The role of IL-36γ/IL-1F9 in developing erythroderma in patients with psoriasis

Cover Page


Cite item

Full Text

Abstract

Erythroderma is the term used for naming any inflammatory skin disease affecting over 90% of cutaneous surface. Numerous etiologic factors may background erythroderma; however, this condition is most often associated with such underlying diseases as eczema, drug hypersensitivity syndrome, cutaneous epidermotropic lymphoma, photosensitization. Being the most severe clinical form of psoriasis, psoriatic erythroderma may be a life hazard in patients with psoriasis, requiring admission and systemic treatment. The paper reviews modern data on psoriasis and psoriatic erythroderma pathogenesis. The biological role of IL-36γ/IL-1F9 - novel specific marker of psoriasis - is described in detail. Data of researches of this marker in different forms of inflammatory skin disease are discussed. Unlike other earlier described markers of psoriasis, for example, S100 A7, A8, A9 proteins, IL-36γ was highly specific to psoriasis, and rarely found at other inflammatory skin diseases (atopic dermatitis, contact dermatitis). The role of IL-36γ in diagnosing erythroderma in patients with psoriasis is described. The most specific and promising marker for distinguishing psoriatic erythroderma from other forms of erythroderma, IL-36γ can be detected at early stages of the disease, allowing to administer early causative treatment, improving treatment effect and preventing complications.

About the authors

D V Zaslavskiy

Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia

Author for correspondence.
Email: Dr.Sidikov@yahoo.com

I N Chuprov

North-Western State Medical University named after I.I. Mechnikov, Saint Petersburg, Russia

Email: Dr.Sidikov@yahoo.com

A A Sydikov

Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia

Email: Dr.Sidikov@yahoo.com

K U Ibragimov

Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia

Email: Dr.Sidikov@yahoo.com

P Wolkenstein

Henri Mondor University Hospital, Paris, France

Email: Dr.Sidikov@yahoo.com

S V Skrek

North-Western State Medical University named after I.I. Mechnikov, Saint Petersburg, Russia

Email: Dr.Sidikov@yahoo.com

R A Nasyrov

Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia

Email: Dr.Sidikov@yahoo.com

References

  1. Знаменская Л.Ф., Егорова Ю.Ю., Зитнер C.B. Механизмы реализации биологического действия фактора некроза опухоли альфа при псориазе // Вестн. дерматол. и венерол. - 2011. - №2. - С. 13-17.
  2. Катунина O.P., Резайкина A.B. Провоспалительные цитокины ИЛ-1 и ФНО-а в очагах поражённой кожи больных псориазом // Вестн. дерматол, и венерол. - 2011. - №4. - С. 25-30.
  3. Кубанова A.A. Клинические рекомендации. Дерматовенерология. - М.: Дэкс-Пресс, 2007. - 300 с.
  4. Кунгуров H.B., Филимонкова H.H., Голубцов В.И., Корхмазова С.А. Генетические факторы этиологии и патогенеза псориаза // Вестн. дерматол. и венерол. - 2011. - №1. - С. 23-27.
  5. Родионов А.Н. Справочник по кожным и венерическим болезням. - СПб: Спутник врача, 2005. - 464 с.
  6. Симбирцев A.C. Цитокины: классификация и биологические функции // Цитокины и воспаление. - 2004. - Т. 3, №2. - С. 16-22.
  7. Хаитов P.M., Игнатьева Г.А., Сидорович И.Г. Иммунология. Норма и патология. - М.: Медицина, 2010. - 752 с.
  8. Bieber T., Cork M., Reitamo S. Atopic dermatitis: a candidate for disease-modifying strategy // Allergy. - 2012. - Vol. 67. - P. 969-975.
  9. Blumberg H., Dinh H., Trueblood E.S. et al. Opposing activities of two novel members of the IL-1 ligand family regulate skin inflammation // J. Exp. Med. - 2007. - Vol. 204. - P. 2603-2614.
  10. Boraschi D., Tagliabue A. The interleukin-1 receptor family // Semin. Immunol. - 2013. - Vol. 25. - Р. 394-407.
  11. Carrier Y., Ma H.L., Ramon H.E. et al. Inter-regulation of Th17 cytokines and the IL-36 cytokines in vitro and in vivo: implications in psoriasis pathogenesis // J. Invest. Dermatol. - 2011. - Vol. 131. - P. 2428-2437.
  12. Chiricozzi A., Guttman-Yassky E., Suarez F. et al. Integrative responses to IL-17 and TNF alpha in human keratinocytes account for key inflammatory pathogenesis circuit in psoriasis // J. Invest. Dermatol. - 2011. - Vol. 131. - P. 677-687.
  13. Dinarello C., Arend W., Sims J. et al. IL-1family nomenclature // Nat. Immunol. - 2010. - Vol. 11. - P. 973.
  14. Esposito M., Mazzotta A., de Falice C. et al. Treatment of erythrodermic psoriasis with etanercept // Br. J. Dermatol. - 2006. - Vol. 155, N 1. - P. 156-159.
  15. Fraga N.A., Paim M.F., Follador I., Ramos A.M. Refractory erythrodermic psoriasis in a child with an excellent outcome by using etanercept Text // An. Bras. Dermatol. - 2011. - Vol. 4, N 1. - P. 144-147.
  16. Glaser R., Meyer-Hoffert U., Harder J. et al. The antimicrobial protein psoriasin (S100A7) is upregulated in atopic dermatitis and after experimental skin barrier disruption // J. Invest. Dermatol. - 2009. - Vol. 129. - P. 641-649.
  17. Gresnigt M.S., van de Veerdonk F.L. Biology of IL-36 cytokines and their role in disease // Semin. Immunol. - 2013. - Vol. 25. - P. 458-465.
  18. Guttman-Yassky E., Krueger J.G. Contrasting pathogenesis of atopic dermatitis and psoriasis - part II: immune cell subsets and therapeutic concepts // J. Allergy Clin. Immunol. - 2011. - Vol. 127. - P. 1420-1432.
  19. Hawilo A., Zaraa A., Benmously A. et al. Erythrodermic psoriasis: epidemiological clinical and therapeutic features about 60 cases // Tunis Med. - 2011. - Vol. 89, N 11. - P. 841-847.
  20. He Q., Chen H.X., Li W. et al. IL-36 cytokine expression and its relationship with p38 MAPK and NF-kappaB pathways in psoriasis vulgaris skin lesions // J. Huazhong Uni. Sci. Technolog. Med. Sci. - 2013. - Vol. 33. - P. 594-549.
  21. Johnston A., Fritz Y., Dawes S.M. et al. Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation // J. Immunol. - 2013. - Vol. 190. - P. 2252-2262.
  22. Kamsteeg M., Jansen P.A., van Vlijmen-Willems I.M. et al. Molecular diagnostics of psoriasis, atopic dermatitis, allergic dermatitis and irritant contact dermatitis // Br. J. Dermatol. - 2010. - Vol. 162. - P. 568-578.
  23. Kerkhoff C., Voss A., Scholzen T.E. et al. Novel insight into the role of S100A/A9 in skin biology // Exp. Dermatol. - 2012. - Vol. 21. - P. 822-826.
  24. Lian L.H., Milora K.A., Manupipatpong K.K. et al. The double-stranded RNA anologue polynosinic-polycytidilic acid induces keratinocyte pyroptosis and release of IL-36 gamma // J. Invest. Dermatol. - 2012. - Vol. 132. - P. 1346-1353.
  25. Liu H., Huang K., Wu Y. et al. The expression of interleukin-22 and S100A7, A8, A9, mRNA in patients with psoriasis vulgaris // J. Huazhong Univ. Sci. Technolog. Med. Sci. - 2007. - Vol. 27. - P. 605-607.
  26. Marrakchi S., Guigue P., Renshaw B.R. et al. Interleukin-36 receptor antagonist deficiency and generalized pustular psoriasis // N. Engl. J. Med. - 2011. - Vol. 365. - P. 620-628.
  27. Muhr P., Zeitvogel J., Heitland I. et al. Expression of interleukin (IL)-1 family members upon stimulation with IL-17 differs in keratinocytes derived from patients with psoriasis and healthy donors // Br. J. Dermatol. - 2011. - Vol. 165. - P. 189-193.
  28. Nickoloff B.J., Xin H., Nestle F.O., Qin J.Z. The cytokine and chemokine network in psoriasis // Clin. Dermatol. - 2007. - Vol. 25. - P. 568-573.
  29. Nold M.F., Nold-Petry C.A., Zepp J.A. IL-37 is a fundamental inhibitor of innate immunity // Nat. Immunol. - 2010. - Vol. 11. - P. 1014-1022.
  30. Onoufriadis A., Simpson M.A., Pink A.E. et al. Mutation in IL36RN/ILF5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis // Am. J. Hum. Genet. - 2011. - Vol. 89. - P. 432-437.
  31. Pedersen M.B., Skov L., Menne T. et al. Gene expression time course in the human skin during elicitation of allergic contact dermatitis // J. Invest. Dermatol. - 2007. - Vol. 127. - P. 2585-2595.
  32. Perera G.K., Di Meglio P., Nestle F.O. Psoriasis // Annu. Rev. Pathol. - 2012. - Vol. 7. - P. 385-422.
  33. Sempirini S., Capon F., Bovolenta S. et al. Genomic structure, promoter characterization and mutation analysis of the S100A7 gene: exclusion of a candidate for familial psoriasis susceptibility // Hum. Genet. - 1999. - Vol. 104. - P. 130-134.
  34. Tortola L., Rosenwald E., Abel B. et al. Psoriasiform dermatitis is driven by IL-36 mediated DC-keratinocyte crosstalk // J. Clin. Invest. - 2012. - Vol. 122. - P. 3965-3976.
  35. Towne J.E., Garka K.E., Renshaw B.R. et al. Interleukin (IL)-1F6, IL-1F8, and IL1F9 signal through IL-1Rrp2 and IL-1RAcP to activate the pathway leading to NF-kappaB and MAPKs // J. Biol. Chem. - 2004. - Vol. 279. - P. 13 677-13 688.
  36. Towne J.E., Sims J.E. IL-36 in psoriasis // Curr. Opin. Pharmacol. - 2012. - Vol. 12. - P. 486-490.
  37. Vigne S., Palmer G., Lamacchia C. et al. IL-36R ligands are potent regulators of dendritic cells and T-cells // Blood. - 2011. - Vol. 118. - P. 5813-5823.
  38. Villanova F., Di Meglio P., Nestle F.O. et al. Biomarkers in psoriasis and psoriatic arthritis // Ann. Rheum. Dis. - 2012. - Vol. 72, suppl. 2. - P. 104-110.
  39. Wenzel J., Peters B., Zahn S. et al. Gene expression profiling of lichen planus reflects CXCL9+ mediated inflammation and distinguishes this disease from atopic dermatitis and psoriasis // J. Invest. Dermatol. - 2008. - Vol. 128. - P. 67-78.
  40. Wolf J., Ferris L.K. Anti-IL-36R-antibodies, potentially useful for the treatment of psoriasis: a patent evaluation of WO2013074569 // Expert Opin. Therap. Pat. - 2014. - Vol. 24, N (4). - P. 477--479.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

© 2015 Zaslavskiy D.V., Chuprov I.N., Sydikov A.A., Ibragimov K.U., Wolkenstein P., Skrek S.V., Nasyrov R.A.

Creative Commons License

This work is licensed
under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.




This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies