Pathogen-associated molecular pattern

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Pathogen-associated molecular patterns, or PAMPs, are molecules associated with groups of pathogens, that are recognized by cells of the innate immune system. These molecules can be referred to as small molecular motifs conserved within a class of microbes. They are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals. A vast array of different types of molecules can serve as PAMPs, including glycans and glycoconjugates.[1]

PAMPs activate innate immune responses, protecting the host from infection, by identifying some conserved non-self molecules. Bacterial lipopolysaccharide (LPS), an endotoxin found on the bacterial cell membrane of a bacterium, is considered to be the prototypical PAMP. LPS is specifically recognised by TLR 4, a recognition receptor of the innate immune system. Other PAMPs include bacterial flagellin (recognized by TLR 5), lipoteichoic acid from Gram positive bacteria, peptidoglycan, and nucleic acid variants normally associated with viruses, such as double-stranded RNA (dsRNA), recognized by TLR 3 or unmethylated CpG motifs, recognized by TLR 9. Although the term "PAMP" is relatively new, the concept that molecules derived from microbes must be detected by receptors from multicellular organisms has been held for many decades, and references to an "endotoxin receptor" are found in much of the older literature.


The term "PAMP" has been criticized on the grounds that most microbes, not only pathogens, express the molecules detected; the term microbe-associated molecular pattern[2] (MAMP),[3] has therefore been proposed. A virulence signal capable of binding to a pathogen receptor, in combination with a MAMP, has been proposed as one way to constitute a (pathogen-specific) PAMP.[4] Plant immunology frequently treats the terms "PAMP" and "MAMP" interchangeably, considering their recognition to be the first step in plant immunity, PTI (PAMP-triggered immunity), a relatively weak immune response that occurs when the host plant does not also recognize pathogenic effectors that damage it or modulate its immune response.[5]

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Notes and references[edit]

  1. ^ Maverakis E, Kim K, Shimoda M, Gershwin M, Patel F, Wilken R, Raychaudhuri S, Ruhaak LR, Lebrilla CB (2015). "Glycans in the immune system and The Altered Glycan Theory of Autoimmunity". J Autoimmun 57 (6): 1–13. doi:10.1016/j.jaut.2014.12.002. PMID 25578468. 
  2. ^ Ausubel (2005). "Are innate immune signaling pathways in plants and animals conserved?". Nature Immunology 6 (10): 973–9. doi:10.1038/ni1253. PMID 16177805. 
  3. ^ Didierlaurent A, Simonet M, Sirard J (2006). "Innate and acquired plasticity of the intestinal immune system". Cell Mol Life Sci 62 (12): 1285–7. doi:10.1007/s00018-005-5032-4. PMC 1865479. PMID 15971103. 
  4. ^ Rumbo M, Nempont C, Kraehenbuhl J, Sirard J (2006). "Mucosal interplay among commensal and pathogenic bacteria: Lessons from flagellin and Toll-like receptor 5". FEBS Letters 580 (12): 2976–84. doi:10.1016/j.febslet.2006.04.036. PMID 16650409.  (Free full text available)
  5. ^ Jones DG, Dangl JL (2006). "The plant immune system". Nature 444 (7117): 323–329. Bibcode:2006Natur.444..323J. doi:10.1038/nature05286. PMID 17108957. 

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