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| Author(s): |
Walmir Cutrim Aragão Filho
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2014-06-27 |
| Examining board members: |
Antonio Condino Neto;
Edson Antunes;
Lucia Rossetti Lopes;
Pérsio Roxo Júnior;
Alexandre Alarcon Steiner
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| Advisor: | Antonio Condino Neto |
| Abstract | |
The NADPH oxidase system is an enzymatic complex that generates superoxide anion, it is formed by gp91-phox, p22-phox, p47-phox, p67-phox and p40-phox subunits. The IL-12/23-IFN-g axis is critical for the phagocytes activation and infection control. Defects in this axis activation result in recurrent infections and MSMD, and can lead to decreased expression of gp91-phox component. In my Master Thesis (Aragão-Filho, 2009), we found that the subunits 1 and 2 of the IFN-g receptor are required for NCF1 and NCF2 gene expression and activation of human NADPH oxidase system in human experimental cell models that we used. Therefore, in the present doctoral work, we continue to investigate the role of IL-12/23-IFN-g axis defects on NADPH oxidase system using new cell lines from patients with IL-12/23-IFN-g axis defects. We verify that there is a secundary defect in the activation of the NADPH oxidase from patients with IL-12/23-IFN-g defects, what represents a new immunopathological mechanism involved in MSMD. (AU) | |