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In atopic dermatitis, DISCOVER WHAT'S AT THE CORE


Current evidence has shown that nonlesional skin is not normal skin, owing to persistent subclinical inflammation throughout the body.1-4 This underlying chronic inflammation is a source of the primary signs and symptoms of atopic dermatitis.1,3,4 Th2 dominance in tissue samples from patients with atopic dermatitis is well documented, with Th2-specific cytokines dominating the immune infiltrate.5

Studies of tissue samples from patients with atopic dermatitis have shown that acute and chronic lesions, as well as nonlesional skin, are associated with an increased1,6-9:

  • Number of immune cells that secrete IL-4 and IL-13
  • Amount of Th2 signaling, compared with samples from healthy controls

Animal and human studies have shown that IL-4 and IL-13 are key drivers of a systemic, chronic inflammatory response.13
Research in animal and in vitro models has demonstrated:

  • IL-13 is considered to be an “effector” cytokine with distinct but overlapping roles from IL-4 in both the normal immune response to parasitic infections and the pathogenesis of atopic dermatitis14

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References: 1. Gittler JK, Shemer A, Suárez-Fariñas M, et al. Progressive activation of Th2/Th22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis. J Allergy Clin Immunol. 2012;130(6):1344-1354. 2. De Benedetto A, Rafaels NM, McGirt LY, et al. Tight junction defects in patients with atopic dermatitis. J Allergy Clin Immunol. 2011;127(3):773-786. 3. Leung DYM, Boguniewicz M, Howell MD, Nomura I, Hamid QA. New insights into atopic dermatitis. J Clin Invest. 2004;113(5):651-657. 4. 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(4):954-964. 5. Guttman-Yassky E, Nograles KE, Krueger JG. Contrasting pathogenesis of atopic dermatitis and psoriasis─Part II: immune cell subsets and therapeutic concepts. J Allergy Clin Immunol. 2011;127(6):1420-1432. 6. Hamid Q, Boguniewicz M, Leung DYM. Differential in situ cytokine gene expression in acute versus chronic atopic dermatitis. J Clin Invest. 1994;94(2):870-876. 7. Lonati A, Licenziati S, Canaris AD, et al. Reduced production of both Th1 and Tc1 lymphocyte subsets in atopic dermatitis (AD). Clin Exp Immunol. 1999;115(1):1-5. 8. Tazawa T, Sugiura H, Sugiura Y, Uehara M. Relative importance of IL-4 and IL-13 in lesional skin of atopic dermatitis. Arch Dermatol Res. 2004;295(11):459-464. 9. Novak N, Bieber T, Leung DYM. Immune mechanisms leading to atopic dermatitis. J Allergy Clin Immunol. 2003;112(6 suppl):S128-S139. 10. Noda S, Kruger JG, Guttman-Yassky E. The translational revolution and use of biologics in patients with inflammatory skin diseases. J Allergy Clin Immunol. 2015;135(2):324-336. 11. Guttman-Yassky E, Dhingra N, Leung DYM. New era of biological therapeutics in atopic dermatitis. Expert Opin Biol Ther. 2013;13(4):549-561. 12. Biedermann T, Skabytska Y, Kaesler S, Volz T. Regulation of T cell immunity in atopic dermatitis by microbes: the yin and yang of cutaneous inflammation. Front Immunol. 2015;6:353. doi:10.3389/fimmu.2015.00353. 13. Brandt EB, Sivaprasad U. Th2 cytokines and atopic dermatitis. J Clin Cell Immunol. 2011;2(3):1-25. 14. Junttila IS, Mizukami K, Dickensheets H, et al. Tuning sensitivity to IL-4 and IL-13: differential expression of IL-4Rɑ, IL-13Rɑ1, and γc regulates relative cytokine sensitivity. J Exp Med. 2008;205(11):2595-2608.