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Progress on mechanisms for pathogensto evade NOD-like receptor and Toll-like receptor signaling pathways / 浙江大学学报·医学版
Journal of Zhejiang University. Medical sciences ; (6): 218-224, 2017.
Artículo en Chino | WPRIM | ID: wpr-819080
ABSTRACT
The innate immune system provides a first line of defense against invading pathogens, in which the pattern recognition receptors (PRR) recognize pathogen-associated molecular patterns (PAMP) and initiate the downstream signaling pathways to eliminate the encountered pathogens. There are two main classes of such signaling pathways NOD-like receptor (NLR) signaling pathway and Toll-like receptor (TLR) signaling pathway. The microbial pathogens under selective pressure have evolved numerous mechanisms to avoid and/or manipulate the NLR and TLR signal transduction for survival and replication. To evade the NLR signaling pathway, pathogens interfere and/or inhibit inflammasome activation in innate immune cells by producing virulence factors or reducing PAMPs expression. The mechanisms for pathogens to evade TLR signaling pathway include inhibition of mitogen activated protein kinases (MAPKs) cascade reaction, inhibition of NF-КB activation, and interference of down-stream signal transduction by producing Toll/interleukin-1 receptor (TIR)-containing proteins which bind directly with TLRs or adaptor proteins in the signaling pathway.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Transducción de Señal / Receptores de Interleucina-1 / Alergia e Inmunología / Receptores Toll-Like / Proteínas NLR / Inmunidad Innata / Metabolismo Idioma: Chino Revista: Journal of Zhejiang University. Medical sciences Año: 2017 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Transducción de Señal / Receptores de Interleucina-1 / Alergia e Inmunología / Receptores Toll-Like / Proteínas NLR / Inmunidad Innata / Metabolismo Idioma: Chino Revista: Journal of Zhejiang University. Medical sciences Año: 2017 Tipo del documento: Artículo