Updates are available Correction dated 2026-08-04

Article History

Received: 16 April 2026

Accepted: 18 July 2026

First Online: 24 July 2026

Change Date: 3 August 2026

Change Type: Update

Change Details: The original online version of this article has been revised. Part of the caption for Figure 2: “In atopic dermatitis, epidermal barrier dysfunction facilitates chronic exposure to allergens and microbial stimuli, including Staphylococcus aureus, leading to the release of epithelial alarmins by keratinocytes, such as TSLP, IL-25, and IL-33. These signals activate cutaneous antigen-presenting cells, including Langerhans cells and dermal dendritic cells, and initiate antigen-dependent T-cell priming in skin-draining lymph nodes through TCR-MHC recognition and early CD28-CD80/CD86 co-stimulation. Inducible co-stimulatory pathways of the TNFR superfamily, particularly the OX40-OX40L axis, become engaged within the skin following this initial activation phase. OX40 signaling promotes effector T cell expansion, survival, and functional persistence, reinforcing type 2 inflammation during acute disease and supporting a mixed Th2/Th17/Th22 immune profile during the transition to chronic inflammation. Sustained OX40-OX40L engagement contributes to the maintenance of skin-resident memory T cells, epidermal hyperplasia, and long-term inflammatory memory in atopic dermatitis, thereby facilitating disease chronicity and relapse. Created with BioRender.com” was inadvertently included as a regular paragraph under the “Atopic Dermatitis” section.

Change Date: 4 August 2026

Change Type: Correction

Change Details: A Correction to this paper has been published:

Change Details: https://doi.org/10.1007/s12016-026-09188-w

Declarations

Competing interests: The authors declare no competing interests.