Abstract
Developing defense mechanisms by the host is fundamental to ensure its survival against various microbial pathogens. At the heart of the host defense against microbes is its ability to initiate an immune response to detect and eliminate potential microbial threats. However, in many cases the aberrant immune response is the cause of the host’s clinical symptoms of infections rather than the microbe itself.
Highlights
Developing defense mechanisms by the host is fundamental to ensure its survival against various microbial pathogens
Myeloid differentiation primary response 88 (Myd88) conduits toll-like receptor 4 (TLR4) surface signaling as a part of a large oligomeric supra-molecular organizing center (SMOC) called Myddosome consisting of oligomers of TLR4, TIR Domain Containing Adaptor Protein (TIRAP), Myd88 and IL-1 receptorassociated kinases (IRAKs) [39,40,41,42,43]
TLR4 dimers interacts with another sorting adaptor called TRIF-related adaptor molecule (TRAM), which seeds the formation of another SMOC, the Triffsome that initiate Toll-interleukin (IL)-1 receptor (TIR)-domain-containing adapter-inducing interferon-β (TRIF)-dependent signaling
Summary
Developing defense mechanisms by the host is fundamental to ensure its survival against various microbial pathogens. Understanding the mechanisms governing the initiation and the regulation of the host’s immune response against various microbial encounters is critical for our understanding of the host-microbe interaction. Charles Janeway Jr. proposed a model of pathogen detection describing two characteristics of innate immune receptors: first, the ability to distinguish between self and non-self molecules, and second is the ability to promote adaptive immune response to the nonself microbial products [2].
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