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http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2252| Título : | Producción defectuosa de citocinas mediada por receptor 9 de tipo Toll en células B de ratones deficientes en tirosina quinasa de Bruton. Defective Toll-like receptor 9-mediated cytokine production in B cells from Bruton's tyrosine kinase-deficient mice. |
| Creador: | Hasan M |
| Nivel de acceso: | Open access |
| Palabras clave : | Linfocitos B - inmunología Citocinas - biosíntesis Proteínas Tirosina Quinasas - inmunología Receptores Toll-Like Inmunología B-Lymphocytes - immunology Cytokines - biosynthesis Protein-Tyrosine Kinases - immunology Toll-Like Receptor immunology Cinasa de la tirosina de Bruton células B receptores Toll-like 9 citoquinas inflamación Bruton's tyrosine kinase B cells Toll-like receptor 9 cytokines inflammation |
| Descripción : | Bruton's tyrosine kinase (Btk), a member of the Tec family of tyrosine kinases, plays an important role in the differentiation and activation of B cells. Mutations affecting Btk cause immunodeficiency in both humans and mice. In this study we set out to investigate the potential role of Btk in Toll-like receptor 9 (TLR9) activation and the production of pro-inflammatory cytokines such as interleukin (IL)-6, tumour necrosis factor (TNF)-alpha and IL-12p40. Our data show that Btk-deficient B cells respond more efficiently to CpG-DNA stimulation, producing significantly higher levels of pro-inflammatory cytokines but lower levels of the inhibitory cytokine IL-10. The quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis presented in this work shows that mRNAproduction of one of the important new members of the IL-12 family, IL-27, was significantly increased in Btk-deficient B cells after CpG-DNA stimulation. In this study, we demonstrate significant differences in CpG responsiveness between transitional 1 (T1) and T2B cells for survival and maturation. Furthermore, TLR9 expression, measured both as protein and as mRNA, was increased in Btk-defective cells, especially after TLR9 stimulation. Collectively, these data provide evidence in support of the theory that Btk regulates both TLR9 activation and expression in mouse splenic B cells. |
| Colaborador(es) u otros Autores: | Lopez-Herrera G Blomberg KE Lindvall JM Berglöf A Smith CI Vargas L |
| Fecha de publicación : | 2008 |
| Tipo de publicación: | Artículo |
| Formato: | |
| Identificador del Recurso : | 10.1111/j.1365-2567.2007.02693.x |
| Fuente: | Immunology. 123(2):239-49 |
| URI : | http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2252 |
| Idioma: | eng |
| Aparece en las colecciones: | Artículos |
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