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Cited by 537

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

The IL-23/T17 pathogenic axis in psoriasis is amplified by keratinocyte responses

Open access
Lowes, Michelle A., Russell, Chris B., Martin, David A., Towne, Jennifer E., Krueger, James G.·2013·Trends in Immunology

Abstract

Psoriasis is a complex inflammatory process resulting from activation of the well-defined IL-23/T17 cytokine axis. We review the role of key cytokines interleukin (IL)-17 and IL-23 in psoriasis, as well as tumor necrosis factor alpha (TNα), focusing on therapeutic cytokine interventions and what they reveal about psoriatic inflammation. The potential role of recently described epidermal IL-36RN and CARD14 genetic mutations in psoriasis pathogenesis will also be explored, as they augment keratinocyte responses to pro-inflammatory cytokines. The discovery of these genetic mutations in familial and pustular psoriasis suggest new links between cytokine-induced gene products and IL-1 family members from keratinocytes, which may regulate features of the disease, including epidermal hyperplasia and neutrophil infiltrating responses.

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Crossref · 10.1016/j.it.2012.11.005

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Metadata

Authors
Lowes, M. A., Russell, C. B., Martin, D. A., Towne, J. E., & Krueger, J. G.
Venue
Trends in Immunology
Publisher
Elsevier BV
Published
2013-04
Volume
34
Issue
4
Pages
174-181
ISSN
1471-4906 (ISSN-L)
OpenAlex
W1981177225
Cited by
537
References
9
FWCI
2.59
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: The IL-23/T17 pathogenic axis in psoriasis is amplified by keratinocyte responses. https://app.cochat.ai/papers/10.1016/j.it.2012.11.005
The paper
Lowes, M. A., Russell, C. B., Martin, D. A., Towne, J. E., & Krueger, J. G. (2013). The IL-23/T17 pathogenic axis in psoriasis is amplified by keratinocyte responses. Trends in Immunology. https://doi.org/10.1016/j.it.2012.11.005

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.