Диссертация (Клиническое значение определения сывороточного маркера активации нейтрофилов – алармина S100A12 при аутовоспалительных заболеваниях), страница 18
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Москва, 1973. 199 c.10213. Breda L. et al. Laboratory tests in the diagnosis and follow-up of pediatricrheumatic diseases: an update // Semin. Arthritis Rheum. 2010. Vol. 40, № 1. P.53–72.14. Kang J.H., Hwang S.M., Chung I.Y. S100A8, S100A9 and S100A12 activateairway epithelial cells to produce MUC5AC via extracellular signal-regulatedkinase and nuclear factor-κB pathways // Immunology. 2015. Vol. 144, № 1.
P. 79–90.15. Kessel C., Holzinger D., Foell D. Phagocyte-derived S100 proteins inautoinflammation: putative role in pathogenesis and usefulness as biomarkers //Clin. Immunol. Orlando Fla. 2013. Vol. 147, № 3. P. 229–241.16. Клатт Э. Атлас патологии Роббинса и Котрана Клатт Э. Логосфера.
Москва,2010.17. French FMF Consortium. A candidate gene for familial Mediterranean fever // Nat.Genet. 1997. Vol. 17, № 1. P. 25–31.18. Masters S.L. et al. Horror autoinflammaticus: the molecular pathophysiology ofautoinflammatory disease // Annu. Rev. Immunol. 2009. Vol. 27. P. 621–668.19.
Ombrello M.J., Kastner D.L. Autoinflammation in 2010: expanding clinicalspectrum and broadening therapeutic horizons // Nat. Rev. Rheumatol. 2011. Vol.7, № 2. P. 82–84.20. Lamkanfi M., Vande Walle L., Kanneganti T.-D. Deregulated inflammasomesignaling in disease // Immunol. Rev.
2011. Vol. 243, № 1. P. 163–173.21. Mayadas T.N., Cullere X., Lowell C.A. The multifaceted functions of neutrophils //Annu. Rev. Pathol. 2014. Vol. 9. P. 181–218.22. Mantovani A. et al. Neutrophils in the activation and regulation of innate andadaptive immunity // Nat. Rev. Immunol. 2011. Vol. 11, № 8. P.
519–531.23. Kolaczkowska E., Kubes P. Neutrophil recruitment and function in health andinflammation // Nat. Rev. Immunol. 2013. Vol. 13, № 3. P. 159–175.24. Amulic B. et al. Neutrophil function: from mechanisms to disease // Annu. Rev.Immunol. 2012. Vol.
30. P. 459–489.10325. Ley K. et al. Getting to the site of inflammation: the leukocyte adhesion cascadeupdated // Nat. Rev. Immunol. 2007. Vol. 7, № 9. P. 678–689.26. Phillipson M. et al. Endothelial domes encapsulate adherent neutrophils andminimize increases in vascular permeability in paracellular and transcellularemigration // PloS One. 2008. Vol. 3, № 2.
P. e1649.27. Carman C.V. et al. Transcellular diapedesis is initiated by invasive podosomes //Immunity. 2007. Vol. 26, № 6. P. 784–797.28. Trinchieri G., Sher A. Cooperation of Toll-like receptor signals in innate immunedefence // Nat. Rev. Immunol. 2007. Vol. 7, № 3. P. 179–190.29. Parker L.C. et al. The expression and roles of Toll-like receptors in the biology ofthe human neutrophil // J.
Leukoc. Biol. 2005. Vol. 77, № 6. P. 886–892.30. Хаитов Р.М. Иммунология: структура и функции иммунной системы: учебноепособие. ГЭОТАР-Медиа. М., 2013. 280 c.31. Rabiet M.-J., Huet E., Boulay F. The N-formyl peptide receptors and theanaphylatoxin C5a receptors: an overview // Biochimie. 2007.
Vol. 89, № 9. P.1089–1106.32. Schymeinsky J., Mócsai A., Walzog B. Neutrophil activation via beta2 integrins(CD11/CD18): molecular mechanisms and clinical implications // Thromb.Haemost. 2007. Vol. 98, № 2. P. 262–273.33. Nordenfelt P., Tapper H. Phagosome dynamics during phagocytosis by neutrophils// J.
Leukoc. Biol. 2011. Vol. 90, № 2. P. 271–284.34. Oppenheim J.J., Yang D. Alarmins: chemotactic activators of immune responses //Curr. Opin. Immunol. 2005. Vol. 17, № 4. P. 359–365.35. Bianchi M.E., Manfredi A.A. Immunology. Dangers in and out // Science. 2009.Vol. 323, № 5922. P. 1683–1684.36. Chan J.K. et al. Alarmins: awaiting a clinical response // J.
Clin. Invest. 2012. Vol.122, № 8. P. 2711–2719.37. Brinkmann V. et al. Neutrophil extracellular traps kill bacteria // Science. 2004.Vol. 303, № 5663. P. 1532–1535.10438. Clark S.R. et al. Platelet TLR4 activates neutrophil extracellular traps to ensnarebacteria in septic blood // Nat. Med. 2007. Vol. 13, № 4. P. 463–469.39. Papayannopoulos V., Zychlinsky A. NETs: a new strategy for using old weapons //Trends Immunol. 2009. Vol. 30, № 11. P. 513–521.40.
Fuchs T.A. et al. Extracellular DNA traps promote thrombosis // Proc. Natl. Acad.Sci. U. S. A. 2010. Vol. 107, № 36. P. 15880–15885.41. Soehnlein O., Weber C., Lindbom L. Neutrophil granule proteins tune monocyticcell function // Trends Immunol. 2009. Vol. 30, № 11. P. 538–546.42. Schultze J.L., Schmieder A., Goerdt S. Macrophage activation in human diseases //Semin.
Immunol. 2015. Vol. 27, № 4. P. 249–256.43. Broderick L. et al. The Inflammasomes and Autoinflammatory Syndromes // Annu.Rev. Pathol. Mech. Dis. 2015. Vol. 10, № 1. P. 395–424.44. Sidiropoulos P.I. et al. Inflammasomes and rheumatic diseases: evolving concepts //Ann.
Rheum. Dis. 2008. Vol. 67, № 10. P. 1382–1389.45. Schmitz J. et al. IL-33, an interleukin-1-like cytokine that signals via the IL-1receptor-related protein ST2 and induces T helper type 2-associated cytokines //Immunity. 2005. Vol. 23, № 5. P. 479–490.46. Thornberry N.A. et al. A novel heterodimeric cysteine protease is required forinterleukin-1 beta processing in monocytes // Nature. 1992. Vol. 356, № 6372. P.768–774.47. Luksch H. et al.
Current knowledge on procaspase-1 variants with reduced orabrogated enzymatic activity in autoinflammatory disease // Curr. Rheumatol. Rep.2015. Vol. 17, № 7. P. 45.48. Mariathasan S. et al. Cryopyrin activates the inflammasome in response to toxinsand ATP // Nature. 2006. Vol. 440, № 7081. P. 228–232.49. Sutterwala F.S. et al. Critical role for NALP3/CIAS1/Cryopyrin in innate andadaptive immunity through its regulation of caspase-1 // Immunity. 2006.
Vol. 24,№ 3. P. 317–327.50. Martinon F. et al. Gout-associated uric acid crystals activate the NALP3inflammasome // Nature. 2006. Vol. 440, № 7081. P. 237–241.10551. Feldmann J. et al. Chronic infantile neurological cutaneous and articular syndromeis caused by mutations in CIAS1, a gene highly expressed in polymorphonuclearcells and chondrocytes // Am. J. Hum.
Genet. 2002. Vol. 71, № 1. P. 198–203.52. Aksentijevich I. et al. De novo CIAS1 mutations, cytokine activation, and evidencefor genetic heterogeneity in patients with neonatal-onset multisystem inflammatorydisease (NOMID): a new member of the expanding family of pyrin-associatedautoinflammatory diseases // Arthritis Rheum. 2002.
Vol. 46, № 12. P. 3340–3348.53. Hoffman H.M. et al. Mutation of a new gene encoding a putative pyrin-like proteincauses familial cold autoinflammatory syndrome and Muckle-Wells syndrome //Nat. Genet. 2001. Vol. 29, № 3. P. 301–305.54. Duncan J.A. et al. Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requiresATP binding to mediate inflammatory signaling // Proc. Natl. Acad. Sci. U. S. A.2007. Vol.
104, № 19. P. 8041–8046.55. Ferrari D. et al. The P2X7 receptor: a key player in IL-1 processing and release // J.Immunol. Baltim. Md 1950. 2006. Vol. 176, № 7. P. 3877–3883.56. Pelegrin P., Barroso-Gutierrez C., Surprenant A. P2X7 receptor differentiallycouples to distinct release pathways for IL-1beta in mouse macrophage // J.Immunol. Baltim. Md 1950. 2008. Vol.
180, № 11. P. 7147–7157.57. Neven B. et al. Molecular basis of the spectral expression of CIAS1 mutationsassociatedwithphagocyticcell-mediatedautoinflammatorydisordersCINCA/NOMID, MWS, and FCU // Blood. 2004. Vol. 103, № 7. P. 2809–2815.58. Hoffman H.M., Wanderer A.A., Broide D.H. Familial cold autoinflammatorysyndrome: phenotype and genotype of an autosomal dominant periodic fever // J.Allergy Clin. Immunol.
2001. Vol. 108, № 4. P. 615–620.59. Stych B., Dobrovolny D. Familial cold auto-inflammatory syndrome (FCAS):characterization of symptomatology and impact on patients’ lives // Curr. Med.Res. Opin. 2008. Vol. 24, № 6. P. 1577–1582.60. Dodé C. et al. New mutations of CIAS1 that are responsible for Muckle-Wellssyndrome and familial cold urticaria: a novel mutation underlies both syndromes //Am. J. Hum.
Genet. 2002. Vol. 70, № 6. P. 1498–1506.10661. Hawkins P.N. et al. Spectrum of clinical features in Muckle-Wells syndrome andresponse to anakinra // Arthritis Rheum. 2004. Vol. 50, № 2. P. 607–612.62. Aganna E. et al. Association of mutations in the NALP3/CIAS1/PYPAF1 genewith a broad phenotype including recurrent fever, cold sensitivity, sensorineuraldeafness, and AA amyloidosis // Arthritis Rheum. 2002. Vol. 46, № 9. P.
2445–2452.63. Goldbach-Mansky R. et al. Neonatal-onset multisystem inflammatory diseaseresponsive to interleukin-1beta inhibition // N. Engl. J. Med. 2006. Vol. 355, № 6.P. 581–592.64. Sibley C.H. et al. Sustained response and prevention of damage progression inpatients with neonatal-onset multisystem inflammatory disease treated withanakinra: a cohort study to determine three- and five-year outcomes // ArthritisRheum. 2012. Vol. 64, № 7. P. 2375–2386.65.