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Pathogen-associated molecular patterns (PAMPs) are small molecular motifs conserved within a class of microbes, but not present in the host. [1] They are recognized by toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals. [ 2 ]
The microbe-specific molecules that are recognized by a given PRR are called pathogen-associated molecular patterns (PAMPs) and include bacterial carbohydrates (such as lipopolysaccharide or LPS, mannose), nucleic acids (such as bacterial or viral DNA or RNA), bacterial peptides (flagellin, microtubule elongation factors), peptidoglycans and ...
The same cells that recognize PAMPs on microbial pathogens may bind to the antigen of a foreign blood cell and recognize it as a pathogen because the antigen is unfamiliar. [11] It is not easy to classify red blood cell recognition as intrinsic or extrinsic, as a foreign cell may be recognized as part of the organism if it has the right antigens.
In contrast to the noninfectious inflammatory response produced by DAMPs, pathogen-associated molecular patterns (PAMPs) initiate and perpetuate the infectious pathogen-induced inflammatory response. [6] Many DAMPs are nuclear or cytosolic proteins with defined intracellular function that are released outside the cell following tissue injury. [7]
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.
Immunological memory is the ability of the immune system to quickly and specifically recognize an antigen that the body has previously encountered and initiate a corresponding immune response. Generally, they are secondary, tertiary and other subsequent immune responses to the same antigen.
Because APCs are not antigen-specific, capable of processing self structures, Charles Janeway proposed the Infectious Non-self Model in 1989. [3] Janeway's theory involved APCs being activated by pattern recognition receptors (PRRs) that recognize evolutionarily conserved pathogen-associated molecular patterns (PAMPs) as infectious non-self ...
At the beginning, there is a binding of collectin to PAMPs or DAMPs. Collectin MBL is involved in activation of the lectin complement pathway. [ 32 ] [ 33 ] There are three serine proteases, MASP-1, 2 and 3 ( MBL-associated serine proteases ), which participate in activation of the lectin pathway.