The Role of T Cells in AD
T cells play a pivotal role in shaping the immune behavior in atopic dermatitis (AD)1,2
T cells may be the key to understanding why AD can remain persistently active.1
On this page:
T cells as drivers of AD chronicity
Meet the key immune cells behind AD's chronic activity
How T-cell activity shapes AD heterogeneity
T cells as drivers of AD chronicity
In AD, immune responses are shaped by coordinated interactions across diverse T-cell populations. Signals from antigen presentation and costimulation guide T-cell growth, survival, and the release of inflammatory signals—impacting the magnitude of the immune response.3,4
Differences in T-cell signaling and function help explain AD’s immune heterogeneity and variable disease expression across patients.1,2,4,5
Meet the key immune cells behind AD’s chronic activity
Explore how each key immune cell type contributes to the immune response seen in AD, from persistent flares to rapid recurrence. Each “Bes-T” character represents a cell which plays an important role in immune defenses, and a specific role in contributing to immune dysregulation and shaping AD chronicity.
ACE
Antigen-presenting cell (APC)
APCs are specialized immune cells that initiate the immune response by presenting antigens (immune triggers) and delivering essential costimulatory signals to T cells. These signals are transmitted through ligand-receptor interactions on the cell surface.2,4
Why it matters in AD: Persistent costimulatory signaling can amplify effector T-cell activity and contribute to the inflammation that characterizes AD.2,4
EFFIE
Effector T cell
When presented with antigens, effector T cells differentiate into specialized subsets and produce inflammatory cytokines—shaping the magnitude and persistence of immune responses depending on the signals they receive.1,2,5
Why it matters in AD: Effector T-cell activity shapes the magnitude and persistence of immune responses in AD, and the self‑perpetuating inflammatory cycle that is seen in the disease. While Th2 cells are often central to AD inflammation, other effector subsets—such as Th1, Th17, and Th22—may also play important roles, highlighting the complexity and heterogeneity of
immune dysregulation in AD.1,4
REGGIE
Regulatory T cell (Treg)
Regulatory T cells help maintain immune homeostasis by providing inhibitory signals that limit excessive effector activity.3
Why it matters in AD: Persistent costimulation by APCs can impair T‑regulatory function, reducing their ability to suppress effector responses. When effector T cells and memory T cells dominate the immune response, regulatory T cells are no longer able to maintain sufficient inhibitory control, leading to the inflammation that drives AD.2,3,6
MEMO
Memory T cell
Memory T cells preserve long‑term immune memory, enabling the system to respond rapidly when antigens reappear.1,2
Why it matters in AD: Memory T cells survive and remain in the skin long after active inflammation subsides, perpetuating AD recurrence and chronicity.1,2
All T cells are important
Each T cell plays a distinct role in immune defense and regulation. Maintaining these populations while potentially addressing immune dysregulation may be important when supporting your patient's immune health.1,3-5
How T‑cell activity shapes AD heterogeneity
AD is driven by multiple effector T-cell subsets that release distinct cytokines shaping inflammation, chronicity, and immune behavior. Each patient has a unique immune signature comprised of inflammatory drivers across Th2, Th1, Th17, and Th22 pathways.1
This complexity in immune signatures helps explain AD’s unpredictability and variability in treatment responses. When outcomes differ across patients, it may reflect underlying immunologic diversity. These differences highlight the need for treatments that consider diverse immune drivers.1,4
Th=T helper.
References: 1. 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 2. 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 3. 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 4. 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 5. Zhang DJ, Hao F, Qian T, Cheng HX. Expression of helper and regulatory T cells in atopic dermatitis: a meta-analysis. Front Pediatr. 2022;10:777992. doi:10.3389/fped.2022.777992 6. Schettini N, Pacetti L, Corazza M, Borghi A. The role of OX40-OX40L axis in the pathogenesis of atopic dermatitis. Dermatitis. 2025;36(1):28-36. doi:10.1089/derm.2024.0058
