Alexandra Golant, MD, discusses highlights from her lecture on Atopic Dermatitis Immunology on Thursday, November 3, 2022, at the PA/NP Elevate-Derm Conference in Tucson, Arizona.

In this video

Dr. Golant frames AD pathophysiology as "two sides of the coin" — the barrier defects patients are born with and the immune-mediated defects seen downstream — tied together by the itch-scratch cycle. She notes the debate over what comes first remains open, but that both contribute to the signs and symptoms of AD, and both must be addressed to get a patient to their therapeutic goal. While AD is primarily a TH2-driven disease, she highlights the growing recognition of TH22, TH17, and even TH1 contributions, especially as lesions move from the acute to the chronic phase.

She emphasizes that "no two patients with atopic dermatitis look exactly alike," with presentation varying by acuity, skin tone, and body location — and points to emerging phenotypes such as Asian patients presenting with more psoriasiform-like features. On treatment, Golant argues that understanding mechanism of action is critical: biologics block cytokines extracellularly, while JAK-STAT inhibitors act on a broader downstream pathway. She urges clinicians to get comfortable with JAK inhibitors early, calling them "here to stay," and says the most rewarding part of her work is finally getting long-undertreated patients clear and giving them a quality of life they didn't think could be theirs.

  • AD pathogenesis has "two sides of the coin" — barrier defects and immune dysfunction, linked by the itch-scratch cycle — and treatment must address both.
  • AD is primarily TH2-driven, but TH22, TH17, and TH1 pathways increasingly contribute to lesion chronicity, particularly as disease shifts from acute to chronic.
  • There is immunologic heterogeneity in AD; "no two patients look exactly alike," and phenotypes vary by acuity, skin tone, and location — watch for atypical presentations such as psoriasiform features in Asian patients.
  • Biologics block cytokines extracellularly, while JAK-STAT inhibitors act more broadly on downstream inflammation, suppressing other cytokines in the same family — understanding mechanism of action guides therapeutic choice.
  • Getting comfortable with JAK inhibitors early matters; they are "here to stay" in dermatology, and this is "just the beginning."