Inflammasoma
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Inflammasoma (-atis, n.) est complexus proteinorum oligomerorum responsa inflammatoria[1] per varios adaptores[2] excitatus. Adaptoribus incitatum his inflammasoma enzymum caspasem 1[3] se immutare impellit ita, ut praecursor interleukini 1 beta macrophagocytis liberatus in formam activam interleukinumi 1 activi (IL-1β) et febrem generantis convertatur ideoque cataracta inflammationis biochemica continuetur.
Inflammasomatum complexus, qui in textu myeloideo locati sunt ex enzymis caspasi 1 ac PYCARD et receptorio NALP et nonnumquam enzymo caspasi 5 compositi sunt. Variae formae receptoriorum NALP complexu ligatae notae sunt.
Natura inflammasomatum[recensere | fontem recensere]
Contextus[recensere | fontem recensere]
Sub inflammationem systema immunitatis innatum machinationem defensionis contestari oportet. Post stimulationem inflammasomate primum liberatio ex cellula cytokinorum conceditur, deinde extra cellulam pyroptosis (mors cellularum programmata) fit[4].
Structura[recensere | fontem recensere]
Inflammasomata sunt complexus ex diversis proteinis compositi, ita ex enzymis caspasi 1 ac PYCARD et receptorio NALP et nonnumquam enzymo caspasi 5. Variae formae rececptoriorum NALP complexu ligatae notae sunt, quo inflammasomata NLRP1 et NLRP3[5] et NLRC4 munerum singularium nominata sunt.
Physiologia[recensere | fontem recensere]
Quando infectio prodit cellulae systematis immunitatis, ut monocyti, macrophagocyti receptoria peculiaria, receptoria exempla cognoscendorum (Anglice Pattern Recognition Receptors, PRR) enim, exprimunt: et superficie membranae et intra cellulam.
Haec PRR′ia modo duo genera stimulorum cognoscunt: PAMP vel DAMP. PAMP est abbreviatura Anglica "pathogenis sociatorum exemplorum molecularis" (pathogen-associated molecular patterns), quae sunt partes corpori alienae, per exemplum lipopolysaccharidi bacteriorum. Pluribus exemplis alienis receptoria propria ex familia receptoriorum typi Toll instar (abbreviatura internationalis: TLR) superficie cellulae sunt; Exemplum flagella bacterialia per TLR 5 superficie membranae cellularum immunitatis recognoscuntur[6]. DAMP sunt "vastitatibus sociata exempla molecularia" (damage-associated molecular patterns), quae sunt partes cellularum vulneratarum corporis poprii denaturatae: Quando damnum cellularum prodit, organella ex cellula liberata signum initii inflammationis fient[7].
Inter cytokina et inflammasomata cellularum immunitatis mutuo signa dantur[8].
Notae[recensere | fontem recensere]
- ↑ Martinon F., Burns K., Tschopp J. (2002). "The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta". Mol Cell 10 (2): 417-26.
- ↑ Mariathasan S., Newton K., Monack D. M., Vucic D., French D. M., Lee W. P., Roose-Girma M., Erickson S., Dixit V. M. (2004). "Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf". Nature 430 (6996): 213-8.
- ↑ seu interleukini 1 beta convertasis
- ↑ Fink S. L., Cookson B. T. (2006). "Caspase-1-dependent pore formation during pyroptosis leads to osmotic lysis of infected host macrophages". Cell Microbiol 8 (11): 1812-25.
- ↑ Lebeaupin C., Proics E., de Bieville C. H., Rousseau D., Bonnafous S., Patouraux S., Adam G., Lavallard V. J., Rovere C., Le Thuc O., Saint-Paul M. C., Anty R., Schneck AS., Iannelli A., Gugenheim J., Tran A., Gual P., Bailly-Maitre B. (2015). "ER stress induces NLRP3 inflammasome activation and hepatocyte death". Cell Death Dis 6: e1879
- ↑ Rumbo M., Nempont C., Kraehenbuhl J. P., Sirard J. C. (2006). "Mucosal interplay among commensal and pathogenic bacteria: lessons from flagellin and Toll-like receptor 5". FEBS Lett 580 (12): 2976-84.
- ↑ Rubartelli A., Lotze M. T. (2007). "Inside, outside, upside down: damage-associated molecular-pattern molecules (DAMPs) and redox". Curr Opin Immunol 23 (5): 591-7.
- ↑ Barker B. R., Taxman D. J., Ting J. P. (2011). "Cross-regulation between the IL-1β/IL-18 processing inflammasome and other inflammatory cytokines". Curr Opin Immunol 23 (5): 591-7.