10 e menos IL-12 e IFN-γ. A baixa mortalidade de animais 5-LOko correlaciona com a produção de PGE 2 e IL-10, produzir muita IL-12 e menos IFN-γ e NO e baixíssima parasitemia. A mortalidade maior de animais controles envolve a produção IFN-γ e altos níveis de LTB 4 , LTC 4 , NO e ausência de IL-10, IL-1β, PGE 2 e números elevados de parasitas circulantes. Ainda macrófagos de animais 5-LOko apresentam maior capacidade de adesão/internalização de tripomastigotas e alta atividade tripanocida por mecanismo independente da geração de NO. Estes dados em conjunto demonstram que mediadores lipídicos produzidos pela enzima 5-lipoxigenase como LTB 4 e LTC 4 modulam negativamente a capacidade dos camundongos para geração de uma resposta imune capaz de controlar os parasitos durante a fase aguda da infecção pelo T. cruzi.

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Anti-Ia treatment modulates specific and polyclonal antibody responses in Trypanosoma cruzi-infected mice

Cited by 12 publications

References 32 publications

A CD4⁺ T_H2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG₂ polyclonal response in vivo

A CD4⁺ T_H2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG₂ polyclonal response in vivo

Trypanosoma cruzimitochondrial malate dehydrogenase triggers polyclonal B-cell activation

Papel dos leucotrienos durante a infecção experimental de camundongos com 'Trypanosoma cruzi'

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Anti-Ia treatment modulates specific and polyclonal antibody responses in Trypanosoma cruzi-infected mice

Cited by 12 publications

References 32 publications

A CD4+ TH2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG2 polyclonal response in vivo

A CD4+ TH2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG2 polyclonal response in vivo

Trypanosoma cruzimitochondrial malate dehydrogenase triggers polyclonal B-cell activation

Papel dos leucotrienos durante a infecção experimental de camundongos com 'Trypanosoma cruzi'

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A CD4⁺ T_H2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG₂ polyclonal response in vivo

A CD4⁺ T_H2 cell line isolated from mice chronically infected with Trypanosoma cruzi induces IgG₂ polyclonal response in vivo