Even when AD appears controlled, many patients still experience ongoing burden1-3
When T cells are out of balance, symptoms can persist.2,4,5
More than 55% of adults with moderate to severe atopic dermatitis report inadequate disease control, even while on treatment.6
The ongoing realities for patients
For many patients, “controlled” atopic dermatitis still comes with visible symptoms and discomfort, even while on treatment. Living with AD often requires continuous care to manage recurring flares and symptoms, impacting routines, social interactions, and overall well‑being.1-3
Understanding the current unmet need in AD
Atopic dermatitis is a heterogeneous disease driven by multiple inflammatory pathways. While many current treatments have made great strides in improving patient outcomes in AD, there still exists an unmet need. Many treatments take an approach of selectively targeting type 2 inflammatory drivers, addressing only part of the immune activity involved in AD.1,2,4
Many current therapies can provide relief of signs and symptoms of AD; however, sustained efficacy may rely on continuous treatment—leaving many in an ongoing cycle of AD management.1,7
How T‑cell imbalance shapes persistent AD
Understanding T cells is crucial to uncovering the patterns that contribute to chronicity. In AD, excessive activation and expansion of effector and memory T cells overwhelm regulatory mechanisms. This imbalance sustains inflammatory loops over time, driving AD chronicity and recurrence.2,4,8
Understanding AD’s complex immune activity
Variations in immune pathways may influence how different patients respond to therapeutic interventions. Understanding the immune pathways—including Th1, Th17, and Th22—that contribute to AD inflammation is crucial in trying to address the immunologic complexity of AD.2
Exploring AD’s inflammatory prequel
The inflammatory prequel is an initiating phase of immune dysregulation in atopic dermatitis. T-cell activation during the inflammatory prequel drives a wide range of inflammatory responses, suggesting it may play a key role in the heterogeneous inflammatory response seen in AD.2,4
OX40 ligand signaling during the inflammatory prequel
During the inflammatory prequel, key signaling via the OX40 ligand pathway contributes to an overactive immune system in AD. Overactivity in this initiating phase of immune dysregulation fuels T-cell imbalance, potentially influencing the wide range of inflammatory drivers involved in the disease.2,4
Th=T helper.
References: 1. Al B, Holzscheck N, Traidl S, et al. Subclinical inflammation precedes atopic dermatitis relapses. J Allergy Clin Immunol. 2025;156(5):1234-1246.e9. doi:10.1016/j.jaci.2025.03.033 2. Croft M, Esfandiari E, Chong C, et al. OX40 in the pathogenesis of atopic dermatitis–a new therapeutic target. Am J Clin Dermatol. 2024;25(3):447-461. doi:10.1007/s40257-023-00838-9 3. Courtney A, Su JC. The psychology of atopic dermatitis. J Clin Med. 2024;13(6):1602. doi:10.3390/jcm13061602 4. Sadrolashrafi K, Guo L, Kikuchi R, et al. An OX-tra’ordinary tale: the role of OX40 and OX40L in atopic dermatitis. Cells. 2024;13(7):587. doi:10.3390/cells13070587 5. Conrad ML, Barrientos G, Cai X, et al. Regulatory T cells and their role in allergic disease. Allergy. 2025;80(1):77-93. doi:10.1111/all.16326 6. Simpson EL, Guttman-Yassky E, Margolis DJ, et al. Association of inadequately controlled disease and disease severity with patient-reported disease burden in adults with atopic dermatitis. JAMA Dermatol. 2018;154(8):903-912. doi:10.1001/jamadermatol.2018.1572 7. Weidinger S, Blauvelt A, Papp KA, et al. Phase 2b randomized clinical trial of amlitelimab, an anti-OX40 ligand antibody, in patients with moderate-to-severe atopic dermatitis. J Allergy Clin Immunol. 2025;155(4):1264-1275. doi:10.1016/j.jaci.2024.10.031 8. Agrawal R, Wisniewski JA, Woodfolk JA. The role of regulatory T cells in atopic dermatitis. Curr Probl Dermatol. 2011;41:112-124. doi:10.1159/000323305
