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Cited by 29Dermatology and Skin DiseasesPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

The DOI matches its Crossref record; 95 of the 96 references it cites were found in a registry or an index, and 1 are not checked yet.

An OX-Tra’Ordinary Tale: The Role of OX40 and OX40L in Atopic Dermatitis

Open access
Sadrolashrafi, Kaviyon, Guo, Lily, Kikuchi, Robin, Hao, Audrey, Yamamoto, Rebecca K., Tolson, Hannah C., Bilimoria, Sara N., Yee, Danielle K., Armstrong, April W.·2024·Cells
DOI 10.3390/cells13070587PMC PMC11011471
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Abstract

The transmembrane glycoprotein OX40 receptor (OX40) and its ligand, OX40L, are instrumental modulators of the adaptive immune response in humans. OX40 functions as a costimulatory molecule that promotes T cell activation, differentiation, and survival through ligation with OX40L. T cells play an integral role in the pathogenesis of several inflammatory skin conditions, including atopic dermatitis (AD). In particular, T helper 2 (TH2) cells strongly contribute to AD pathogenesis via the production of cytokines associated with type 2 inflammation (e.g., IL-4, IL-5, IL-13, and IL-31) that lead to skin barrier dysfunction and pruritus. The OX40-OX40L interaction also promotes the activation and proliferation of other T helper cell populations (e.g., TH1, TH22, and TH17), and AD patients have demonstrated higher levels of OX40 expression on peripheral blood mononuclear cells than healthy controls. As such, the OX40-OX40L pathway is a potential target for AD treatment. Novel therapies targeting the OX40 pathway are currently in development, several of which have demonstrated promising safety and efficacy results in patients with moderate-to-severe AD. Herein, we review the function of OX40 and the OX40-OX40L signaling pathway, their role in AD pathogenesis, and emerging therapies targeting OX40-OX40L that may offer insights into the future of AD management.

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Crossref · 10.3390/cells13070587

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  • The OX40-OX40 L interaction suppresses the production of TREGs, attenuating their suppressive function in inflammation/immune response.

    “The OX40-OX40 L interaction suppresses the production of TREGs, attenuating their suppressive function in inflammation/immune response.”

    From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [67]

  • During the acute phase of inflammation in AD, OX40/OX40 L signaling promotes differentiation of Th2 cells, which express more OX40 and secrete cytokines that will promote rupture of the epidermal barrier, activating antigen-presenting cells that will subsequently express OX40 L.

    “During the acute phase of inflammation in AD, OX40/OX40 L signaling promotes differentiation of Th2 cells, which express more OX40 and secrete cytokines that will promote rupture of the epidermal barrier, activating antigen-presenting cells that will subsequently express OX40 L.”

    From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [67]

  • Effector memory T cells express OX40 and are overexpressed in AD lesions, which may offer a potential immune explanation for AD recurrence and chronicity.

    “Effector memory T cells express OX40 and are overexpressed in AD lesions, which may offer a potential immune explanation for AD recurrence (exacerbations or flares) and AD chronicity.”

    From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [67]

  • The OX40-OX40 L interaction allows a relevant co-stimulatory pathway in inducing the clonal expansion of effector CD4+ and CD8+ cells, intensifying the expression of pro-inflammatory cytokines, and facilitating the generation of memory T cells.

    “The OX40-OX40 L interaction allows a relevant co-stimulatory pathway in inducing the clonal expansion of effector CD4+ and CD8+ cells, intensifying the expression of pro-inflammatory cytokines, and facilitating the generation of memory T cells.”

    From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [67]

  • During the chronic phase of AD, other T cell subtypes express OX40 (Th1, Th17 and Th22), which are recruited to the inflammatory microenvironment.

    “During the chronic phase of AD, other T cell subtypes express OX40 (Th1, Th17 and Th22), which are recruited to the inflammatory microenvironment.”

    From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [67]

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Research works printed but not linked: 1

  1. Croft, M., Salek-Ardakani, S., Song, J., So, T., and Bansal-Pakala, P. (2024, January 25). Regulation of T Cell Immunity by OX40 and OX40L, Madame Curie Bioscience Database [Internet], Available online: https://www.ncbi.nlm.nih.gov/books/NBK5990/.

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Metadata

Authors
Sadrolashrafi, K., Guo, L., Kikuchi, R., Hao, A., Yamamoto, R. K., Tolson, H. C., Bilimoria, S. N., Yee, D. K., & Armstrong, A. W.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Armstrong, April W.
ORCID
Venue
Cells
Publisher
MDPI AG
Published
2024-03-28
Volume
13
Issue
7
Pages
587
ISSN
2073-4409 (ISSN-L)
DOI
10.3390/cells13070587
PMC
PMC11011471
OpenAlex
W4393279176
Cited by
28
References
95
Citations by year
2026: 9 · 2025: 14 · 2024: 5
FWCI
2.19
Type
journal article
Language
en
Open access
Licence
Locations
  • Cells (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
OX40, OX40L, atopic dermatitis, costimulation, T cell activation, type 2 inflammation, Th2 cells, Th17 cells, Th22 cells, IL-4, IL-13, IL-31, pruritus, skin barrier dysfunction, inflammatory skin diseases
MeSH terms
Cell Differentiation, Dermatitis, Atopic, Humans, Inflammation, Leukocytes, Mononuclear, Cytokines, Receptors, OX40, OX40 Ligand

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