Russian Journal of AllergyRussian Journal of AllergyРоссийский Аллергологический Журнал1810-88302686-682XPublishing House ABV Press156810.36691/RJA1568ReviewsНаучные обзорыReview ArticleSpecificity of the condition of the skin barrier in patients with congenital epidermolysis bullosa as a factor of transcutaneous sensitization by food allergensОсобенности состояния кожного барьера у больных врождённым буллёзным эпидермолизом как фактор транскутанной сенсибилизации пищевыми аллергенамиhttps://orcid.org/0000-0002-6701-38722960-6185GalimovaAlbina A.ГалимоваАльбина Альбертовна
Russian Federation

MD

albina86@yandex.ruhttps://orcid.org/0000-0002-3056-403X2094-2840MakarovaSvetlana G.МакароваСветлана Геннадиевна
Russian Federation

MD, Dr. Sci. (Med.), Professor

д.м.н., профессор

sm27@yandex.ruhttps://orcid.org/0000-0003-2252-85705906-9724MurashkinNikolay N.МурашкинНиколай Николаевич
Russian Federation

MD, Dr. Sci. (Med.), Professor

д.м.н., профессор

m_nn2001@mail.ruNational Medical Research Center for Children’s HealthНациональный медицинский исследовательский центр здоровья детейLomonosov Moscow State UniversityМосковский государственный университет имени М.В. ЛомоносоваThe First Sechenov Moscow State Medical UniversityПервый Московский государственный медицинский университет имени И.М. Сеченова (Сеченовский Университет)Central State Medical Academy of Department of Presidential AffairsЦентральная государственная медицинская академия Управления делами Президента Российской Федерации09122022051220221945085182607202201122022Copyright ©; 2022, Pharmarus Print MediaCopyright ©; 2022, Фармарус Принт Медиа2022Pharmarus Print MediaФармарус Принт Медиаhttps://rusalljournal.ru/raj/article/view/1568

Congenital epidermolysis bullosa is a heterogeneous group of hereditary dermatoses resulting from a pathogenic variant of the genome-encoding proteins of the dermo-epidermal junction. Epidermolysis bullosa is mainly manifested as the formation of blisters and erosions on the skin and mucous membranes in response to minor mechanical action. Itching is one of the most common symptoms of epidermolysis bullosa, reduces the quality of life, and causes additional skin damage.

The influence of comorbid pathology, which can increase itching, is not excluded. Skin inflammation secondary to a disruption in the skin barrier, wound-healing cascades, and unregulated activation of epidermal sensitive nerve endings are involved in the pathophysiology of itching at the molecular and cellular levels. Diffuse damage to the skin and mucous membranes, leading to the loss of their barrier properties, contributes to the excessive intake of antigens, including allergens of food and non-food origin, and to transcutaneous sensitization. However, food sensitization and food allergy in these patients have not been sufficiently studied. Understanding the causes of these processes may be crucial for the development of optimized techniques for managing children with congenital epidermolysis bullosa and improvement of their quality of life.

This review summarizes updated data on clinical and genetic aspects of congenital epidermolysis bullosa.

Врождённый буллёзный эпидермолиз (ВБЭ) представляет собой гетерогенную группу наследственных дерматозов, возникающих в результате патогенного варианта генома, кодирующего белки дермо-эпидермального соединения (зона базальной мембраны). Основными клиническими проявлениями буллёзного эпидермолиза является образование пузырей и/или эрозий на коже и слизистых оболочках в ответ на незначительное механическое воздействие. К одному из наиболее распространённых симптомов при буллёзном эпидермолизе относится зуд, который не только снижает качество жизни, но и вызывает дополнительные повреждения кожи. Не исключается также влияние коморбидной патологии, которая может усиливать зуд.

Вполне вероятно, что воспаление кожи, вторичное по отношению к нарушению кожного барьера, каскады заживления ран и нерегулируемая активация эпидермальных чувствительных нервных окончаний вовлечены в патофизиологию зуда на молекулярном и клеточном уровне. Диффузное поражение кожи и слизистых оболочек, приводящее к потере ими барьерных свойств, способствует избыточному поступлению антигенов, в том числе аллергенов пищевого и непищевого происхождения, и может способствовать транскутанной сенсибилизации. Однако вопросы пищевой сенсибилизации и пищевой аллергии у данной категории больных изучены недостаточно. Понимание причин возникновения этих процессов может иметь решающее значение для разработки оптимизированной тактики ведения детей с врождённым буллёзным эпидермолизом и улучшения качества их жизни.

В обзоре обобщены обновлённые данные о клинических и генетических аспектах врождённого буллёзного эпидермолиза.

congenital epidermolysis bullosafood allergyfood sensitizationtranscutaneous sensitizationchildrenврождённый буллёзный эпидермолизпищевая аллергияпищевая сенсибилизациятранскутанная сенсибилизациядетиHas C, Fischer J. Inherited epidermolysis bullosa: New diagnostics and new clinical phenotypes. Exp Dermatol. 2019;28(10):1146–1152. doi: 10.1111/exd.13668Has C., Fischer J. Inherited epidermolysis bullosa: New diagnostics and new clinical phenotypes // Exp Dermatol. 2019. Vol. 28, N 10. Р. 1146–1152. doi: 10.1111/exd.13668Mariath LM, Santin JT, Schuler-Faccini L, Kiszewski AE. Inherited epidermolysis bullosa: Update on the clinical and genetic aspects. An Bras Dermatol. 2020;95(5):551–569. doi: 10.1016/j.abd.2020.05.001Mariath L.M., Santin J.T., Schuler-Faccini L., Kiszewski A.E. Inherited epidermolysis bullosa: update on the clinical and genetic aspects // An Bras Dermatol. 2020. Vol. 95, N 5. Р. 551–569. doi: 10.1016/j.abd.2020.05.001Has C, Bauer JW, Bodemer C, et al. Consensus reclassification of inherited epidermolysis bullosa and other disorders with skin fragility. Br J Dermatol. 2020;183(4):614–627. doi: 10.1111/bjd.18921Has C., Bauer J.W., Bodemer C., et al. Consensus reclassification of inherited epidermolysis bullosa and other disorders with skin fragility // Br J Dermatol. 2020. Vol. 183, N 4. Р. 614–627. doi: 10.1111/bjd.18921Fine J. Epidemiology of inherited epidermolysis bullosa based on incidence and prevalence estimates from the national epidermolysis bullosa registry. JAMA Dermatol. 2016;152(11):1231–1238. doi: 10.1001/jamadermatol.2016.2473Fine J. Epidemiology of inherited epidermolysis bullosa based on incidence and prevalence estimates from the national epidermolysis bullosa registry // JAMA Dermatol. 2016. Vol. 152, N 11. Р. 1231–1238. doi: 10.1001/jamadermatol.2016.2473Tadini G, Gualandri L, Colombi M, et al. Th e Italian registry of hereditary epidermolysis bullosa. Ital Dermatol Venereol. 2005; 140(4):359–372.Tadini G., Gualandri L., Colombi M., et al. Th e Italian registry of hereditary epidermolysis bullosa // Ital Dermatol Venereol. 2005. Vol. 140, N 4. Р. 359–372.Mellerio JE. Epidermolysis bullosa care in the United Kingdom. Dermatol Clin. 2010;28(2):395–396, xiv. doi: 10.1016/j.det.2010.02.015Mellerio J.E. Epidermolysis bullosa care in the United Kingdom // Dermatol Clin. 2010. Vol. 28, N 2. Р. 395–396, xiv. doi: 10.1016/j.det.2010.02.015Kubanov AA, Albanova VI, Karamova AE, et al. Prevalence of congenital epidermolysis bullosa in the population of the Russian Federation. Bulletin Dermatol Venereol. 2015;(3):21–30. (In Russ).Кубанов А.А., Альбанова В.И., Карамова А.Э., и др. Распространенность врожденного буллезного эпидермолиза у населения Российской Федерации // Вестник дерматологии и венерологии. 2015. № 3. C. 21–30.Epidermolysis bullosa: A guide for doctors. Ed. by N.N. Murashkin, L.S. Namazova-Baranova. Moscow: Pediatr”; 2019. 443 р. (In Russ).Буллезный эпидермолиз: руководство для врачей / под ред. Н.Н. Мурашкина, Л.С. Намазовой-Барановой. Москва: ПедиатрЪ, 2019. 443 с.Yuen WY, Pas HH, Sinke RJ. Junctional epidermolysis bullosa of late onset explained by mutations in COL17A1. Br J Dermatol. 2011;164(2):1280–1284. doi: 10.1111/j.1365-2133.2011.10359.xYuen W.Y., Pas H.H., Sinke R.J. Junctional epidermolysis bullosa of late onset explained by mutations in COL17A1 // Br J Dermatol. 2011. Vol. 164, N 2. Р. 1280–1284. doi: 10.1111/j.1365-2133.2011.10359.xBruckner-Tuderman L, Has C. Molecular heterogeneity of blistering disorders: the paradigm of epidermolysis bullosa. J Invest Dermatol. 2012;132(Suppl 3):E2–5. doi: 10.1038/skinbio.2012.2Bruckner-Tuderman L., Has C. Molecular heterogeneity of blistering disorders: the paradigm of epidermolysis bullosa // J Invest Dermatol. 2012. Vol. 132, Suppl 3. Р. E2–5. doi: 10.1038/skinbio.2012.2Goldschneider KR, Lucky AW. Pain management in epidermolysis bullosa. Dermatol Clin. 2010;28(2):273–282, Ix. doi: 10.1016/j.det.2010.01.008Goldschneider K.R., Lucky A.W. Pain management in epidermolysis bullosa // Dermatol Clin. 2010. Vol. 28, N 2. Р. 273–282, Ix. doi: 10.1016/j.det.2010.01.008Van Scheppingen C, Lettinga AT, Duipmans JC, et al. Main problems experienced by children with epidermolysis bullosa: A qualitative study with semi-structured interviews. Acta Derm Venereol. 2008;88(2):143–150. doi: 10.2340/00015555-0376Van Scheppingen C., Lettinga A.T., Duipmans J.C., et al. Main problems experienced by children with epidermolysis bullosa: a qualitative study with semi-structured interviews // Acta Derm Venereol. 2008. Vol. 88, N 2. Р. 143–150. doi: 10.2340/00015555-0376Papanikolaou M, Onoufriadis A, Mellerio JE, et al. Prevalence, pathophysiology and management of itch in epidermolysis bullosa. Br J Dermatol. 2021;184(5):816–825. doi: 10.1111/bjd.19496Papanikolaou M., Onoufriadis A., Mellerio J.E., et al. Prevalence, pathophysiology and management of itch in epidermolysis bullosa // Br J Dermatol. 2021. Vol. 184, N 5. Р. 816–825. doi: 10.1111/bjd.19496Bruckner AL, Losow M, Wisk J, et al. The challenges of living with and managing epidermolysis bullosa: insights from patients and caregivers. Orphanet J Rare Dis. 2020;15(1):1. doi: 10.1186/s13023-019-1279-yBruckner A.L., Losow M., Wisk J., et al. The challenges of living with and managing epidermolysis bullosa: Insights from patients and caregivers // Orphanet J Rare Dis. 2020. Vol. 15, N 1. Р. 1. doi: 10.1186/s13023-019-1279-yEng VA, Solis DC, Gorell ES, et al. Patient reported outcomes and quality of life in recessive dystrophic epidermolysis bullosa: A global cross-sectional survey. J Am Acad Dermatol. 2021;85(5):1161–1167. doi: 10.1016/j.jaad.2020.03.028Eng V.A., Solis D.C., Gorell E.S., et al. Patient reported outcomes and quality of life in recessive dystrophic epidermolysis bullosa: a global cross-sectional survey // J Am Acad Dermatol. 2021. Vol. 85, N 5. Р. 1161–1167. doi: 10.1016/j.jaad.2020.03.028Danial C, Adeduntan R, Gorell ES, et al. Prevalence and characterization of pruritus in epidermolysis bullosa. Pediatr Dermatol. 2015;32(1):53–59. doi: 10.1111/pde.12391Danial C., Adeduntan R., Gorell E.S., et al. Prevalence and characterization of pruritus in epidermolysis bullosa // Pediatr Dermatol. 2015. Vol. 32, N 1. Р. 53–59. doi: 10.1111/pde.12391Jeon IK, On HR, Kim SC. Quality of life and economic burden in recessive dystrophic epidermolysis bullosa. Ann Dermatol. 2016;28(1):6–14. doi: 10.5021/ad.2016.28.1.6Jeon I.K., On H.R., Kim S.C. Quality of life and economic burden in recessive dystrophic epidermolysis bullosa // Ann Dermatol. 2016. Vol. 28, N 1. Р. 6–14. doi: 10.5021/ad.2016.28.1.6Schräder NH, Korte EW, Duipmans JC, et al. Identifying epidermolysis bullosa patient needs and perceived treatment benefits: an explorative study using the patient benefit index. J Clin Med. 2021;10(24):5836. doi: 10.3390/jcm10245836Schräder N.H., Korte E.W., Duipmans J.C., et al. Identifying epidermolysis bullosa patient needs and perceived treatment benefits: An explorative study using the patient benefit index // J Clin Med. 2021. Vol. 10, N 24. Р. 5836. doi: 10.3390/ jcm10245836Snauwaert JJ, Yuen WY, Jonkman MF, et al. Burden of itch in epidermolysis bullosa. Br J Dermatol. 2014;171(1):73–78. doi: 10.1111/bjd.12885Snauwaert J.J., Yuen W.Y., Jonkman M.F., et al. Burden of itch in epidermolysis bullosa // Br J Dermatol. 2014. Vol. 171, N 1. Р. 73–78. doi: 10.1111/bjd.12885Dawn A, Papoiu AD, Chan YH, et al. Itch characteristics in atopic dermatitis: results of a web-based questionnaire. Br J Dermatol. 2009;160(4):642–644. doi: 10.1111/j.1365-2133.2008.08941.xDawn A., Papoiu A.D., Chan Y.H., et al. Itch characteristics in atopic dermatitis: results of a web-based questionnaire // Br J Dermatol. 2009. Vol. 160, N 4. Р. 642–644. doi: 10.1111/j.1365-2133.2008.08941.xFine JD, Johnson LB, Weiner M, Suchindran C. Assessment of mobility, activities and pain in different subtypes of epidermolysis bullosa. Clin Exp Dermatol. 2004;29(2):122–127. doi: 10.1111/j.1365-2230.2004.01428.xFine J.D., Johnson L.B., Weiner M., Suchindran C. Assessment of mobility, activities and pain in different subtypes of epidermolysis bullosa // Clin Exp Dermatol. 2004. Vol. 29, N 2. Р. 122–127. doi: 10.1111/j.1365-2230.2004.01428.xChoi S, Solis D, Nazaroff J, et al. 224 Quality of life in recessive dystrophic epidermolysis bullosa: The AltaVoice patient registry, 2012–2015. J Investig Dermatol. 2017;137(5):S38.Choi S., Solis D., Nazaroff J., et al. 224 Quality of life in recessive dystrophic epidermolysis bullosa: The altavoice patient registry, 2012–2015 // J Investig Dermatol. 2017. Vol. 137, N 5. Р. S38.Dawn A, Papoiu AD, Chan YH, et al. Itch characteristics in atopic dermatitis: Results of a web-based questionnaire. Br J Dermatol. 2009;160(3):642–644. doi: 10.1111/j.1365-2133.2008.08941.xDawn A., Papoiu A.D., Chan Y.H., et al. Itch characteristics in atopic dermatitis: results of a web-based questionnaire // Br J Dermatol. 2009. Vol. 160, N 3. Р. 642–644. doi: 10.1111/j.1365-2133.2008.08941.xYosipovitch G, Goon A, Wee J, et al. The prevalence and clinical characteristics of pruritus among patients with extensive psoriasis. Br J Dermatol. 2000;143(3):969–973. doi: 10.1046/j.1365-2133.2000.03829.xYosipovitch G., Goon A., Wee J., et al. The prevalence and clinical characteristics of pruritus among patients with extensive psoriasis // Br J Dermatol. 2000. Vol. 143, N 3. Р. 969–973. doi: 10.1046/j.1365-2133.2000.03829.xMuraro A, Roberts G, Worm M, et al. Food allergy and anaphylaxis guidelines. Allergy. 2014;69(8):1026–1045.Muraro A., Roberts G., Worm M., et al. Food allergy and anaphylaxis guidelines // Allergy. 2014. Vol. 69, N 8. Р. 1026–1045.Eiwegger T, Hung L, San Diego KE, et al. Recent developments and highlights in food allergy. Allergy. 2019;74(12):2355–2367. doi: 10.1111/all.14082Eiwegger T., Hung L., San Diego K.E., et al. Recent developments and highlights in food allergy // Allergy. 2019. Vol. 74, N 12. Р. 2355–2367. doi: 10.1111/all.14082Renz H, Allen KJ, Sicherer SH, et al. Food allergy. Nat Rev Dis Primers. 2018;(4):17098. doi: 10.1038/nrdp.2017.98Renz H., Allen K.J., Sicherer S.H., et al. Food allergy // Nat Rev Dis Primers. 2018. N 4. Р. 17098. doi: 10.1038/nrdp.2017.98De Martinis M, Sirufo MM, Viscido A, Ginaldi L. Food allergy insights: A changing landscape. Arch Immunol Ther Exp (Warsz). 2020;68(2):8. doi: 10.1007/s00005-020-00574-6De Martinis M., Sirufo M.M., Viscido A., Ginaldi L. Food allergy insights: А changing landscape // Arch Immunol Ther Exp (Warsz). 2020. Vol. 68, N 2. Р. 8. doi: 10.1007/s00005-020-00574-6Turner PJ, Gowland MH, Sharma V, et al. Increase in anaphylaxis-related hospitalizations but no increase in fatalities: an analysis of United Kingdom national anaphylaxis data, 1992–2012. J Allergy Clin Immunol. 2015;135(4):956–963.e1. doi: 10.1016/j.jaci.2014.10.021Turner P.J., Gowland M.H., Sharma V., et al. Increase in anaphylaxis-related hospitalizations but no increase in fatalities: An analysis of United Kingdom national anaphylaxis data, 1992–2012 // J Allergy Clin Immunol. 2015. Vol. 35, N 4. Р. 956–963.e1. doi: 10.1016/j.jaci.2014.10.021Pouessel G, Beaudouin E, Tanno LK, et al. Food-related anaphylaxis fatalities: analysis of the Allergy Vigilance Network(R) database. Allergy. 2019;74(6):1193–1196. doi: 10.1111/all.13717Pouessel G., Beaudouin E., Tanno L.K., et al. Food-related anaphylaxis fatalities: Analysis of the Allergy Vigilance Network(R) database // Allergy. 2019. Vol. 74, N 6. Р. 1193–1196. doi: 10.1111/all.13717Gupta RS, Warren CM, Smith BM, et al. The public health impact of parent-reported childhood food allergies in the United States. Pediatrics. 2018;142(6):e20181235. doi: 10.1542/peds.2018-1235Gupta R.S., Warren C.M., Smith B.M., et al. The public health impact of parent-reported childhood food allergies in the United States // Pediatrics. 2018. Vol. 142, N 6. Р. e20181235. doi: 10.1542/peds.2018-1235Burney PG, Potts J, Kummeling I, et al. The prevalence and distribution of food sensitization in European adults. Allergy. 2014; 69(3):365–371. doi: 10.1111/all.12341Burney P.G., Potts J., Kummeling I., et al. The prevalence and distribution of food sensitization in European adults // Allergy. 2014. Vol. 69, N 3. Р. 365–371. doi: 10.1111/all.12341Lyons SA, Burney PG, Ballmer-Weber BK, et al. Food allergy in adults: substantial variation in prevalence and causative foods across Europe. J Allergy Clin Immunol Pract. 2019;7(6):1920–1928.e11. doi: 10.1016/j.jaip.2019.02.044Lyons S.A., Burney P.G., Ballmer-Weber B.K., et al. Food allergy in adults: substantial variation in prevalence and causative foods across Europe // J Allergy Clin Immunol Pract. 2019. Vol. 7, N 6. Р. 1920–1928.e11. doi: 10.1016/j.jaip.2019.02.044Lyons SA, Clausen M, Knulst AC, et al. Prevalence of food sensitization and food allergy in children across Europe. J Allergy Clin Immunol Pract. 2020;8(8):2736–2746.e9. doi: 10.1016/j.jaip.2020.04.020Lyons S.A., Clausen M., Knulst A.C., et al. Prevalence of food sensitization and food allergy in children across Europe // J Allergy Clin Immunol Pract. 2020. Vol. 8, N 8. Р. 2736–2746.e9. doi: 10.1016/j.jaip.2020.04.020Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol. 2008;121(6):1331–1336. doi: 10.1016/j.jaci.2008.04.032Lack G. Epidemiologic risks for food allergy // J Allergy Clin Immunol. 2008. Vol. 121, N 6. Р. 1331–1336. doi: 10.1016/j.jaci.2008.04.032Martin PE, Eckert JK, Koplin JJ, et al. Which infants with eczema are at risk of food allergy? Results from a population-based cohort. Clin Exp Allergy. 2015;45(1):255–264. doi: 10.1111/cea.12406Martin P.E., Eckert J.K., Koplin J.J., et al. Which infants with eczema are at risk of food allergy? Results from a population-based cohort // Clin Exp Allergy. 2015. Vol. 45, N 1. Р. 255–264. doi: 10.1111/cea.12406Grimshaw KE, Roberts G, Selby A, et al. Risk factors for hen’s egg allergy in Europe: EuroPrevall birth cohort. J Allergy Clin Immunol Pract. 2020;8(4):1341–1348.e1345. doi: 10.1016/j.jaip.2019.11.040Grimshaw K.E., Roberts G., Selby A., et al. Risk factors for hen’s egg allergy in Europe: EuroPrevall birth cohort // J Allergy Clin Immunol Pract. 2020. Vol. 8, N 4. Р. 1341–1348.e1345. doi: 10.1016/j.jaip.2019.11.040Chinthrajah RS, Tupa D, Prince BT, et al. Diagnosis of food allergy. Pediatr Clin N Am. 2015;62(6):1393–1408. doi: 10.1016/j.pcl.2015.07.009Chinthrajah R.S., Tupa D., Prince B.T., et al. Diagnosis of food allergy // Pediatr Clin N Am. 2015. Vol. 62, N 6. Р. 1393–1408. doi: 10.1016/j.pcl.2015.07.009Johnston LK, Chien KB, Bryce PJ. The immunology of food allergy. J Immunol. 2014;192(6):2529–2534. doi: 10.4049/jimmunol.1303026Johnston L.K., Chien K.B., Bryce P.J. The immunology of food allergy // J Immunol. 2014. Vol. 192, N 6. Р. 2529–2534. doi: 10.4049/jimmunol.1303026Aalberse RC, Platts-Mills TA, Rispens T. The developmental history of IgE and IgG4 antibodies in relation to atopy, eosinophilic esophagitis and the modified Th2 response. Curr Allergy Asthma Rep. 2016;16(6):45. doi: 10.1007/s11882-016-0621-xAalberse R.C., Platts-Mills T.A., Rispens T. The developmental history of IgE and IgG4 antibodies in relation to atopy, eosinophilic esophagitis and the modified TH2 response // Curr Allergy Asthma Rep. 2016. Vol. 16, N 6. Р. 45. doi: 10.1007/s11882-016-0621-xSatitsuksanoa P, Jansen K, Głobińska A, et al. Regulatory immune mechanisms in tolerance to food allergy. Front Immunol. 2018;(9):2939. doi: 10.3389/fimmu.2018.02939Satitsuksanoa P., Jansen K., Głobińska A., et al. Regulatory immune mechanisms in tolerance to food allergy // Front Immunol. 2018. N 9. Р. 2939. doi: 10.3389/fimmu.2018.02939Chinthrajah RS, Hernandez JD, Boyd SD, et al. Molecular and cellular mechanisms of food allergy and food tolerance. J Allergy Clin Immunol. 2016;137(4):984–997. doi: 10.1016/j.jaci.2016.02.004Chinthrajah R.S., Hernandez J.D., Boyd S.D., et al. Molecular and cellular mechanisms of food allergy and food tolerance // J Allergy Clin Immunol. 2016. Vol. 137, N 4. Р. 984–997. doi: 10.1016/j.jaci.2016.02.004Huang YJ, Marsland BJ, Bunyavanich S, et al. The microbiome in allergic disease: Current understanding and future opportunities-2017 PRACTALL document of the American Academy of Allergy, Asthma, Immunology and the European Academy of Allergy and Clinical Immunology. J Allergy Clin Immunol. 2017;139(4):1099–1110. doi: 10.1016/j.jaci.2017.02.007Huang Y.J., Marsland B.J., Bunyavanich S., et al. The microbiome in allergic disease: Current understanding and future opportunities-2017 PRACTALL document of the American Academy of Allergy, Asthma, Immunology and the European Academy of Allergy and Clinical Immunology // J Allergy Clin Immunol. 2017. Vol. 139, N 4. Р. 1099–1110. doi: 10.1016/j.jaci.2017.02.007De Martinis M, Sirufo MM, Viscido A, Ginaldi L. Food allergy insights: a changing landscape. Arch Immunol Ther Exp (Warsz). 2020;68(2):8. doi: 10.1007/s00005-020-00574-6De Martinis M., Sirufo M.M., Viscido A., Ginaldi L. Food allergy insights: A changing landscape // Arch Immunol Ther Exp (Warsz). 2020. Vol. 68, N 2. Р. 8. doi: 10.1007/s00005-020-00574-6Yu LC. Intestinal epithelial barrier dysfunction in food hypersensitivity. J Allergy (Cairo). 2012;2012:596081. doi: 10.1155/2012/596081Yu L.C. Intestinal epithelial barrier dysfunction in food hypersensitivity // J Allergy (Cairo). 2012. Vol. 2012. Р. 596081. doi: 10.1155/2012/596081Nakajima-Adachi H, Shibahara K, Fujimura Y, et al. Critical role of intestinal interleukin-4 modulatingregulatory T cells for desensitization, tolerance, and inflammation of food allergy. PLoS ONE. 2017;12(2):e0172795. doi: 10.1371/journal.pone.0172795Nakajima-Adachi H., Shibahara K., Fujimura Y., et al. Critical role of intestinal interleukin-4 modulatingregulatory T cells for desensitization, tolerance, and inflammation of food allergy // PLoS ONE. 2017. Vol. 12, N 2. Р. e0172795. doi: 10.1371/journal.pone.0172795Eiwegger T, Hung L, San Diego KE, et al. Recent developments and highlights in food allergy. Allergy. 2019;74(12):2355–2367. doi: 10.1111/all.14082Eiwegger T., Hung L., San Diego K.E., et al. Recent developments and highlights in food allergy // Allergy. 2019. Vol. 74, N 12. Р. 2355–2367. doi: 10.1111/all.14082Cabanillas B, Brehler AC, Novak N. Atopic dermatitis phenotypes and the need for personalized medicine. Curr Opin Allergy Clin Immunol. 2017;17(4):309–315. doi: 10.1097/ACI.0000000000000376Cabanillas B., Brehler A.C., Novak N. Atopic dermatitis phenotypes and the need for personalized medicine // Curr Opin Allergy Clin Immunol. 2017. Vol. 17, N 4. Р. 309–315. doi: 10.1097/ACI.0000000000000376Schmiechen ZC, Weissler KA, Frischmeyer-Guerrerio PA. Recent developments in understanding the mechanisms of food allergy. Curr Opin Pediatr. 2019;31(6):807–814. doi: 10.1097/MOP.0000000000000806Schmiechen Z.C., Weissler K.A., Frischmeyer-Guerrerio P.A. Recent developments in understanding the mechanisms of food allergy // Curr Opin Pediatr. 2019. Vol. 31, N 6. Р. 807–814. doi: 10.1097/MOP.0000000000000806Leyva-Castillo JM, Galand C, Kam C, et al. Mechanical skin injury promotes food anaphylaxis by driving intestinal mast cell expansion. Immunity. 2019;50(5):1262–1275. doi: 10.1016/j.immuni.2019.03.023Leyva-Castillo J.M., Galand C., Kam C., et al. Mechanical skin injury promotes food anaphylaxis by driving intestinal mast cell expansion // Immunity. 2019. Vol. 50, N 5. Р. 1262–1275. doi: 10.1016/j.immuni.2019.03.023Kim JE, Kim JS, Cho DH, Park HJ. Molecular mechanisms of cutaneous inflammatory disorder: atopic dermatitis. Int J Mol Sci. 2016;17(8):1234. doi: 10.3390/ijms17081234Kim J.E., Kim J.S., Cho D.H., Park H.J. Molecular mechanisms of cutaneous inflammatory disorder: Atopic dermatitis // Int J Mol Sci. 2016. Vol. 17, N 8. Р. 1234. doi: 10.3390/ijms17081234Belkaid Y, Segre JA. Dialogue between skin microbiota and immunity. Science. 2014;346(6212):954–959. doi: 10.1126/science.1260144Belkaid Y., Segre J.A. Dialogue between skin microbiota and immunity // Science. 2014. Vol. 346, N 6212. Р. 954–959. doi: 10.1126/science.1260144Nakatsuji T, Chen TH, Narala S, et al. Antimicrobials from human skin commensal bacteria protect against Staphylococcus aureus and are deficient in atopic dermatitis. Sci Transl Med. 2017;9(378):eaah4680. doi: 10.1126/scitranslmed.aah4680Nakatsuji T., Chen T.H., Narala S., et al. Antimicrobials from human skin commensal bacteria protect against Staphylococcus aureus and are deficient in atopic dermatitis // Sci Transl Med. 2017. Vol. 9, N 378. Р. eaah4680. doi: 10.1126/scitranslmed.aah4680Chambers ES, Vukmanovic-Stejic M. Skin barrier immunity and ageing. Immunology. 2020;160(2):116–125. doi: 10.1111/imm.13152Chambers E.S., Vukmanovic-Stejic M. Skin barrier immunity and ageing // Immunology. 2020. Vol. 160, N 2. Р. 116–125. doi: 10.1111/imm.13152Harder J, Meyer-Hoffert U, Wehkamp K, et al. Differential gene induction of human β-defensins (hBD-1, -2, -3, and -4) in keratinocytes is inhibited by retinoic acid. J Invest Dermatol. 2004;123(3):522–529. doi: 10.1111/j.0022-202X.2004.23234.xHarder J., Meyer-Hoffert U., Wehkamp K., et al. Differential gene induction of human β-defensins (hBD-1, -2, -3, and -4) in keratinocytes is inhibited by retinoic acid // J Invest Dermatol. 2004. Vol. 123, N 3. Р. 522–529. doi: 10.1111/j.0022-202X.2004.23234.xBraff MH, Di Nardo A, Gallo RL. Keratinocytes store the antimicrobial peptide cathelicidin in lamellar bodies. J Invest Dermatol. 2005;124(2):394–400. doi: 10.1111/j.0022-202X.2004.23443.xBraff M.H., Di Nardo A., Gallo R.L. Keratinocytes store the antimicrobial peptide cathelicidin in lamellar bodies // J Invest Dermatol. 2005. Vol. 124, N 2. Р. 394–400. doi: 10.1111/j.0022-202X.2004.23443.xKollisch G, Kalali BN, Voelcker V, et al. Various members of the Toll-like receptor family contribute to the innate immune response of human epidermal keratinocytes. Immunology. 2005;114(4):531–541. doi: 10.1111/j.1365-2567.2005.02122.xKollisch G., Kalali B.N., Voelcker V., et al. Various members of the Toll-like receptor family contribute to the innate immune response of human epidermal keratinocytes // Immunology. 2005. Vol. 114, N 4. Р. 531–541. doi: 10.1111/j.1365-2567.2005.02122.xYao C, Oh JH, Lee DH, et al. Toll-like receptor family members in skin fibroblasts are functional and have a higher expression compared to skin keratinocytes. Int J Mol Med. 2015;35(5): 1443–1450. doi: 10.3892/ijmm.2015.2146Yao C., Oh J.H., Lee D.H., et al. Toll-like receptor family members in skin fibroblasts are functional and have a higher expression compared to skin keratinocytes // Int J Mol Med. 2015. Vol. 35, N 5. Р. 1443–1450. doi: 10.3892/ijmm.2015.2146Izadi N, Luu M, Ong PY, Tam JS. The role of skin barrier in the pathogenesis of food allergy. Children (Basel). 2015;2(3):382–402. doi: 10.3390/children2030382Izadi N., Luu M., Ong P.Y., Tam J.S. The role of skin barrier in the pathogenesis of food allergy // Children (Basel). 2015. Vol. 2, N 3. Р. 382–402. doi: 10.3390/children2030382Marcelo H, Grunwald MD, Amichai MD, et al. Dystrophic epidermolysis bullosa associated with eosinophilic infiltrate and elevated serum IgE. Pediatric Dermatology. 1999;16(1):16–18. doi: 10.1046/j.1525-1470.1999.99004.xMarcelo H., Grunwald M.D., Amichai M.D., et al. Dystrophic epidermolysis bullosa associated with eosinophilic infiltrate and elevated serum IgE // Pediatric Dermatology. 1999. Vol. 16, N 1. Р. 16–18. doi: 10.1046/j.1525-1470.1999.99004.xMakarova S, Murashkin N, Epishev R, et al. Food allergy as comorbid condition in children with epidermolysis bullosa. The results of the observational study. Acta Dermato-Venereologica. 2020; 100(S200):33–34. doi: 10.2340/00015555-3586Makarova S., Murashkin N., Epishev R., et al. Food allergy as comorbid condition in children with epidermolysis bullosa. The results of the observational study // Acta Dermato-Venereologica. 2020. Vol. 100, N S200. Р. 33–34. doi: 10.2340/00015555-3586Makarova S, Valenta R, Lupinek S, et al. Patients with epidermolysis bullosa (eb) due to mutations in collagen type 7 show markedly higher ige sensitizations to allergens than eb patients with mutations in keratins. Allergy. 2018;73(S105):729.Makarova S., Valenta R., Lupinek S., et al. Patients with epidermolysis bullosa (eb) due to mutations in collagen type 7 show markedly higher ige sensitizations to allergens than eb patients with mutations in keratins // Allergy. 2018. Vol. 73, N S105. Р. 729.Galimova AA, Makarova SG, Murashkin NN, et al. Food allergy as a comorbid background in a child with congenital epidermolysis bullosa. Russ Pediatric J. 2021;24(4):250. (In Russ).Галимова А.А., Макарова С.Г., Мурашкин Н.Н., и др. Пищевая аллергия как коморбидный фон у ребенка с врожденным буллезным эпидермолизом // Российский педиатрический журнал. 2021. Т. 24, № 4. С. 250.