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Randow, F., MacMicking, J. D., & James, L. C. (2013). Cellular self-defense: How cell-autonomous immunity protects against pathogens. Science, 340(6133), 701–706. Added by: Dr. Enrique Feoli (23/03/2024, 17:21) Last edited by: Dr. Enrique Feoli (23/03/2024, 17:36) |
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| Resource type: Journal Article DOI: 10.1126/science.1233028 BibTeX citation key: Randow2013 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Innate Immunity Keywords: , Creators: James, MacMicking, Randow Collection: Science |
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Conclusiones
Fig. 3 Multilayered defenses synergistically inhibit infection and pathogen replication.
To infect cells and complete their life cycle, retroviruses, such as HIV-1, must pass through multiple compartment borders and access distinct cellular compartments. Virions must recruit and retask cellular cofactors to negotiate their way through the cell and to replicate successfully. Meanwhile, antiviral factors adapted to specific cellular microenvironments target and inhibit specific steps of the viral life cycle. At each stage, only a fraction of virions are successful, which provides a highly synergistic defense system capable of inhibiting even quickly evolving pathogens. LEDGF, PC4 and SFRS1 interacting protein–1; ZAP, zinc finger CCCH-type antiviral protein–1.
Added by: Dr. Enrique Feoli |
| Abstract |
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Provided a pathogen can enter the body and survive coughing and spluttering, peristalsis, and mucus, the first active responses the host evokes to an invading organism will be at the level of the first cell encountered, well before classical cellular immunity and antibody responses are initiated. Randow et al. (p. 701) review the range of intracellular defenses against incoming pathogens and describe how compartmental boundaries within the cell provide multiple levels at which pathogens can be thwarted in their attempts to subjugate the cell to do their bidding. Baxt et al. (p. 697) review the range of evasion tactics that bacterial pathogens can summon to counter host repulsion and establish a niche in which to replicate and ensure onward transmission. Our prevailing view of vertebrate host defense is strongly shaped by the notion of a specialized set of immune cells as sole guardians of antimicrobial resistance. Yet this view greatly underestimates a capacity for most cell lineages—the majority of which fall outside the traditional province of the immune system—to defend themselves against infection. This ancient and ubiquitous form of host protection is termed cell-autonomous immunity and operates across all three domains of life. Here, we discuss the organizing principles that govern cellular self-defense and how intracellular compartmentalization has shaped its activities to provide effective protection against a wide variety of microbial pathogens.
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| Notes |
Fig. 1 Compartmentalization promotes cellular self-defense.
Eukaryotic cells are composed of compartments separated by selectively permeable borders that control their composition. Cell and compartment borders can physically prevent pathogen invasion, and they house sensors that are “tripped” as pathogens try to cross them. Pathogen-induced damage to borders alters compartment composition; the resulting mislocalization of host molecules can be perceived as a danger signal. Control over compartment composition allows potent antimicrobial effectors that otherwise might damage the cell to be safely sequestered. Finally, each cellular compartment represents its own microenvironment that can be made hostile to pathogens.
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