Diverse activation and differentiation of multiple B-cell subsets in patients with atopic dermatitis but not in patients with psoriasis - 07/01/16
, Juana Gonzalez, PhD b, Kathleen M. Bonifacio, MD a, Avner Shemer, MD c, Peng Xiangyu, MSc d, Norma Kunjravia, MD a, Dana Malajian, BA a, e, Judilyn Fuentes-Duculan, MD a, Hitokazu Esaki, MD a, d, Shinji Noda, MD a, Yeriel Estrada, BSc d, Hui Xu, MSc d, Xiuzhong Zheng, MSc a, James G. Krueger, MD, PhD a, Emma Guttman-Yassky, MD, PhD a, dAbstract |
Background |
Atopic dermatitis (AD) and psoriasis pathogeneses involve skin barrier impairment and immune dysregulation; however, the contribution of B-cell imbalances to these diseases has not yet been determined.
Objective |
We sought to quantify B-cell populations and antibody-secreting cells in the blood of patients with AD, patients with psoriasis, and control subjects.
Methods |
We studied 34 adults with moderate-to-severe AD (mean SCORAD score, 65), 24 patients with psoriasis (mean Psoriasis Area and Severity Index score, 16), and 27 healthy subjects using an 11-color flow cytometric antibody panel. IgD/CD27 and CD24/CD38 core gating systems were used to determine frequencies of plasmablasts and naive, memory, transitional, and activated B cells.
Results |
We measured increased CD19+CD20+ B-cell counts in the skin and blood of patients with AD (P < .01). Significantly higher frequencies of chronically activated CD27+ memory and nonswitched memory B cells were observed in patients with AD (P < .05), with lower values of double-negative populations (4% for patients with AD vs 7% for patients with psoriasis [P = .001] and 6% for control subjects [P = .02]). CD23 expression was highest in patients with AD and correlated with IgE levels (P < .01) and disease severity (r = 0.6, P = .0002). Plasmablast frequencies and IgE expression were highest in all memory subsets of patients with AD (P < .01). Finally, CD19+CD24++CD38++ transitional and CD19+CD24−CD38− new memory B-cell counts were higher in patients with AD versus those in patients with psoriasis (2.8% vs 1.4% [P = .001] and 9.2% vs 5.7% [P = .02], respectively).
Conclusions |
AD is accompanied by systemic expansion of transitional and chronically activated CD27+ memory, plasmablast, and IgE-expressing memory subsets. These data create a critical basis for the future understanding of this debilitating skin disease.
Le texte complet de cet article est disponible en PDF.Key words : Atopic dermatitis, psoriasis, B cells
Abbreviations used : AD, ASC, CLA, DN, IHC, NSM, PASI, SwMe, TCM, TEM, TLR, Treg
Plan
| T.C. was cosponsored by the Center for Basic and Translational Research on Disorders of the Digestive System through the generosity of the Leona M. and Harry B. Helmsley Charitable Trust. J.G. was supported in part by grant no. UL1TR0000 from the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health (NIH) Clinical and Translational Science Award (CTSA) program. D.M. received funding from the American Dermatological Association Medical Student Fellowship. J.G.K. was supported by grant no. 5UL1RR024143-02 from the National Center for Research Resources (NCRR), a component of the NIH, and the NIH Roadmap for Medical Research. E.G.-Y. was supported by the Dermatology Foundation Physician Scientist Career Development Award. |
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| Disclosure of potential conflict of interest: J. G. Krueger has received research support (grants paid to his institution) and/or personal fees from Pfizer, Amgen, Janssen, Lilly, Merck, Novartis, Kadmon, Dermira, Boehringer, Innovaderm, Kyowa, BMS, Serono, BiogenIdec, Delenex, AbbVie, Sanofi, Baxter, Paraxel, 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, Steifel/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. |
Vol 137 - N° 1
P. 118 - janvier 2016 Retour au numéro
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