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The first function described for TLR4 was the recognition of exogenous molecules from pathogens (PAMPs), in particular LPS molecules from gram-negative bacteria. [13] As pattern recognition receptor, TLR4 plays a fundamental role in pathogen recognition and activation of innate immunity which is the first line of defense against invading micro-organisms.
The ability of the immune system to recognize molecules that are broadly shared by pathogens is, in part, due to the presence of immune receptors called toll-like receptors (TLRs) that are expressed on the membranes of leukocytes including dendritic cells, macrophages, natural killer cells, cells of the adaptive immunity T cells, and B cells, and non-immune cells (epithelial and endothelial ...
The innate immune system recognizes microbial pathogens through Toll-like receptors (TLRs), which identify pathogen-associated molecular patterns. Different TLRs recognize different pathogen-associated molecular patterns and all TLRs have a Toll-interleukin 1 receptor (TIR) domain, which is responsible for signal transduction.
Toll-like receptors were first discovered in Drosophila and trigger the synthesis and secretion of cytokines and activation of other host defense programs that are necessary for both innate or adaptive immune responses. 10 functional members of the TLR family have been described in humans so far. [5]
Kagan is recognized for pioneering the cell biological analysis of innate immunity, which revealed a map of the subcellular sites of innate immune signal transduction. His work identified subdomains of the plasma membrane that permit Toll-like Receptor 4 (TLR4) signaling and identified endosomes as a key site from which TLR4 signaling occurs.
Beutler and his team thus proved that one of the mammalian Toll-like receptors, TLR4, acts as the membrane-spanning component of the mammalian LPS receptor complex. [ 2 ] [ 40 ] [ 41 ] They also showed that while mouse TLR4 is activated by a tetra-acylated LPS-like molecule (lipid IVa), human TLR4 is not, recapitulating the species specificity ...
This response is crucial for recruiting adipose tissue macrophages, facilitated by AIM-induced chemokine production through toll-like receptor 4 (TLR4) activation. Administering recombinant AIM to TLR4-deficient mice induces lipolysis without chemokine production, preventing inflammatory macrophage infiltration into adipose tissue and ...
The cascade begins with endotoxin-mediated activation of the Toll-like receptor 4 and CD14, receptors on the Kupffer cell that internalize endotoxin. This in turn activates the transcription of pro-inflammatory cytokines and tumor necrosis factor-alpha (TNFα), with concurrent production of superoxides .