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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 ...
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 ...
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 ...
Bruce Beutler was awarded a portion of the 2011 Nobel Prize in Physiology or Medicine for his work demonstrating that TLR4 is the LPS receptor. [36] [37] As part of the cellular stress response, superoxide is one of the major reactive oxygen species induced by LPS in various cell types that express TLR (toll-like receptor). [38]
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 ...
Lipid A (and LPS) has been demonstrated to activate cells via Toll-like receptor 4 , MD-2 and CD14 on the cell surface. [9] [10] [11] Consequently, lipid A analogs like eritoran can act as TLR4 antagonists. They are being developed as drugs for the treatment of excessive inflammatory responses to infections with gram-negative bacteria. [12]
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.