UMMS Affiliation

Department of Medicine, Division of Infectious Diseases and Immunology

Date

7-9-2014

Document Type

Article

Subjects

Antigens, CD40; CD40 Ligand; Cells, Cultured; Glycoproteins; Glycosylphosphatidylinositols; Humans; Interferon-gamma; Interleukin-12; Monocytes; Mucins; Protein Binding; Trypanosoma cruzi

Disciplines

Immunopathology | Parasitic Diseases | Parasitology

Abstract

Chagas disease, caused by the protozoan parasite Trypanosoma cruzi (T. cruzi), is characterized by immunopathology driven by IFN-gamma secreting Th1-like T cells. T. cruzi has a thick coat of mucin-like glycoproteins covering its surface, which plays an important role in parasite invasion and host immunomodulation. It has been extensively described that T. cruzi or its products-like GPI anchors isolated from GPI-anchored mucins from the trypomastigote life cycle stage (tGPI-mucins)-are potent inducers of proinflammatory responses (i.e., cytokines and NO production) by IFN-gamma primed murine macrophages. However, little is known about whether T. cruzi or GPI-mucins exert a similar action in human cells. We therefore decided to further investigate the in vitro cytokine production profile from human mononuclear cells from uninfected donors exposed to T. cruzi as well as tGPI-mucins. We observed that both living T. cruzi trypomastigotes and tGPI-mucins are potent inducers of IL-12 by human peripheral blood monocytes and this effect depends on CD40-CD40L interaction and IFN-gamma. Our findings suggest that the polarized T1-type cytokine profile seen in T. cruzi infected patients might be a long-term effect of IL-12 production induced by lifelong exposure to T. cruzi tGPI-mucins.

Rights and Permissions

Citation: Mediators Inflamm. 2014;2014:345659. doi: 10.1155/2014/345659. Epub 2014 Jul 9. Link to article on publisher's site

DOI of Published Version

10.1155/2014/345659

Comments

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Related Resources

Link to Article in PubMed

Journal Title

Mediators of inflammation

PubMed ID

25120285

Creative Commons License

Creative Commons Attribution 3.0 License
This work is licensed under a Creative Commons Attribution 3.0 License.

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