Conference summaries


Atopic dermatitis and psoriasis: On a spectrum?

Presented by: Emma Guttman-Yassky, MD, PhD
Icahn School of Medicine, Mount Sinai Medical School, New York, NY; USA
  • Psoriasis (PsO) and atopic dermatitis (AD) are common, chronic inflammatory skin diseases. 
  • Treating PsO today is relatively easy.
  • AD is more difficult to treat as there is more immune activation and more heterogeneity.
  • Both PsO vulgaris and chronic AD are generally characterized by psoriasiform dermatitis.
  • At a mechanistic level both diseases can be classified as epidermal hyperplasia responses to cytokines produced by activated T-cells in skin lesions [1].
  • PsO and AD are diseases of distinct T-cell ‘polar’ subsets.
  • Targeting Th17/IL-17 is an extremely effective treatment for PsO.
  • Targeting Th2/IL-4 & IL-13 is a highly effective treatment for AD [2].
  • See Table 1.
  • A paradigm shift in the pathogenesis of AD has been proven, revealing a progressive activation of Th2 and Th22 immune axes from the acute to chronic phases [3].
  • See Figure 1.
  • Systemic inflammation is well established in psoriasis but the concept of AD being a systemic disease is emerging.
  • There is an activated T cell response and circulatory cytokines and cardiovascular associated markers compared to control patients, and these differences are also observed when compared to psoriasis patients too [4].
  • Additionally, other studies have underlined the associations of AD with atherosclerotic signaling [5], cardiovascular disease [6] and coronary artery disease [7].
  • Further, the non-lesional AD skin is practically abnormal, unlike non-lesional skin in PsO (Th2 and Th22) [8].
  • The high-grade systemic immune activation in AD (T-cells, B cells, circulating cytokines) is responsible for the development of atopic co-morbidities (such as asthma) and other co-morbidities, such as cardiovascular and infection [9].
  • Therefore, in a patient with >10% body surface area involvement, a topical approach will not resolve the disease.
  • A systemic treatment approach is therefore necessary in moderate-to-severe AD due to the high level of systemic immune activation.
  • No. There are multiple phenotypes associated with AD and the immune polarizations and epidermal barriers are different [10].
  • All AD subtypes share robust Th2 activation, but stratifications of biomarkers specific to different AD phenotypes may be important for developing a personalized AD medical approach.
  • Asian AD has been suggested to be different from European AD in terms of clinical phenotype, epidemiological and blood and skin data (Th17+ and IL-17+ cells) [11].
  • Asian AD is characterized by increased hyperplasia, marked parakeratosis and focal hypogranulosis, but there is a similar Th2 axis [12].
  • There is therefore, a blended phenotype between PsO and European AD.
  • At the mechanistic level both PsO and AD can be classified as epidermal responses to cytokines produced by activated T-cells in skin lesions.
  • Broad T-cell targeting approaches are effective in both AD and PsO.
  • Targeting polar T-cells can now be done with different drugs in AD vs. PsO, but it seems that cross treatment approaches could be possible.


  • IL4Rα mAb potentially inhibits both IL4 and IL-13 signaling.
  • 4-week dose response – EASI 50 was achieved in 71% of patients on the highest dose [13].
  • No difference response was independent of baseline IgE or FLG mutation status [13].
  • More evident down regulation of multiple markers in the DPL300 group [13].
  • In a longer study, the AD transcriptome was progressively reversed and at week 16 the LS phenotype of the lesional and non-lesional skin were similar, with a major reversal of dysregulated genes at Week 16 [14].
  • The AD barrier defect was also reversed at Week 16 [14].
  • This establishes the Th2 axis and IL-4 and IL-13 cytokines as pathogenic in AD and cements AD as a reversible, immune driven disease, like psoriasis.


  • Small study of 60 patients showed that in severe patients a significant difference in SCORAD was observed, but not in the non-severe patients [15].
  • According to baseline IL-22 expression above or below the median, the higher IL-22 baseline patients largely improved, where the other group saw no improvement with occasional worsening [15].


  • Treating psoriasis today is relatively easy as Th17 is shared across all variants.
  • Th2 axis is also common across the spectrum of AD subsets.
  • AD is more difficult to treat as there is more immune activation and more heterogeneity.
  • AD may require targeting of more than 1 cytokine axis or different targeting in different endotypes (personalized medicine approach).



  1. Guttman-Yassky E, Lowes MA, Fuentes-Duculan J, et al. Major differences in inflammatory dendritic cells and their products distinguish atopic dermatitis from psoriasis. J Allergy Clin Immunol. 2007;119:1210
  2. Guttman-Yassky E, Krueger JDE. Atopic dermatitis and psoriasis: two different immune diseases or one spectrum? Curr Opin Immunol. 2017;48:68-73
  3. Gittler JK, Shemer A, Suárez-Fariñas M, et al. Progressive activation of T(H)2/T(H)22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis. J Allergy Clin Immunol. 2012;130:1344-54
  4. Czarnowicki T, Malajian D, Shemer A, et al. Skin-homing and systemic T-cell subsets show higher activation in atopic dermatitis versus psoriasis. J Allergy Clin Immunol. 2015;136:208-11
  5. Ewald DA, Malajian D, Krueger JG, et al. Meta-analysis derived atopic dermatitis (MADAD) transcriptome defines a robust AD signature highlighting the involvement of atherosclerosis and lipid metabolism pathways. BMC Med Genomics. 2015;8:60
  6. Silverberg JI. Association between adult atopic dermatitis, cardiovascular disease, and increased heart attacks in three population-based studies. Allergy. 2015;70:1300-8
  7. Hjuler KF, Böttcher M, Vestergaard C, et al. Increased Prevalence of Coronary Artery Disease in Severe Psoriasis and Severe Atopic Dermatitis. Am J Med. 2015;128:1325-34.e2
  8. Suárez-Fariñas M, Tintle SJ, Shemer A, et al. Nonlesional atopic dermatitis skin is characterized by broad terminal differentiation defects and variable immune abnormalities. J Allergy Clin Immunol. 2011;127:954-64
  9. Ungar B, Garcet S, Gonzalez J, et al. An Integrated Model of Atopic Dermatitis Biomarkers Highlights the Systemic Nature of the Disease. J Invest Dermatol. 2017;137:603-613
  10. Czarnowicki T, He H, Krueger JG, Guttman-Yassky E. Atopic dermatitis endotypes and implications for targeted therapeutics. J Allergy Clin Immunol. 2019;143:1-11
  11. Koga C, Kabashima K, Shiraishi N, et al. Possible pathogenic role of Th17 cells for atopic dermatitis. J Invest Dermatol. 2008;128:2625-30
  12. 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. J Allergy Clin Immunol. 2015;136:1254-64
  13. Beck LA, Thaçi D, Hamilton JD, et al. Dupilumab treatment in adults with moderate-to-severe atopic dermatitis. N Engl J Med. 2014;10;371:130-9
  14. Guttman-Yassky E, Bissonnette R, Ungar B, et al. Dupilumab progressively improves systemic and cutaneous abnormalities in patients with atopic dermatitis. J Allergy Clin Immunol. 2019;143:155-172
  15. Brunner PM, Pavel AB, Khattri S, et al. Baseline IL-22 expression in patients with atopic dermatitis stratifies tissue responses to fezakinumab. J Allergy Clin Immunol. 2019;143:142-154

Presenter disclosure(s): [none provided]

Written by: Johanna Chester, BA

Reviewed by: Martina Lambertini, MD

All report

Welcome to the SPIN 2019 Highlights

Jo Lambert, MD, PhD

With this collection of summaries from selected presentations at SPIN 2019, and interviews with international experts, we hope to share with you some of the highlights of this year’s congress. The international network met … [ Read all ]



Atopic dermatitis and psoriasis: On a spectrum?

Presented by: Emma Guttman-Yassky, MD, PhD



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