host–pathogen interactions a biological rendez-vous of the infectious nonself and danger modelshost-pathogen交互感染的生物一起异物和危险模型.pdfVIP

host–pathogen interactions a biological rendez-vous of the infectious nonself and danger modelshost-pathogen交互感染的生物一起异物和危险模型.pdf

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host–pathogen interactions a biological rendez-vous of the infectious nonself and danger modelshost-pathogen交互感染的生物一起异物和危险模型

Opinions Host–Pathogen Interactions: A Biological Rendez-Vous of the Infectious Nonself and Danger Models? Jean-Nicolas Tournier*, Anne Quesnel-Hellmann ‘‘Les phenomenes biologiques presentent une telle complexite que system in nonpathogen-associated situations such as allograft ´ ` ´ ´ lorsqu’on a etabli une regle les concernant, il faut toujours s’attendre a rejection or autoimmunity. For autoimmunity, recent works ´ ` ` des exceptions plus ou moins nombreuses. [Biological phenomena are so demonstrate a crucial role of TLR activation in at least two complex, that when a new rule has been established, it is expected to murine models of autoimmune diseases such as type 1 find several exceptions.] ’’ —Elie Metchnikov [1] diabetes and lupus [9,10]. In the early 90s, Polly Matzinger proposed the ‘‘danger’’ ntil recently, immunologists had thought of the model as an alternative and comprehensive view of the U immune system as a complex cellular web aimed at immune system, where endogenous danger signals (e.g., protecting the body against marauding microbes, by cytokines) released from infected cells could affect the producing a highly specialized, specific, and adaptive function of antigen-presenting cells (APCs) without directly response. This adaptive response involves the production of a exposing APCs to PAMPs [11]. The danger model had broader specific receptor for each antigenic motif (e.g., B cell implications than the INS model, since it could predict the receptors, antibodies, and T cell rec

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