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TLR4 is a transmembrane protein of approximately 95 kDa that is encoded by the TLR4 gene. TLR4 belongs to the toll-like receptor family which is representative of the pattern recognition receptors (PRR), so named for their ability to recognize evolutionarily conserved components of microorganisms (bacteria, viruses, fungi and parasites) called ...
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 ...
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 ...
This is the conserved structural motif that is recognized by TLR4, particularly the TLR4-MD2 complex. [ 11 ] [ 12 ] Microbes have two main strategies in which they try to avoid the immune system, either by masking lipid A or directing their LPS towards an immunomodulatory receptor.
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 .
The MD-2 protein appears to associate with toll-like receptor 4 on the cell surface and confers responsiveness to lipopolysaccharide (LPS), thus providing a link between the receptor and LPS signaling. [7] That is, the primary interface between TLR4 and MD-2 is formed before binding LPS and the dimerization interface is induced by binding LPS. [8]
Membrane-bound PRRs include toll-like receptors (TLRs) and C-type lectin receptors (CLRs). Cytoplasmic PRRs include NOD-like receptors (NLRs) and RIG-I-like receptors (RLRs). PRRs were first discovered in plants. [6] Since that time many plant PRRs have been predicted by genomic analysis (370 in rice; 47 in Arabidopsis). Unlike animal PRRs ...
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.