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Master's Dissertation
DOI
10.11606/D.42.2009.tde-08072009-150021
Document
Author
Full name
Walmir Cutrim Aragão Filho
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2009
Supervisor
Committee
Condino Neto, Antonio (President)
Muscara, Marcelo Nicolas
Roxo Júnior, Pérsio
Title in Portuguese
O papel do fator nuclear kappa B (NF-kB) e do eixo IL-12/23-IFN-g na ativação do sistema NADPH oxidase.
Keywords in Portuguese
Déficit
Displasia ectodérmica anidrótica com imunodeficiência
Eixo IL-12/23-IFN-g
Fator nuclear kappa B
Imunologia
NADPH oxidase
Abstract in Portuguese
O sistema NADPH oxidase é um complexo enzimático gerador de superóxido. O NF-kB é um fator de transcrição envolvido no controle da expressão de diversos genes ligados à resposta inflamatória. Defeitos no eixo IL-12/23-IFN-g resultam em infecções recorrentes e à susceptibilidade mendeliana a micobacterioses, podendo diminuir a expressão do componente gp91-phox da NADPH oxidase. Estudamos qual é a relação direta do NF-kB e de defeitos no eixo IL-12/23-IFN-g na regulação dos genes CYBA, NCF1, NCF2 e NCF4 do sistema NADPH oxidase humano em células U937, células B EBV transformadas provenientes de pacientes com EDA-ID, DGC, ou de pacientes com defeitos no eixo IL-12/23-IFN-g. A expressão dos genes NCF1 e NCF2 foi diminuída em células com defeitos no eixo (IFNGR1 e INFGR2) e em células U937 IkB S32A/S36A. A expressão do gene NCF1 também foi diminuída em células EDA-ID S32I e em células EDA-ID NEMO/IKKg W420X. O NF-kB e os IFNGR1 e INFGR2 são necessários para a expressão dos genes NCF1 e NCF2 e para a ativação do sistema NADPH oxidase humano neste sistema modelo.
Title in English
The role of nuclear factor kappa B (NF-kB) and the IL-12/23-IFN-g axis in the activation of the NADPH oxidase system.
Keywords in English
Anhidrotic ectodermal dysplasia with immunodeficiency
Axis IL-12/23-IFN-gama
Deficit
Immunology
NADPH oxidase
Nuclear factor kappa B
Abstract in English
The NADPH oxidase system is an enzymatic complex that generates superoxide. The NF-kB is a transcriptional factor involved in the expression of several genes related to the inflammatory response. The IL-12/23-IFN-g axis defects lead to recurrent infections and to the mendelian susceptibility of mycobacterial disease (MSMD), and they can decrease the gp91-phox expression (a NADPH oxidase component). We studied the NF-kB and the IL-12/23-IFN-g axis defects consequences on the regulation of CYBA, NCF1, NCF2 and NCF4 genes of the human NADPH oxidase system in U937 cells, and in B EBV cells from patients with EDA-ID, DGC, or patients with IL-12/23-IFN-g axis defects. The NCF1 and NCF2 gene expression was decreased in IL-12/23-IFN-g axis defects cells (IFNGR1 and INFGR2) and in U937 IkB S32A/S36A cells. NCF1 gene expression was decreased in EDA-ID S32I and in EDA-ID NEMO/IKKg W420X cell lineages. The NF-kB and the IFNGR1 and INFGR2 are necessary for NCF1 and NCF2 gene expression and activation of the human NADPH oxidase in this model system.
 
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Publishing Date
2009-08-17
 
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