PAF as an endogenous modulator of Dendritic Cells phenotype and function.

Author(s)

Marianna Mainardi Koga

• Document type: Doctoral Thesis
• Press: São Paulo.
• Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI)
• Defense date: 2015-10-16

Examining board members

Sonia Jancar Negro; Jose Alexandre Marzagao Barbuto; Ana Campa; Roger Chammas; Lucia Helena Faccioli

• Advisor: Sonia Jancar Negro; Francisco José Oliveira Rios

Abstract

In the present work we show that BALB/c mice dendritic cells (DCs) express the PAF (platelet-activating factor) receptor and that its activation promotes a tolerogenic phenotype via IL10 and PGE2 production. Blocking PAFR by selective antagonists markedly enhanced DCs ability to induce T cell proliferation. The antagonist WEB2170 potentiated the in vivo immune response the IgG2a OVA-specific levels were 30 fold increased in the treated group; IgG1 concentration was similar for both groups. The PAFR blockade in mice immunized with OVA in complete Freunds adjuvant enhanced both IgG1 and IgG2a OVA-specific antibody production. In OVA/alum immunized mice, the antagonist did not change IgG1 production. These results suggest that PAFR activation in DCs modulates their antigen-presenting function through IL10 and PGE2 production. Blocking PAFR may be useful to induce DCs activation in DCs-based vaccination protocols and/or as a co-adjuvant in immunization protocols. (AU)

• FAPESP's process: 10/09120-0 - Modulation of dendritic cell phenotype by the Platelet-Activating Factor Receptor (PAFR) and the consequences for the immune response
• Grantee: Marianna Mainardi Koga
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)