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Journal of Allergy and Clinical Immunology

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The Asian atopic dermatitis phenotype combines features of atopic dermatitis and psoriasis with increased TH17 polarization - 06/11/15

Doi : 10.1016/j.jaci.2015.08.015 
Shinji Noda, MD, PhD a, Mayte Suárez-Fariñas, PhD a, b, c, d, Benjamin Ungar, BA a, b, Soo Jung Kim, MD, PhD b, Cristina de Guzman Strong, PhD e, Hui Xu, MSc b, Xiangyu Peng, MSc b, Yeriel D. Estrada, BSc b, Saeko Nakajima, MD, PhD f, Tetsuya Honda, MD, PhD f, Jung U. Shin, MD g, Hemin Lee, MD g, James G. Krueger, MD, PhD a, Kwang-Hoon Lee, MD, PhD g, Kenji Kabashima, MD, PhD f, Emma Guttman-Yassky, MD, PhD a, b, h, ⁎
a Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 
b Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY 
c Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY 
h Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 
d Department of Genetics and Genomics Science, Icahn Institute for Genomics and Multiscale Biology, New York, NY 
e Division of Biology and Biomedical Sciences, Washington University, St Louis, Mo 
f Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan 
g Department of Dermatology & Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea 

∗Corresponding author: Emma Guttman-Yassky, MD, PhD, Department of Dermatology, Icahn School of Medicine at Mount Sinai Medical Center, 5 E 98th St, New York, NY 10029.

Abstract

Background

Atopic dermatitis (AD) shows very high prevalence in Asia, with a large unmet need for effective therapeutics. Direct comparisons between European American (EA) and Asian patients with AD are unavailable, but earlier blood studies detected increased IL-17+–producing cell counts in Asian patients with AD.

Objective

We sought to characterize the Asian AD skin phenotype and compare it with the EA AD skin phenotype.

Methods

We performed genomic profiling (real-time PCR) and immunohistochemistry on lesional and nonlesional biopsy specimens from 52 patients with AD (25 EAs and 27 Asians), 10 patients with psoriasis (all EAs), and 27 healthy subjects (12 EAs and 15 Asians).

Results

Although disease severity/SCORAD scores were similar between the AD groups (58.0 vs 56.7, P = .77), greater acanthosis, higher Ki67 counts, and frequent parakeratosis were characteristics of lesional epidermis from Asian patients with AD (P < .05). Most (24/27) Asian patients had high IgE levels. A principal component analysis using real-time PCR data clustered the Asian AD phenotype between the EA AD and psoriasis phenotypes. TH2 skewing characterized both Asian and EA patients with AD but not patients with psoriasis. Significantly higher TH17 and TH22 (IL17A, IL19, and S100A12 in lesional and IL-22 in nonlesional skin; P < .05) and lower TH1/interferon (CXCL9, CXCL10, MX1, and IFNG in nonlesional skin; P < .05) gene induction typified AD skin in Asian patients.

Conclusion

The Asian AD phenotype presents (even in the presence of increased IgE levels) a blended phenotype between that of EA patients with AD and those with psoriasis, including increased hyperplasia, parakeratosis, higher TH17 activation, and a strong TH2 component. The relative pathogenic contributions of the TH17 and TH2 axes in creating the Asian AD phenotype need to be tested in future clinical trials with appropriate targeted therapeutics.

El texto completo de este artículo está disponible en PDF.

Key words : Atopic dermatitis, TH1, TH2, TH17, TH22, acanthosis, parakeratosis, psoriasis, Asian, European American

Abbreviations used : AD, DC, EA, FCH, FLG, IHC, LC, PCA, RT-PCR, STAT1


Esquema


 Supported by a research grant (EGY) from Leo Pharma. S.N., B.U., M.S.-F., and J.G.K. were supported by grant no. 5UL1RR024143-02 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and the NIH Roadmap for Medical Research. S.N. was supported in part by grant no. UL1 TR000043 from the National Center for Advancing Translational Sciences (NCATS), NIH Clinical and Translational Science Award (CTSA) program.
 Disclosure of potential conflict of interest: S. Noda has received research support from the CTSA program. C. de Guzman Strong has received research support from the National Institutes of Health (NIH; R01 AR065523). J. G. Krueger has received research support (grants paid to his institution) and personal fees from Novartis, Pfizer, Janssen, Lilly, Merck, Kadmon, Dermira, Boehringer, BMS, and Paraxel during the conduct of the study and has received research support (grants paid to his institution) from Amgen, Innovaderm, and Kyowa and personal fees from Serono, BiogenIdec, Delenex, AbbVie, Sanofi, Baxter, Xenoport, and Kineta. E. Guttman-Yassky is a board member for Sanofi Aventis, Regeneron, Stiefel/GlaxoSmithKline, Medimmune, Celgene, Anacor, and Leo Pharma; has received consultancy fees from Regeneron, Sanofi Aventis, Medimmune, Celgene, Stiefel/GlaxoSmithKline, Celsus, BMS, Amgen, and Drais; and has received research support from Regeneron, Celgene, BMS, and Janssen. The rest of the authors declare that they have no relevant conflicts of interest.


© 2015  American Academy of Allergy, Asthma & Immunology. Publicado por Elsevier Masson SAS. Todos los derechos reservados.
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Vol 136 - N° 5

P. 1254-1264 - novembre 2015 Regresar al número
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