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Other forms of innate immunity

[edit]Host defense in prokaryotes (в прокариотах)

Bacteria (and perhaps other prokaryotic organisms), utilize a unique defense mechanism, called the restriction modification system to protect themselves from pathogens, such as bacteriophages. In this system, bacteria produceenzymes, called restriction endonucleases, that attack and destroy specific regions of the viral DNA of invading bacteriophages. Methylation of the host's own DNA marks it as "self" and prevents it from being attacked by endonucleases.[11] Restriction endonucleases and the restriction modification system exist exclusively in prokaryotes.

[edit]Host defense in invertebrates (в беспозвоночных)

Invertebrates do not possess lymphocytes or an antibody-based humoral immune system, and it is likely that a multicomponent, adaptive immune system arose with the first vertebrates.[12] Nevertheless, invertebrates possess mechanisms that appear to be precursors of these aspects of vertebrate immunity. Pattern recognition receptors are proteins used by nearly all organisms to identify molecules associated with microbial pathogens. Toll-like receptors are a major class of pattern recognition receptor, that exists in all coelomates (animals with a body-cavity), including humans.[13] The complement system, as discussed above, is a biochemical cascade of the immune system that helps clear pathogens from an organism, and exists in most forms of life. Some invertebrates, including various insects, crabs, and worms utilize a modified form of the complement response known as the prophenoloxidase (proPO) system.[12]

Antimicrobial peptides are an evolutionarily conserved component of the innate immune response found among all classes of life and represent the main form of invertebrate systemic immunity. Several species of insect produce antimicrobial peptides known as defensins and cecropins.

[edit]Host defense in plants (в растениях)

Members of every class of pathogen which infect humans also infect plants. Although the exact pathogenic species vary with the infected species, bacteria, fungi, viruses, nematodes and insects can all cause plant disease. As with animals, plants attacked by insects or other pathogens use a set of complex metabolic responses that lead to the formation of defensive chemical compounds that fight infection or make the plant less attractive to insects and other herbivores.[14](see: plant defense against herbivory). = (см. растения защищаются против травоядных!!!)

Like invertebrates, plants neither generate antibody or T-cell responses nor possess mobile cells that detect and attack pathogens. In addition, in case of infection, parts of some plants are treated as disposable and replaceable, in ways that very few animals are able to do. Walling off or discarding a part of a plant helps stop spread of an infection.[14]

Most plant immune responses involve systemic chemical signals sent throughout a plant. Plants use pattern-recognition receptors to identify pathogens and to start a basal response, which produces chemical signals that aid in warding off infection. When a part of a plant becomes infected with a microbial or viral pathogen, in case of an incompatible interaction triggered by specific elicitors, the plant produces a localized hypersensitive response (HR), in which cells at the site of infection undergo rapid programmed cell death to prevent the spread of the disease to other parts of the plant. HR has some similarities to animal pyroptosis, such as a requirement of caspase-1-like proteolytic activity of VPEγ, acysteine protease that regulates cell disassembly during cell death.[15]

"Resistance" (R) proteins, encoded by R genes, are widely present in plants and detect pathogens. These proteins contain domains similar to the NOD Like Receptors and Toll-like receptors utilized in animal innate immunity. Systemic acquired resistance (SAR) is a type of defensive response that renders the entire plant resistant to a broad spectrum of infectious agents.[16] SAR involves the production of chemical messengers, such as salicylic acid or jasmonic acid. Some of these travel through the plant and signal other cells to produce defensive compounds to protect uninfected parts, e.g., leaves.[17] Salicylic acid itself, although indispensable for expression of SAR, is not the translocated signal responsible for the systemic response. Recent evidence indicates a role for jasmonates in transmission of the signal to distal portions of the plant. RNA silencing mechanisms are also important in the plant systemic response, as they can block virus replication.[18] The jasmonic acid response, is stimulated in leaves damaged by insects, and involves the production of methyl jasmonate.[14]

[edit]See also



References

  1. a b c d Alberts, Bruce; Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walters (2002). Molecular Biology of the Cell; Fourth Edition. New York and London: Garland Science. ISBN 0-8153-3218-1.
  2. a b c d e f Janeway, Charles; Paul Travers, Mark Walport, and Mark Shlomchik (2001). Immunobiology; Fifth Edition. New York and London: Garland Science. ISBN 0-8153-4101-6..
  3. a b c d e f g Stvrtinová, Viera; Ján Jakubovský and Ivan Hulín (1995). Inflammation and Fever from Pathophysiology: Principles of Disease. Computing Centre, Slovak Academy of Sciences: Academic Electronic Press.
  4. a b Janeway CA, Jr. et al. (2005). Immunobiology. (6th ed. ed.). Garland Science. ISBN 0-443-07310-4.
  5. a b c d Unless else specified in boxes, then ref is: Lippincott's Illustrated Reviews: Immunology. Paperback: 384 pages. Publisher: Lippincott Williams & Wilkins; (July 1, 2007). Language: English. ISBN 0781795435ISBN 978-0781795432. Page 172
  6. ^ Kennedy, Alan. "Immune Evasion by bacteria".
  7. ^ Finlay B, McFadden G (2006). "Anti-immunology: evasion of the host immune system by bacterial and viral pathogens". Cell 124 (4): 767–82. doi:10.1016/j.cell.2006.01.034PMID 16497587.
  8. ^ Finlay B, Falkow S (1997). "Common themes in microbial pathogenicity revisited". Microbiol Mol Biol Rev 61 (2): 136–69. PMID9184008.
  9. ^ Dorland WAN (editor) (2003). Dorland's Illustrated Medical Dictionary (30th ed.). W.B. Saunders. ISBN 0-7216-0146-4.
  10. ^ Kobayashi H (2005). "Airway biofilms: implications for pathogenesis and therapy of respiratory tract infections". Treat Respir Med 4(4): 241–53. doi:10.2165/00151829-200504040-00003PMID 16086598.
  11. ^ Restriction Enzymes Access Excellence Classic Collection Background Paper.
  12. a b Beck, Gregory and Habicht, Gail S. Immunity and the Invertebrates Scientific American. November 1996:60-66.
  13. ^ Imler JL, Hoffmann JA. (2001) Toll receptors in innate immunity. Trends Cell Biol. Jul;11(7):304-11. Review. PMID 11413042
  14. a b c Schneider, David (2005) Plant immune responses Stanford University Department of Microbiology and Immunology.
  15. ^ Rojo, E. et al. (2004). "VPEgamma exhibits a caspase-like activity that contributes to defense against pathogens.". Curr Biol. 14 (21): 1897–1906. doi:10.1016/j.cub.2004.09.056PMID 15530390.
  16. ^ "Chitosan derived from chitin, Chitosan Natural Biocontrol for Agricutlural & Horticultural use".
  17. ^ "Linden, J., Stoner, R., Knutson, K. Gardner-Hughes, C. “Organic Disease Control Elicitors”. Agro Food Industry Hi-Te (p12-15 Oct 2000)".
  18. ^ Baulcombe D (2004). "RNA silencing in plants". Nature 431 (7006): 356–63. doi:10.1038/nature02874PMID 15372043.

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