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IN ATOPIC DERMATITIS, KEY TYPE 2 CYTOKINES MAY BE AT THE CORE OF PERSISTENT,
UNDERLYING INFLAMMATION

IL-4 and IL-13 are drivers of chronic Type 2 inflammation1

Current evidence has shown that nonlesional skin is not normal skin, owing to persistent subclinical inflammation throughout the body.2-4 This underlying 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 increased expression of Th2-specific cytokines.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 Type 2 cytokine signaling, compared with samples from healthy controls

Explore the Type 2 pathway by tapping the following icons:

IL-4 and IL-13 Cytokines in Th2 Signaling IL-4 and IL-13 Cytokines in Th2 Signaling IL-4 and IL-13 Cytokines in Th2 Signaling
IL-4 and IL-13 Cytokines in Th2 Signaling IL-4 and IL-13 Cytokines in Th2 Signaling IL-4 and IL-13 Cytokines in Th2 Signaling IL-4 and IL-13 Cytokines in Th2 Signaling
IL-4 and IL-13 Cytokines in Th2 Signaling IL-4 and IL-13 Cytokines in Th2 Signaling IL-4 and IL-13 Cytokines in Th2 Signaling

Animal and human studies have shown that IL-4 and IL-13 may be drivers of a systemic, chronic inflammatory response.13

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This has increased my understanding of the mechanism of underlying inflammation

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.