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While traditionally associated with type 2 inflammation, its role extends across multiple barrier tissues, including the skin and respiratory mucosa, where it integrates epithelial signals with adaptive immune responses.\u00a0To provide a comprehensive and integrative overview of the OX40-OX40L axis as a shared driver of immune persistence across skin and airway inflammatory diseases and to discuss its therapeutic implications.\u00a0A narrative review was conducted based on a focused literature search of PubMed, Scopus, and Web of Science up to February 2026. Experimental, translational, and clinical studies addressing OX40-OX40L biology and therapeutic targeting were included.\u00a0OX40 signaling acts as a late co-stimulatory pathway that sustains effector T-cell survival, promotes tissue-resident memory T-cell formation, and modulates regulatory T-cell function. In barrier tissues, epithelial-derived alarmins such as TSLP and IL-33 induce OX40L expression on antigen-presenting cells, reinforcing type 2-polarized immune responses. This axis contributes to chronic inflammation in atopic dermatitis, asthma, allergic rhinitis, and nasal polyposis, supporting the concept of shared mechanisms of immune persistence across type 2 inflammatory diseases. Beyond type 2 immunity, OX40-OX40L signaling also participates in Th1-, Th17-, and Th22-mediated responses, as well as in autoimmune, fibrosing, and lymphoproliferative disorders. Therapeutic targeting of this pathway, particularly with monoclonal antibodies such as amlitelimab, has demonstrated clinically meaningful efficacy and suggests potential for durable disease modification.\u00a0The OX40-OX40L axis represents an important immunological pathway linking epithelial activation to adaptive immune memory across barrier tissues. Its role in sustaining immune persistence provides a conceptual framework for understanding chronic inflammatory diseases and supports continued investigation of therapies targeting upstream co-stimulatory pathways.<\/jats:p>","DOI":"10.1007\/s12016-026-09187-x","type":"journal-article","created":{"date-parts":[[2026,7,24]],"date-time":"2026-07-24T16:33:04Z","timestamp":1784910784000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The OX40-OX40L Co-Stimulatory Pathway as a Shared Driver of Immune Persistence in Skin and Airway Inflammation"],"prefix":"10.1007","volume":"69","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5454-3671","authenticated-orcid":false,"given":"Francisco Jos\u00e9","family":"Navarro-Trivi\u00f1o","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiago","family":"Torres","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ricardo","family":"Ruiz-Villaverde","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9 Luis","family":"Moreno-Amador","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pedro","family":"Mendes-Bastos","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,7,24]]},"reference":[{"key":"9187_CR1","doi-asserted-by":"publisher","first-page":"13","DOI":"10.1016\/j.molimm.2017.01.006","volume":"83","author":"J Willoughby","year":"2017","unstructured":"Willoughby J, Griffiths J, Tews I et al (2017) OX40: Structure and function \u2013 What questions remain? 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Part of the caption for Figure 2: \u201cIn 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\u201d was inadvertently included as a regular paragraph under the \u201cAtopic Dermatitis\u201d section.","order":7,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"4 August 2026","order":8,"name":"change_date","label":"Change Date","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"Correction","order":9,"name":"change_type","label":"Change Type","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"A Correction to this paper has been published:","order":10,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"https:\/\/doi.org\/10.1007\/s12016-026-09188-w","URL":"https:\/\/doi.org\/10.1007\/s12016-026-09188-w","order":11,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"The authors declare no competing interests.","order":1,"name":"Ethics","label":"Competing interests","group":{"name":"EthicsHeading","label":"Declarations"}}],"article-number":"59"}}