Toll-Like Receptors - Biochemistry

Toll-like receptors found on immune cells recognize pathogens and recruit other immune cells to clear the pathogen. These toll-like receptors are found in both innate immune system (macrophages and neutrophils) and in adaptive immune system (lymphocytes). Recall that acute inflammation is mediated by neutrophils and macrophages whereas chronic inflammation is mediated by lymphocytes; therefore, toll-like receptors can activate both acute and chronic inflammation. Complements are part of the innate immune system and serve as markers (opsonins) for pathogen recognition. Complements bind to an infected cell or to an antibody-antigen complex and signal immune cells to eliminate the pathogen. They do not utilize toll-like receptors.

Upon activation, toll-like receptors activate a transcription factor called nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB). This transcription factor ultimately activates genes in the genome that are involved in immune response. Upon activation of NF-KB, genes undergo transcription and produce mRNA which can eventually be converted to proteins that facilitate the immune response; therefore, activation of toll-like receptors (TLR's) activates transcription.

Toll-like receptors can be activated by bacterial components such as lipopolysaccharide, peptidoglycan, flagellin, and bacterial DNA. Toll-like receptors activate transcription factors and immune regulatory factors.Activation triggers the production of pro-inflammatory cytokines such as interleukins.

Toll-like receptors are special molecules that recognize specific portions of pathogens called PAMPs (pathogen associated molecular patterns). The toll-like receptors on the immune cells recognize PAMPs on the pathogen. One of the most common PAMPs recognized by toll-like receptors is peptidoglycan on the cell walls of the bacteria.

Toll-like receptors found on immune cells recognize pathogens and recruit other immune cells to clear the pathogen. These toll-like receptors are found in both innate immune system (macrophages and neutrophils) and in adaptive immune system (lymphocytes). Recall that acute inflammation is mediated by neutrophils and macrophages whereas chronic inflammation is mediated by lymphocytes; therefore, toll-like receptors can activate both acute and chronic inflammation. Complements are part of the innate immune system and serve as markers (opsonins) for pathogen recognition. Complements bind to an infected cell or to an antibody-antigen complex and signal immune cells to eliminate the pathogen. They do not utilize toll-like receptors.

Upon activation, toll-like receptors activate a transcription factor called nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB). This transcription factor ultimately activates genes in the genome that are involved in immune response. Upon activation of NF-KB, genes undergo transcription and produce mRNA which can eventually be converted to proteins that facilitate the immune response; therefore, activation of toll-like receptors (TLR's) activates transcription.

Toll-like receptors can be activated by bacterial components such as lipopolysaccharide, peptidoglycan, flagellin, and bacterial DNA. Toll-like receptors activate transcription factors and immune regulatory factors.Activation triggers the production of pro-inflammatory cytokines such as interleukins.

Toll-like receptors are special molecules that recognize specific portions of pathogens called PAMPs (pathogen associated molecular patterns). The toll-like receptors on the immune cells recognize PAMPs on the pathogen. One of the most common PAMPs recognized by toll-like receptors is peptidoglycan on the cell walls of the bacteria.

Toll-like receptors found on immune cells recognize pathogens and recruit other immune cells to clear the pathogen. These toll-like receptors are found in both innate immune system (macrophages and neutrophils) and in adaptive immune system (lymphocytes). Recall that acute inflammation is mediated by neutrophils and macrophages whereas chronic inflammation is mediated by lymphocytes; therefore, toll-like receptors can activate both acute and chronic inflammation. Complements are part of the innate immune system and serve as markers (opsonins) for pathogen recognition. Complements bind to an infected cell or to an antibody-antigen complex and signal immune cells to eliminate the pathogen. They do not utilize toll-like receptors.

Upon activation, toll-like receptors activate a transcription factor called nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB). This transcription factor ultimately activates genes in the genome that are involved in immune response. Upon activation of NF-KB, genes undergo transcription and produce mRNA which can eventually be converted to proteins that facilitate the immune response; therefore, activation of toll-like receptors (TLR's) activates transcription.

Toll-like receptors can be activated by bacterial components such as lipopolysaccharide, peptidoglycan, flagellin, and bacterial DNA. Toll-like receptors activate transcription factors and immune regulatory factors.Activation triggers the production of pro-inflammatory cytokines such as interleukins.

Toll-like receptors are special molecules that recognize specific portions of pathogens called PAMPs (pathogen associated molecular patterns). The toll-like receptors on the immune cells recognize PAMPs on the pathogen. One of the most common PAMPs recognized by toll-like receptors is peptidoglycan on the cell walls of the bacteria.

Toll-like receptors found on immune cells recognize pathogens and recruit other immune cells to clear the pathogen. These toll-like receptors are found in both innate immune system (macrophages and neutrophils) and in adaptive immune system (lymphocytes). Recall that acute inflammation is mediated by neutrophils and macrophages whereas chronic inflammation is mediated by lymphocytes; therefore, toll-like receptors can activate both acute and chronic inflammation. Complements are part of the innate immune system and serve as markers (opsonins) for pathogen recognition. Complements bind to an infected cell or to an antibody-antigen complex and signal immune cells to eliminate the pathogen. They do not utilize toll-like receptors.

Upon activation, toll-like receptors activate a transcription factor called nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB). This transcription factor ultimately activates genes in the genome that are involved in immune response. Upon activation of NF-KB, genes undergo transcription and produce mRNA which can eventually be converted to proteins that facilitate the immune response; therefore, activation of toll-like receptors (TLR's) activates transcription.

Toll-like receptors can be activated by bacterial components such as lipopolysaccharide, peptidoglycan, flagellin, and bacterial DNA. Toll-like receptors activate transcription factors and immune regulatory factors.Activation triggers the production of pro-inflammatory cytokines such as interleukins.