graphic created by ADKeySuspect.com of a magnifying glass over inflamed skin. il-13 is embedded in the skin under the magnifying glass.
THE SPECIFIC DRIVERS OF ATOPIC DERMATITIS AREN’T ALWAYS IN PLAIN SIGHT1,2

EXPLORE A KEY SUSPECT 
BEHIND AD INFLAMMATION 
IN THE SKIN: IL-132

Several Th2 cytokines, including IL-13, are key drivers of inflammation in atopic dermatitis.2,3

illustration of a woman with atopic dermatitis on neck and face

UNCOVER THE BURDEN OF DISEASE

The chronic, persistent nature of atopic dermatitis (AD) means it’s always there, even when patients may appear asymptomatic. The cycle of chronic itch and inflammation can have a significant impact on patients.1,4
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Table created by ADKeySuspect.com highlighting a study of skin samples taken from 90 patients with atopic dermatitis and 20 healthy controls to assess protein levels in lesional skin using a skin–tape stripping methodology; the data demonstrated high levels of IL-13 in all skin samples and low or undetectable IL-4 levels

EXPLORE THE Th2 CYTOKINES 
THAT DRIVE AD

Th2 cytokines are the key drivers of the inflammatory cascade associated with atopic dermatitis. How these manifest can differ across non-lesional, acute lesional, and chronic lesional skin.5

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IL13 cytokine created by ADKeySuspectcom

DISCOVER THE ROLE OF IL-13 IN AD

IL-13 plays a key role in the inflammation underlying AD signs and symptoms. In AD skin, overexpression of IL-13 leads to a variety of pathophysiologic issues, including disruption of the skin barrier and amplified inflammation.6-12
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References

  1. Suárez-Fariñas M, Tintle S, Shemer A, et al. Non-lesional atopic dermatitis (AD) skin is characterized by broad terminal differentiation defects and variable immune abnormalities. J Allergy Clin Immunol. 2011;127(4):954-964.e1-4.
  2. 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.
  3. 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.
  4. Silverberg JI, Kantor R. The role of interleukins 4 and/or 13 in the pathophysiology and treatment of atopic dermatitis. Dermatol Clin. 2017;35(3):327-334.
  5. Weidinger S, Beck LA, Bieber T, Kabashima K, Irvine AD. Atopic dermatitis. Nat Rev Dis Primers. 2018;4(1):1-20.
  6. Kim BE, Leung DY, Boguniewicz M, Howell MD. Loricrin and involucrin expression is down-regulated by Th2 cytokines through STAT-6. Clin Immunol. 2008;126(3):332-337.
  7. Berdyshev E, Golvea E, Bronova I, et al. Lipid abnormalities in atopic skin are driven by type 2 cytokines. JCI Insight. 2018;3(4):e98006.
  8. Nomura I, Goleva E, Howell MD, et al. Cytokine milieu of atopic dermatitis, as compared to psoriasis, skin prevents induction of innate immune response genes.
    J Immunol. 2003;171(6):3262-3269.
  9. Purwar R, Werfel T, Wittmann M. IL-13-stimulated human keratinocytes preferentially attract CD4+CCR4+ T cells: possible role in atopic dermatitis. J Invest Dermatol. 2006;126(5):1043-1051.
  10. Oetjen LK, Mack MR, Feng J, et al. Sensory neurons co-opt classical immune signaling pathways to mediate chronic itch. Cell. 2017;171(1):217-28.e13.
  11. Moriya C, Jinnin M, Yamane K, et al. Expression of matrix metalloproteinase-13 is controlled by IL-13 via PI3K/Akt3 and PKC-δ in normal human dermal fibroblasts.
    J Invest Dermatol. 2011;131(3):655-661.
  12. Mack MR, Kim BS. The itch-scratch cycle: a neuroimmune perspective. Trends Immunol. 2018;39(12):980-991.