Abstract
Psoriasis is an (auto)immune-mediated disease that manifests as widespread desquamative erythema. The TNF-α/IL-23/IL-17A axis is crucial to its pathogenesis, which is demonstrated by its excellent therapeutic response to biologics that target this axis. There is a strong association between HLA-C*0602 and psoriasis, and researchers have identified autoantigens that are restricted to this major histocompatibility class I molecule. These auto-Ags include LL-37, A disintegrin and metalloprotease domain containing thrombospondin type 1 motif-like 5 (ADAMTSL5), and keratin 17. IL-17A-producing T cells have been identified in T cell populations that are reactive to these auto-Ags. In addition, lipid Ags have surfaced as candidate auto-Ags that activate IL-17A-producing T cells in a CD1a-restricted manner. In this article, we review the candidate auto-Ags that may contribute to the activation of the IL-17A-deviated immune response in psoriasis.
| Original language | English |
|---|---|
| Pages (from-to) | 337-343 |
| Number of pages | 7 |
| Journal | Innate Immunity |
| Volume | 25 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Aug 1 2019 |
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All Science Journal Classification (ASJC) codes
- Microbiology
- Immunology
- Molecular Biology
- Cell Biology
- Infectious Diseases
Cite this
The contribution of IL-17 to the development of autoimmunity in psoriasis. / Furue, Masutaka; Kadono, Takafumi.
In: Innate Immunity, Vol. 25, No. 6, 01.08.2019, p. 337-343.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - The contribution of IL-17 to the development of autoimmunity in psoriasis
AU - Furue, Masutaka
AU - Kadono, Takafumi
PY - 2019/8/1
Y1 - 2019/8/1
N2 - Psoriasis is an (auto)immune-mediated disease that manifests as widespread desquamative erythema. The TNF-α/IL-23/IL-17A axis is crucial to its pathogenesis, which is demonstrated by its excellent therapeutic response to biologics that target this axis. There is a strong association between HLA-C*0602 and psoriasis, and researchers have identified autoantigens that are restricted to this major histocompatibility class I molecule. These auto-Ags include LL-37, A disintegrin and metalloprotease domain containing thrombospondin type 1 motif-like 5 (ADAMTSL5), and keratin 17. IL-17A-producing T cells have been identified in T cell populations that are reactive to these auto-Ags. In addition, lipid Ags have surfaced as candidate auto-Ags that activate IL-17A-producing T cells in a CD1a-restricted manner. In this article, we review the candidate auto-Ags that may contribute to the activation of the IL-17A-deviated immune response in psoriasis.
AB - Psoriasis is an (auto)immune-mediated disease that manifests as widespread desquamative erythema. The TNF-α/IL-23/IL-17A axis is crucial to its pathogenesis, which is demonstrated by its excellent therapeutic response to biologics that target this axis. There is a strong association between HLA-C*0602 and psoriasis, and researchers have identified autoantigens that are restricted to this major histocompatibility class I molecule. These auto-Ags include LL-37, A disintegrin and metalloprotease domain containing thrombospondin type 1 motif-like 5 (ADAMTSL5), and keratin 17. IL-17A-producing T cells have been identified in T cell populations that are reactive to these auto-Ags. In addition, lipid Ags have surfaced as candidate auto-Ags that activate IL-17A-producing T cells in a CD1a-restricted manner. In this article, we review the candidate auto-Ags that may contribute to the activation of the IL-17A-deviated immune response in psoriasis.
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U2 - 10.1177/1753425919852156
DO - 10.1177/1753425919852156
M3 - Review article
C2 - 31122103
AN - SCOPUS:85068994866
VL - 25
SP - 337
EP - 343
JO - Innate Immunity
JF - Innate Immunity
SN - 1753-4259
IS - 6
ER -