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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Microneme Proteins 1 and 4 From Toxoplasma gondii Induce IL-10 Production by Macrophages Through TLR4 Endocytosis

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Author(s):
Ricci-Azevedo, Rafael [1, 2] ; Costa Mendonca-Natividade, Flavia [1] ; Carolina Santana, Ana [3] ; Alcoforado Diniz, Juliana [4] ; Cristina Roque-Barreira, Maria [1]
Total Authors: 5
Affiliation:
[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Cell & Mol Biol & Pathogen Bioagents, Lab Immunochem & Glycobiol, Ribeirao Preto - Brazil
[2] Univ Brest, Brest Hosp, Grp Etud Thrombose Bretagne Occidentale GETBO, EA 3878, Brest - France
[3] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Cell & Mol Biol & Pathogen Bioagents, Lab Cellular & Mol Biol Mast Cells, Ribeirao Preto - Brazil
[4] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Cell & Mol Biol & Pathogen Bioagents, Lab Mol Parasitol, Ribeirao Preto - Brazil
Total Affiliations: 4
Document type: Journal article
Source: FRONTIERS IN IMMUNOLOGY; v. 12, APR 12 2021.
Web of Science Citations: 0
Abstract

The protozoan parasite Toxoplasma gondii modulates host cell responses to favor its success in the early stage of infections by secreting proteins from its apical organelles. Some of these proteins, including microneme proteins (MICs) 1 and 4, trigger pro-inflammatory host cell responses. The lectins MIC1 and MIC4 interact with N-linked glycans on TLR2 and TLR4, activating NF-kappa B and producing IL-12, TNF-alpha, and IL-6. Interestingly, MIC1 and MIC4 also trigger secretion of the anti-inflammatory cytokine IL-10 through mechanisms as yet unknown. Herein, we show that the ability of these MICs to induce macrophages to produce IL-10 depends on TLR4 internalization from the cell surface. Macrophages subjected to blockade of endocytosis by Dynasore continued to release TNF-alpha, but failed to produce IL-10, in response to MIC1 or MIC4 exposure. Similarly, IL-10 was not produced by Dynasore-conditioned T. gondii-infected macrophages. Furthermore, MIC1- or MIC4-stimulated macrophages gained transient tolerance to LPS. We report a previously undiscovered mechanism by which well-defined T. gondii components inhibit a host inflammatory response. (AU)

FAPESP's process: 13/04088-0 - Lectin from pathogens
Grantee:Maria Cristina Roque Antunes Barreira
Support type: Research Projects - Thematic Grants
FAPESP's process: 17/02998-0 - Effects of Toxoplasma gondii and Paracoccidioides brasiliensis, exerted through their respective lectins on intracellular pathways activated by the recognition of N-linked glycans to toll like receptors on neutrophils
Grantee:Rafael Ricci de Azevedo
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 16/10446-4 - Mechanisms of immunomodulation by ArtinM: basis for the development of new anti-fungal therapy
Grantee:Maria Cristina Roque Antunes Barreira
Support type: Regular Research Grants
FAPESP's process: 14/13324-1 - Interaction of microneme proteins of Toxoplasma gondii with N-linked glycans of TLR4: effects on innate immunity
Grantee:Flávia Costa Mendonça Natividade
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 16/14657-0 - Methylation mediated by PRMT7 on the differentiation process of promastigotes into amastigotes and the parasite Leishmania major virulence
Grantee:Juliana Alcoforado Diniz
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 18/21708-5 - Application of immunomoduladors, by carbohydrate recognition, as therapeutic agents: mechanism of action to immunotherapy
Grantee:Maria Cristina Roque Antunes Barreira
Support type: Research Projects - Thematic Grants