Psoriasis in an Asian patient with atopic dermatitis treated with dupilumab

Mami Ishibashi, Reiko Koga, Eriko Adachi, Yuna Yamagami, Masami Ichinona, Yoshiaki Yoshikawa

Article ID: 1286
Vol 5, Issue 1, 2021

VIEWS - 1323 (Abstract) 321 (PDF)


Dupilumab is a monoclonal antibody against the alpha subunit of the interleukin (IL)-4 receptor that inhibits IL-4 and IL-13 signaling, which plays a central role in Th2 inflammation in AD.

Here, we report the first Asian case of psoriasis unexpectedly induced by dupilumab therapy for AD. Compared with European and American AD phenotype, Asian AD phenotype is characterized by changes in the psoriasiform phenotype, associating with higher Th17 activation. The blockade of IL-4/IL-13 signaling by dupilumab may induce psoriasis eruption corresponding to shift from a Th2- to Th17- mediated inflammatory response in the skin.


Dupilumab; Atopic Dermatitis; Psoriasis; Th2; Th17

Full Text:



1. Nomura T, Wu J, Kabashima K, et al. Endophenotypic variations of atopic dermatitis by age, race, and ethnicity. The Journal of Allergy and Clinical Immunology: In Practice 2020; 8(6): 1840–1852.

2. Beck LA, Thaçi D, Hamilton JD, et al. Dupilumab treatment in adults with moderate-to-severe atopic dermatitis. New England Journal of Medicine 2014; 371(2): 130–139.

3. Noda S, Suárez-Fariñas M, Ungar B, et al. The Asian atopic dermatitis phenotype combines features of atopic dermatitis and psoriasis with increased TH17 polarization. Journal of Allergy and Clinical Immunology 2015; 136(5): 1254–1264.

4. Guttman-Yassky E, Krueger JG. Atopic dermatitis and psoriasis: two different immune diseases or one spectrum? Current Opinion in Immunology 2017; 48: 68–73.

5. Guenova E, Skabytska Y, Hoetzenecker W, et al. IL-4 abrogates TH17 cell-mediated inflammation by selective silencing of IL-23 in antigen-presen- ting cells. Proceedings of the National Academy of Sciences 2015; 112(7): 2163–2168.



  • There are currently no refbacks.

Copyright (c) 2021 Mami Ishibashi

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

This site is licensed under a Creative Commons Attribution 4.0 International License.