La notion de danger.

Abstract

Pendant de nombreuses années, les recherches en immunologie ont été centrées sur la réponse immunitaire adaptative, et la plupart des immunologistes considéraient que sa fonction principale était de faire la distinction entre soi et non soi. Plus récemment, plusieurs équipes ont proposé que la fonction principale du système immunitaire est en réalité d’éliminer les agents pathogènes. Or, c’est le système immunitaire inné, longtemps négligé, qui joue un rôle essentiel dans l’induction d’une réponse contre les microorganismes. Ce système réagit précocement aux infections, voire instantanément, puis il induit et oriente la réponse du système adaptatif. Plusieurs théories ont été élaborées pour expliquer comment les systèmes inné et adaptatif collaborent dans la réponse immunitaire et la tolérance.

Immunologists have traditionally focused on the adaptive immune response, and have considered that its main function is to distinguish between self (endogenous) and non-self (foreign) antigens. In contrasts, a number of researchers have recently proposed that the main function of the immune system is to eliminate microbial pathogens. The innate immune system, largely neglected in the past, plays an essential role in initiating anti-microbial responses. This system reacts rapidly against infections, and in parallel, it activates and influences the adaptive systems. Several theories have been proposed to explain how the innate and adaptive immune response and affect immune tolerance. According to the model of << immune danger >>, any agent capable of destroying tissue through necrosis and inflammation can trigger an immune response. The << danger model >> has recently converged with a second one, which proposes that the innate system recognizes microorganisms mainly through specific structural motifs expressed by pathogens but not by the host. In contrast, a competing model claims that activation of the immune system is determined by the location and the dose of the antigen, and by the duration of antigen exposure. All three models often invoke microbial pathogens (known or still unknown) to account for autoimmune pathologies.