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High molecular weight components from Ascaris suum inhibit the OVA specific response by a mechanism dependent on MYD88 adapter molecule

S R Silva J F Jacysyn; Mahasti Sahihi de Macedo; E L Faquim-Mauro; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)

Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006

São Paulo 2006

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  • Título:
    High molecular weight components from Ascaris suum inhibit the OVA specific response by a mechanism dependent on MYD88 adapter molecule
  • Autor: S R Silva
  • J F Jacysyn; Mahasti Sahihi de Macedo; E L Faquim-Mauro; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)
  • Assuntos: IMUNOLOGIA
  • É parte de: Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006
  • Notas: Disponível em CD-ROM
  • Descrição: Introduction and Objectives: We have demonstrated that high molecular weight (P1) components from A. suum inhibit in vivo the expression of the molecules involved in antigen presentation in dendritic cells (DCs) from OVA+PI-primed mice and the ability of these cells to induce T cell proliferation compared to DC from OVA-primed mice. Here we evaluate the in vitro ability of PI to modulate the expression of MHC-II and co-stimulatory molecules by already activated CD11c+cells from OVA-immunized mice and the potential of these cells to stimulate OVA-specific T cells, plus the role of the Myd88 adapter protein in its in vivo suppressive effect. Methods and Results: Purified CD11c+ cells from mice immunized with OVA in CFA were incubated with OVA or OVA+P1 for 18 h, labeled with FITC- or PE-conjugated anti-MHC-II, -CD80, -CD86 or -CD40 mAbs, and analyzed by flow cytometry or cultured with OVA-specific T cells. We observed that PI suppressed the MHC-II and co-stimulatory molecules expression by CD11c+cells from OVA-immunized mice pulsed with OVA+P1 compared to that obtained on CD11c+ cells pulsed only with OVA. Reduction of 53% in the proliferation of OVA-specific T cells was obtained when they were cultured with CD11c+cells pulsed with OVA+PI. In addition, MHCII and co-stimulatory molecule expression was evaluated on lymph node cells from C57BL/6 WT or Myd88KO mice immunized with OVA or OVA+P1 in CFA. The expression of these molecules was reduced by 43-50%
    on cells from OVA+PI-primed WT mice compared to those from OVAprimed mice. In contrast, no difference was obtained in Myd88KO mice primed in either way. OVA-specific T cell proliferation was only suppressed when antigen-presenting cells form OVA+PI-immunized WT were used in culture. Conclusion: PI has a potent modulatory effect on the fenotype and function of DCs and this effect is related to Myd88 signaling pathway.
  • Editor: São Paulo
  • Data de criação/publicação: 2006
  • Formato: res. IR.027.
  • Idioma: Inglês

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