The Continuous Burden of Atopic Dermatitis can Have Far-Reaching Impact

  • The burden of inadequately controlled atopic dermatitis may become chronic, or even cumulative, impacting patients throughout their lives1,2

~70 - 80%

of atopic dermatitis patients develop additional type 2 inflammatory diseases, such as asthma or allergic rhinitis, which correlate with atopic dermatitis severity5,6
* The age of children included in the Eczema Society of Canada Atopic Dermatitis Quality of Life Report survey ranged from 0 to 18 years

~70 - 80%

of atopic dermatitis patients develop additional type 2 inflammatory diseases, such as asthma or allergic rhinitis, which correlate with atopic dermatitis severity5,6
* The age of children included in the Eczema Society of Canada Atopic Dermatitis Quality of Life Report survey ranged from 0 to 18 years

~70 - 80%

of atopic dermatitis patients develop additional type 2 inflammatory diseases, such as asthma or allergic rhinitis, which correlate with atopic dermatitis severity5,6

* The age of children included in the Eczema Society of Canada Atopic Dermatitis Quality of Life Report survey ranged from 0 to 18 years
    1. Zuberbier T et al. J Allergy Clin Immunol 2006; 118:226–232.
    2. Ibler K and Jemec GBE. Dermatol Rep 2011; 31; 3(1):8–10.
    3. Eczema Society of Canada. Atopic Dermatitis Quality of Life Report. 2017.
    4. Stocker RPJ et al. Arch Clin Neuropsychol 2017; 32:349–368.
    5. Davis DM et al. Semin Cutan Med Surg 2017; 36(3):95–99.
    6. Eckert L et al. Global Aware. Report Global 2018.
    7. Holm EA et al. J Eur Acad Dermat Venereol 2006; 20(3):255–259.

Around 3 in 5 Adult Moderate-to-Severe Atopic Dermatitis Patients are Inadequately Controlled Despite Treatment1*

A chronic, inadequately controlled disease driven by persistent underlying inflammation7,8
Patients may experience intensified disease activity for 30–50% of the year2
Current treatment paradigm (OCS/ immunosuppressants) primarily addresses disease manifestation using a reactive, episodic approach9
Length of treatment with systemic steroids and other immunosuppressants is limited by common side effects and chance of rebounds11

Continuous Treatment of Underlying Inflammation is Warranted for Long-Term Disease Control10

A more sustainable treatment paradigm proactively targets the persistent underlying inflammation with a safety profile that allows for continuous treatment10-12
Adequately controlled disease with long-term improvements in signs, symptoms, and quality of life.
    1. Wei W et al. J Dermatol 2018; 45:150–157.
    2. Zuberbier T et al. J Allergy Clin Immunol 2006; 118:226–232.
    3. International Alliance of Dermatology Patient Organizations. Atopic Dermatitis: A Collective Global Voice for Improving Care. February 2018.
    4. Hajar T et al. An Bras Dermatol 2018; 93:104–107.
    5. Boguniewicz M et al. J Allergy Clin Immunol Pract 2017; 5:1519–1531.
    6. Ibler K & Jemec GBE. Dermatol Rep 2011; 3:e5.
    7. Gittler J et al. J Allergy Clin Immunol 2012; 130:1344–1354.
    8. Guttman-Yassky E et al. J Allergy Clin Immunol 2011; 127:1420–1432.
    9. Leung DYM et al. J Clin Invest 2004; 113:651–657.
    10. Wollenberg A et al. Ann Dermatol 2012; 24(3):253–260.
    11. Wollenberg A et al. J Eur Acad Dermatol Venereol 2018; 32(6):850–878.
    12. Wollenberg A et al. J Eur Acad Dermatol Venereol 2018; 32:657–682.

Dysregulation of the Type 2 Immune Response Pathway Leads to Underlying Type 2 Inflammation in Atopic Dermatitis and Other Type 2 Inflammatory Diseases*

INFLAMMATORY PATHWAY TYPE 1 TYPE 2 TYPE 3
Primary immune cells1-3
Key cytokines1-4
Associated intracellular signaling pathway4,5
Natural defensive roles against:1,3,6 Viral infection
Intracellular bacterialinfection
Cancer cells		 Allergens
Parasites		 Extracellular bacteria
Fungi
Associated diseases when dysregulated7-8 Psoriasis
Psoriatic arthritis		 Atopic dermatitis
Asthma
CRSwNP		 Psoriasis
Psoriatic arthritis
*Simplified depiction based on key published information; not meant to be exhaustive in nature.
    1. Kaiko GE et al. Immunol 2008; 123:326–338.
    2. Eyerich K & Eyerich S. J Eur Acad 2017; 32:692–703.
    3. Raphael I et al. Cytokine 2015; 74:5–17.
    4. Schwartz DM et al. Nat Rev Rheumatol 2016; 12(1):25–36.
    5. Murray PJ. J Immunol 2007; 178(5):2623–2629.
    6. Annunziato F et al. J Allergy Clin Immunol 2014; 136(3):626–635.
    7. Schleimer R. Annu Rev Pathol 2017; 12:331–357.
    8. Nakayama T et al. Annu Rev Immunol 2017; 35:53–84.
    9. Coates LC et al. Semin Arthritis Rheum 2016; 46:291–304.

In Atopic Dermatitis, Type 2 Inflammation is Always Present Throughout the Body, Even in Nonlesional or Normal-Looking Skin1–3

  • Dysregulation of the type 2 immune response and increased IL-4 and IL-13 signaling drives and perpetuates type 2 inflammation, which contributes to clinical disease features in atopic dermatitis and other type 2 inflammatory diseases3-5
  • IL-4 and IL-13 are produced by various cell types such as Th2 and ILC2 cells in response to increased signaling through the IL-4Rα present on those cells6-8
    1. Leung DYM et al. J Clin Invest 2004; 113:651–657.
    2. Suárez-Fariñas M et al. J Allergy Clin Immunol 2011; 127:954–964.
    3. Gittler JK et al. J Allergy Clin Immunol 2012; 130:1344–1354.
    4. Biedermann T et al. Front Immunol 2015; 6:353.
    5. Gandhi NA et al. Nat Rev Drug Discov 2016; 15:35–50.
    6. Artis D & Spits H. Nature 2015; 517:293–301.
    7. McLeod JJA et al. Cytokine 2015; 75(1):57–61.
    8. Guttman-Yassky E et al. J Allergy Clin Immunol 2019; 143:155–172.

Nonlesional Skin is not Normal Skin

In atopic dermatitis, subclinical inflammation is also present in nonlesional skin1–3
    1. Leung DYM et al. J Clin Invest 2004; 113:651–657.
    2. Suárez-Fariñas M et al. J Allergy Clin Immunol 2011; 127:954–964.
    3. Gittler JK et al. J Allergy Clin Immunol 2012; 130:1344–1354.
    4. Biedermann T et al. Front Immunol 2015; 6:353.
    5. Gandhi NA et al. Nat Rev Drug Discov 2016; 15:35–50.
    6. Artis D & Spits H. Nature 2015; 517:293–301.
    7. McLeod JJA et al. Cytokine 2015; 75(1):57–61.
    8. Guttman-Yassky E et al. J Allergy Clin Immunol 2019; 143:155–172.

MAT-BH-2100439/V1/June 2021