TY - JOUR
T1 - Characteristic Clinical Features of Korean Atopic Dermatitis Patients with Interleukin-17 Receptor A Gene Mutation
AU - Lee, Jong Won
AU - Yu, Kwangmin
AU - Lee, Hyeyoung
AU - Choi, Eung Ho
N1 - Publisher Copyright:
© 2021 Korean Dermatological Association. All rights reserved.
PY - 2021
Y1 - 2021
N2 - Background: Thl7 cytokines such as interleukin-17 and interleukin-22 are expressed in atopic dermatitis lesions. Previous studies have reported increased levels of interleukin-17A, -17E, and -17F in patients with atopic dermatitis. As interleukin-17 A, -17E and -17F act through a common receptor composed of interleukin-17RA, it is speculated that interleukin-17RA gene (IL17RA) mutation could affect the clinical characteristics of atopic dermatitis. Objective: This study aimed to characterize the clinical featiu-es of atopic dermatitis according to the presence of an IL17RA mutation in patients with atopic dermatitis. Methods: We performed reverse blot hybridization assay to detect IL17RA mutations in Korean patients with atopic dermatitis. The clinical features of atopic dermatitis were compared between atopic dermatitis patients with and without IL17RA mutation. Results: Of 332 patients with atopic dermatitis, 27 (8.1%) were found to have IL17RA mutation compared to 8 of 245 controls without atopic diseases (3.27%), which was statistically significant. Furthermore, 272 of atopic dermatitis patients (81.9%) had extrinsic type atopic dermatitis and 60 (18.1%) had intrinsic type. All patients with IL17RA mutations had extrinsic type, hi addition, atopic dermatitis with IL17RA mutation was associated with longer disease duration, more frequent keratosis pilaris, higher blood eosinophil count, higher serum total immunoglobulin E level, higher house dust mite allergen-specific immunoglobulin E levels, and more need for systemic treatment than that in patients without IL17RA mutation. Conclusion: IL17RA mutation is associated with the more severe extrinsic type atopic dermatitis. So, it may predict the progress to severe atopic dermatitis.
AB - Background: Thl7 cytokines such as interleukin-17 and interleukin-22 are expressed in atopic dermatitis lesions. Previous studies have reported increased levels of interleukin-17A, -17E, and -17F in patients with atopic dermatitis. As interleukin-17 A, -17E and -17F act through a common receptor composed of interleukin-17RA, it is speculated that interleukin-17RA gene (IL17RA) mutation could affect the clinical characteristics of atopic dermatitis. Objective: This study aimed to characterize the clinical featiu-es of atopic dermatitis according to the presence of an IL17RA mutation in patients with atopic dermatitis. Methods: We performed reverse blot hybridization assay to detect IL17RA mutations in Korean patients with atopic dermatitis. The clinical features of atopic dermatitis were compared between atopic dermatitis patients with and without IL17RA mutation. Results: Of 332 patients with atopic dermatitis, 27 (8.1%) were found to have IL17RA mutation compared to 8 of 245 controls without atopic diseases (3.27%), which was statistically significant. Furthermore, 272 of atopic dermatitis patients (81.9%) had extrinsic type atopic dermatitis and 60 (18.1%) had intrinsic type. All patients with IL17RA mutations had extrinsic type, hi addition, atopic dermatitis with IL17RA mutation was associated with longer disease duration, more frequent keratosis pilaris, higher blood eosinophil count, higher serum total immunoglobulin E level, higher house dust mite allergen-specific immunoglobulin E levels, and more need for systemic treatment than that in patients without IL17RA mutation. Conclusion: IL17RA mutation is associated with the more severe extrinsic type atopic dermatitis. So, it may predict the progress to severe atopic dermatitis.
KW - Atopic dermatitis. Extrinsic
KW - Reverse blot hybridization
KW - hiterieukin-17 receptor A
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M3 - Article
AN - SCOPUS:85133502504
SN - 0494-4739
VL - 59
SP - 290
EP - 295
JO - Korean Journal of Dermatology
JF - Korean Journal of Dermatology
IS - 4
ER -