3/16/2024 0 Comments System shock 1 data fragment 3![]() ![]() ![]() Uric acid, a byproduct of nucleotide metabolism, is released upon necrotic cell death ( 5). ![]() The precise nature of these intracellular-host-derived signals is emerging. Although TLR engagement by infectious agents can activate the innate immune response, so too can the cellular products released during necrotic cell death. In their model, such signals could be derived from either the host or infectious agents. This fact led Fuchs and Matzinger ( 2, 3, 4) to propose a model in which the immune system is activated by danger signals. However, such molecules do not directly explain immune responses generated against transplanted organs and tumors. Indeed, PAMPS can account for immune responses against infectious agents. To account for these observations, Janeway posited that the immune system responds to pathogen-associated molecular patterns (PAMPS) 4 that are inherent to the make-up of infectious agents and distinguish them from host molecules ( 1). Inherent to two signal models of immune activation is the fact that the Ags are not the critical determinant of whether recognition will lead to activation or tolerance, but rather molecules that have the ability to activate APCs. ![]()
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