Эозинофилы в крови и коже – сложная роль в патогенезе псориаза

Псориаз – хроническое воспалительное папулосквамозное заболевание кожи, однако патологический спектр псориатических поражений далеко не исчерпывается кожными элементами. Псориаз является сложным заболеванием, вызванным взаимодействием между генетической предрасположенностью, экологическими триггерами и дисрегуляцией иммунной системы. В хроническом псориатическом воспалении принимают участие кератиноциты, а также разнообразные клеточные и гуморальные факторы, проникающие из крови. В настоящее время большой научный интерес вызывают эозинофилы, которые принимают активное участие в патогенезе псориаза. Данная научная работа является описательным обзором литературы и охватывает клинические и эпидемиологические исследования, а также описательные и систематические обзоры литературы. Информация, представленная в нашей научной статье, получена из ранее проведенных исследований. Согласно проанализированным данным, эозинофилы – плейотропные многофункциональные лейкоциты, участвующие в иммунной защите. Эозинофилы играют важную роль в реакциях гиперчувствительности и в ряде аутоиммунных заболеваний, могут мигрировать из кровяного русла в кожу в ответ на различные аттракторы и вырабатывать различные цитокины. Показано, что эозинофилы способны к секреции эозинофильного катионного белка в коже пациентов с псориазом. Степень эозинофилии может быть маркером тяжести и прогноза псориаза. Некоторые исследователи считают, что эозинофилия периферической крови связана с тяжелыми формами псориаза (генерализованная пустулезная и эритродермическая). Ряд ученых выявил важную негативную роль цитокина IL-31, который секретируют эозинофилы как основного фактора кожного зуда. Многочисленные научные работы свидетельствуют о важной роли эозинофилов в развитии псориатического воспаления. Необходимы дальнейшие исследования для изучения эозинофилов и их потенциального влияния на прогрессирование псориаза с целью совершенствования лечения и улучшения качества жизни пациентов.

1. Khalili M, Kooshesh A, Shamsi-Meymandi S, Mehrolhasani N, Amiri R, Rezaei Zadeh Rukerd M, Aflatoonian M. Exploring the Significance of Eosinophil Infiltration in Diagnosis of Psoriasis: A Cross-sectional Analysis. Iran J Pathol. 2025;20(1):18–23. https://doi.org/10.30699/ijp.2024.2013501.3191.

2. Арсеньева АА, Мигачева НБ, Лямин АВ, Курмаев ДП. Иммунобиологическая терапия псориаза: современное состояние проблемы. Российский аллергологический журнал. 2024;21(4):502–519. https://doi.org/10.36691/RJA16974.

3. Malakou LS, Gargalionis AN, Piperi C, Papadavid E, Papavassiliou AG, Basdra EK. Molecular mechanisms of mechanotransduction in psoriasis. Ann Transl Med. 2018;6(12):245. https://doi.org/10.21037/atm.2018.04.09.

4. Park S, Jang J, Kim HJ, Jung Y. Unveiling multifaceted roles of myeloid innate immune cells in the pathogenesis of psoriasis. Mol Aspects Med. 2024;99:101306. https://doi.org/10.1016/j.mam.2024.101306.

5. Шафиева ИА, Булгакова СВ, Курмаев ДП, Тренева ЕВ. Применение тофацитиниба при псориатическом артрите (обзор литературы). Медицинский совет. 2024;(12):114–122. https://doi.org/10.21518/ms2024-230.

6. Memariani M, Memariani H. New horizons in the treatment of psoriasis: Modulation of gut microbiome. Heliyon. 2025;11(1):e41672. https://doi.org/10.1016/j.heliyon.2025.e41672.

7. Caro-Chang LA, Fung MA. The role of eosinophils in the differential diagnosis of inflammatory skin diseases. Hum Pathol. 2023;140:101–128. https://doi.org/10.1016/j.humpath.2023.03.017.

8. Conrad C, Gilliet M. Psoriasis: from pathogenesis to targeted therapies. Clin Rev Allergy Immunol. 2018;54(1):102–113. https://doi.org/10.1007/s12016-018-8668-1.

9. Shao S, Cao T, Jin L, Li B, Fang H, Zhang J et al. Increased lipocalin-2 contributes to the pathogenesis of psoriasis by modulating neutrophil chemotaxis and cytokine secretion. J Invest Dermatol. 2016;136(7):1418–1428. https://doi.org/10.1016/j.jid.2016.03.002.

10. Armstrong AW, Read C. Pathophysiology, clinical presentation, and treatment of psoriasis: a review. JAMA. 2020;323(19):1945–1960. https://doi.org/10.1001/jama.2020.4006.

11. Rendon A, Schäkel K. Psoriasis pathogenesis and treatment. Int J Mol Sci. 2019;20(6):1475. https://doi.org/10.3390/ijms20061475.

12. Laga AC, Vleugels RA, Qureshi AA, Velazquez EF. Histopathologic spectrum of psoriasiform skin reactions associated with tumor necrosis factor-α inhibitor therapy. A study of 16 biopsies. Am J Dermatopathol. 2010;32(6):568–573. https://doi.org/10.1097/DAD.0b013e3181cb3ff7.

13. Rao A, Khandpur S, Kalaivani M. A study of the histopathology of palmoplantar psoriasis and hyperkeratotic palmo-plantar dermatitis. Indian J Dermatol Venereol Leprol. 2018;84(1):27–33. https://doi.org/10.4103/ijdvl.IJDVL_71_16.

14. Lundin A, Fredens K, Michaëlsson G, Venge P. The eosinophil granulocyte in psoriasis. Br J Dermatol. 1990;122(2):181–193. https://doi.org/10.1111/j.1365-2133.1990.tb08264.x.

15. Moy AP, Murali M, Kroshinsky D, Duncan LM, Nazarian RM. Immunologic Overlap of Helper T-Cell Subtypes 17 and 22 in Erythrodermic Psoriasis and Atopic Dermatitis. JAMA Dermatol. 2015;151(7):753–760. https://doi.org/10.1001/jamadermatol.2015.2.

16. Mansur AT, Göktay F, Yaşar Ş. Peripheral blood eosinophilia in association with generalized pustular and erythrodermic psoriasis. J Eur Acad Dermatol Venereol. 2008;22(4):451–455. https://doi.org/10.1111/j.14683083.2007.02489.x.

17. Zhou G, Ren X, Tang Z, Li W, Chen W, He Y et al. Exploring the association and causal effect between white blood cells and psoriasis using largescale population data. Front Immunol. 2023;14:1043380. https://doi.org/10.3389/fimmu.2023.1043380.

18. Rothenberg ME, Hogan SP. The eosinophil. Annu Rev Immunol. 2006;24:147–174. https://doi.org/10.1146/annurev.immunol.24.021605.090720.

19. Radonjic-Hoesli S, Brüggen MC, Feldmeyer L, Simon HU, Simon D. Eosinophils in skin diseases. Semin Immunopathol. 2021;43(3):393–409. https://doi.org/10.1007/s00281-021-00868-7.

20. Wechsler ME, Munitz A, Ackerman SJ, Drake MG, Jackson DJ, Wardlaw AJ et al. Eosinophils in Health and Disease: A State-of-the-Art Review. Mayo Clin Proc. 2021;96(10):2694–2707. https://doi.org/10.1016/j.mayocp.2021.04.025.

21. Long H, Zhang G, Wang L, Lu Q. Eosinophilic Skin Diseases: A Comprehensive Review. Clin Rev Allergy Immunol. 2016;50(2):189–213. https://doi.org/10.1007/s12016-015-8485-8.

22. Gigon L, Fettrelet T, Yousefi S, Simon D, Simon HU. Eosinophils from A to Z. Allergy. 2023;78(7):1810–1846. https://doi.org/10.1111/all.15751.

23. Луговская СА, Почтарь МЕ (ред.). Гематологический атлас. М.; 2011. 368 с.

24. Mori Y, Iwasaki H, Kohno K, Yoshimoto G, Kikushige Y, Okeda A et al. Identification of the human eosinophil lineage-committed progenitor: revision of phenotypic definition of the human common myeloid progenitor. J Exp Med. 2009;206(1):183–193. https://doi.org/10.1084/jem.20081756.

25. Jeong BM, Walker MT, Rodriguez R, Coden ME, Nagasaka R, Doan TC et al. More than neutrophils: Lin(+)Ly6G(+)IL-5Rα(+) multipotent myeloid cells (MMCs) are dominant in normal murine bone marrow and retain capacity to differentiate into eosinophils and monocytes. J Leukoc Biol. 2022;111(1):113–122. https://doi.org/10.1002/JLB.1AB0519-170RR.

26. Johnston LK, Hsu CL, Krier-Burris RA, Chhiba KD, Chien KB, McKenzie A et al. IL-33 Precedes IL-5 in Regulating Eosinophil Commitment and Is Required for Eosinophil Homeostasis. J Immunol. 2016;197(9):3445–3453. https://doi.org/10.4049/jimmunol.1600611.

27. Antosz K, Batko J, Błażejewska M, Gawor A, Sleziak J, Gomułka K. Insight into IL-5 as a Potential Target for the Treatment of Allergic Diseases. Biomedicines. 2024;12(7):1531. https://doi.org/10.3390/biomedicines12071531.

28. Dyer KD, Percopo CM, Rosenberg HF. IL-33 promotes eosinophilia in vivo and antagonizes IL-5-dependent eosinophil hematopoiesis ex vivo. Immunol Lett. 2013;150(1-2):41–47. https://doi.org/10.1016/j.imlet.2012.12.002.

29. Wang Y, He C, Xin S, Liu X, Zhang S, Qiao B et al. A Deep View of the Biological Property of Interleukin-33 and Its Dysfunction in the Gut. Int J Mol Sci. 2023;24(17):13504. https://doi.org/10.3390/ijms241713504.

30. Tsuzuki H, Arinobu Y, Miyawaki K, Takaki A, Ota SI, Ota Y et al. Functional interleukin-33 receptors are expressed in early progenitor stages of allergy-related granulocytes. Immunology. 2017;150(1):64–73. https://doi.org/10.1111/imm.12667.

31. Mack EA, Stein SJ, Rome KS, Xu L, Wertheim GB, Melo RCN, Pear WS. Trib1 regulates eosinophil lineage commitment and identity by restraining the neutrophil program. Blood. 2019;133(22):2413–2426. https://doi.org/10.1182/blood.2018872218.

32. Margelidon-Cozzolino V, Tsicopoulos A, Chenivesse C, de Nadai P. Role of Th17 Cytokines in Airway Remodeling in Asthma and Therapy Perspectives. Front Allergy. 2022;3:806391. https://doi.org/10.3389/falgy.2022.806391.

33. Tian BP, Hua W, Xia LX, Jin Y, Lan F, Lee JJ et al. Exogenous interleukin-17A inhibits eosinophil differentiation and alleviates allergic airway inflammation. Am J Respir Cell Mol Biol. 2015;52(4):459–470. https://doi.org/10.1165/rcmb.2014-0097OC.

34. Bochner BS. The eosinophil: For better or worse, in sickness and in health. Ann Allergy Asthma Immunol. 2018;121(2):150–155. https://doi.org/10.1016/j.anai.2018.02.031.

35. Willebrand R, Voehringer D. Regulation of eosinophil development and survival. Curr Opin Hematol. 2017;24(1):9–15. https://doi.org/10.1097/MOH.0000000000000293.

36. Farahi N, Loutsios C, Tregay N, Summers C, Lok LSC, Ruparelia P et al. Radiolabelled leucocytes in human pulmonary disease. Br Med Bull. 2018;127(1):69–82. https://doi.org/10.1093/bmb/ldy022.

37. Weller PF, Spencer LA. Functions of tissue-resident eosinophils. Nat Rev Immunol. 2017;17(12):746–760. https://doi.org/10.1038/nri.2017.95.

38. Leiferman KM, Peters MS. Eosinophil-related disease and the skin. J Allergy Clin Immunol Pract. 2018;6(5):1462–1482. https://doi.org/10.1016/j.jaip.2018.06.002.

39. Shomali W, Gotlib J. World Health Organization-defined eosinophilic disorders: 2022 update on diagnosis, risk stratification, and management. Am J Hematol. 2022;97(1):129–148. https://doi.org/10.1002/ajh.26352.

40. Leru PM. Eosinophilic disorders: evaluation of current classification and diagnostic criteria, proposal of a practical diagnostic algorithm. Clin Transl Allergy. 2019;9(1):36. https://doi.org/10.1186/s13601-019-0277-4.

41. Gotlib J. World Health Organization – defined eosinophilic disorders: 2017 update on diagnosis, risk stratification and management. Am J Hematol. 2017;92(11):1243–1259. https://doi.org/10.1002/ajh.24880.

42. Acharya KR, Ackerman SJ. Eosinophil granule proteins: form and function. J Biol Chem. 2014;289(25):17406–17415. https://doi.org/10.1074/jbc.R113.546218.

43. Zhao Y, Tian J, Gao C, Liu L, Pan L, Song Z. Retrospective Analysis of 397 Dermatoses Inpatients Associated with Blood Eosinophilia. Clin Cosmet Investig Dermatol. 2023;16:3455–3463. https://doi.org/10.2147/CCID.S429183.

44. Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker JNWN. Psoriasis. Lancet. 2021;397(10281):1301–1315. https://doi.org/10.1016/S0140-6736(20)32549-6.

45. Hahn M, Ghoreschi K. The role of IL-4 in psoriasis. Expert Rev Clin Immunol. 2017;13(3):171–173. https://doi.org/10.1080/1744666X.2017.1279054.

46. Kim DS, Shin D, Lee MS, Kim HJ, Kim DY, Kim SM, Lee MG. Assessments of neutrophil to lymphocyte ratio and platelet to lymphocyte ratio in Korean patients with psoriasis vulgaris and psoriatic arthritis. J Dermatol. 2016;43(3):305–310. https://doi.org/10.1111/1346-8138.13061.

47. Gibbs BF, Patsinakidis N, Raap U. Role of the Pruritic Cytokine IL-31 in Autoimmune Skin Diseases. Front Immunol. 2019;10:1383. https://doi.org/10.3389/fimmu.2019.01383.

48. Cataldi C, Mari NL, Lozovoy MAB, Martins LMM, Reiche EMV, Maes M et al. Proinflammatory and anti-inflammatory cytokine profiles in psoriasis: use as laboratory biomarkers and disease predictors. Inflamm Res. 2019;68(7):557–567. https://doi.org/10.1007/s00011-019-01238-8.

49. Dong Y, Hu H, Fu D, Zheng S, Wang Q, Song X et al. Serum Expression of IL-33 and ST2 in Patients with Psoriasis Vulgaris. Arch Iran Med. 2021;24(9):689–695. https://doi.org/10.34172/aim.2021.99.

50. Michalak-Stoma A, Bartosińska J, Raczkiewicz D, Kowal M, Kozak J, Gujski M et al. Multiple Cytokine Analysis of Th1/Th2/Th9/Th17/Th22/Treg Cytokine Pathway for Individual Immune Profile Assessment in Patients with Psoriasis. Med Sci Monit. 2022;28:e938277. https://doi.org/10.12659/MSM.938277.

51. Rosa G, Fernandez AP, Schneider S, Billings SD. Eosinophils are rare in biopsy specimens of psoriasis vulgaris. J Cutan Pathol. 2017;44(12):1027–1032. https://doi.org/10.1111/cup.13042.

52. Chau T, Parsi KK, Ogawa T, Kiuru M, Konia T, Li CS et al. Psoriasis or not? Review of 51 clinically confirmed cases reveals an expanded histopathologic spectrum of psoriasis. J Cutan Pathol. 2017;44(12):1018–1026. https://doi.org/10.1111/cup.13033.

53. Cesinaro AM, Nannini N, Migaldi M, Pepe P, Maiorana A. Psoriasis vs allergic contact dermatitis in palms and soles: a quantitative histologic and immunohistochemical study. APMIS. 2009;117(8):629–634. https://doi.org/10.1111/j.1600-0463.2009.02513.x.

54. Aydin O, Engin B, Oğuz O, Ilvan S, Demirkesen C. Non-pustular palmoplantar psoriasis: is histologic differentiation from eczematous dermatitis possible? J Cutan Pathol. 2008;35(2):169–173. https://doi.org/10.1111/j.1600-0560.2007.00782.x

55. Kamyab-Hesari K, Safaei-Naraghi Z, Ghanadan A, Nikoo A, Sabaghi M. Palmoplantar psoriasis versus eczema: major histopathologic clues for diagnosis. Iran J Pathol. 2014;9(4):251–256. Available at: https://ijp.iranpath.org/article_7043_cabdce676c0dc51b0af5caaece5f8a5f.pdf

56. Kardaun SH, Kuiper H, Fidler V, Jonkman MF. The histopathological spectrum of acute generalized exanthematous pustulosis (AGEP) and its differentiation from generalized pustular psoriasis. J Cutan Pathol. 2010;37(12): 1220–1229. https://doi.org/10.1111/j.1600-0560.2010.01612.x.

57. Penn L, Brinster NK. Eosinophils among the histological features of psoriasis. Am J Dermatopathol. 2019;41(5):347–349. https://doi.org/10.1097/DAD.0000000000001303.

58. Kim TY, Park HJ, Kim CW. Eosinophil cationic protein (ECP) level and its correlation with eosinophil number or IgE level of peripheral blood in patients with various skin diseases. J Dermatol Sci. 1997;15(2):89–94. https://doi.org/10.1016/s0923-1811(97)00614-2.

59. Kim HJ, Roh JY, Jung Y. Eosinophils Accelerate Pathogenesis of Psoriasis by Supporting an Inflammatory Milieu that Promotes Neutrophil Infiltration. J Invest Dermatol. 2018;138(10):2185–2194. https://doi.org/10.1016/j.jid.2018.03.1509.

60. Kahremany S, Hofmann L, Harari M, Gruzman A, Cohen G. Pruritus in psoriasis and atopic dermatitis: current treatments and new perspectives. Pharmacol Rep. 2021;73(2):443–453. https://doi.org/10.1007/s43440-020-00206-y.

61. Sonkoly E, Muller A, Lauerma AI, Pivarcsi A, Soto H, Kemeny L et al. IL-31: a new link between T cells and pruritus in atopic skin inflammation. J Allergy Clin Immunol. 2006;117(2):411–417. https://doi.org/10.1016/j.jaci.2005.10.033.

62. Neis MM, Peters B, Dreuw A, Wenzel J, Bieber T, Mauch C et al. Enhanced expression levels of IL-31 correlate with IL-4 and IL-13 in atopic and allergic contact dermatitis. J Allergy Clin Immunol. 2006;118(4):930–937. https://doi.org/10.1016/j.jaci.2006.07.015.

63. Nobbe S, Dziunycz P, Mühleisen B, Bilsborough J, Dillon SR, French LE, Hofbauer GF. IL-31 expression by inflammatory cells is preferentially elevated in atopic dermatitis. Acta Derm Venereol. 2012;92(1):24–28. https://doi.org/10.2340/00015555-1191.

64. Narbutt J, Olejniczak I, Sobolewska-Sztychny D, Sysa-Jedrzejowska A, Słowik-Kwiatkowska I, Hawro T, Lesiak A. Narrow band ultraviolet B irradiations cause alteration in interleukin-31 serum level in psoriatic patients. Arch Dermatol Res. 2013;305(3):191–195. https://doi.org/10.1007/s00403012-1293-6.

65. Nattkemper LA, Tey HL, Valdes-Rodriguez R, Lee H, Mollanazar NK, Albornoz C et al. The Genetics of Chronic Itch: Gene Expression in the Skin of Patients with Atopic Dermatitis and Psoriasis with Severe Itch. J Invest Dermatol. 2018;138(6):1311–1317. https://doi.org/10.1016/j.jid.2017.12.029.

66. Niyonsaba F, Ushio H, Hara M, Yokoi H, Tominaga M, Takamori K et al. Antimicrobial peptides human beta-defensins and cathelicidin LL-37 induce the secretion of a pruritogenic cytokine IL-31 by human mast cells. J Immunol. 2010;184(7):3526–3534. https://doi.org/10.4049/jimmunol.0900712.

67. Czarnecka-Operacz M, Polańska A, Klimańska M, Teresiak-Mikołajczak E, Molińska-Glura M, Adamski Z, Jenerowicz D. Itching sensation in psoriatic patients and its relation to body mass index and IL-17 and IL-31 concentrations. Postepy Dermatol Alergol. 2015;32(6):426–430. https://doi.org/10.5114/pdia.2015.56097.