Induction of Interleukin-22 (IL-22) production in CD4+ T Cells by IL-17A Secreted from CpG-Stimulated Keratinocytes
Annals of Dermatology
;
: 579-585, 2016.
Article
in English
| WPRIM
| ID: wpr-59031
ABSTRACT
BACKGROUND:
Interleukin-17A (IL-17A) is mainly secreted from Th17 cells that are activated by various stimuli including CpG oligodeoxynucleotide, a Toll-like receptor 9 (TLR9) ligand. Recently, it has been demonstrated that keratinocytes play an important role in the pathogenesis of psoriasis.OBJECTIVE:
To investigate the potential role of keratinocytes, we examined whether TLR9 ligand CpG induces IL-17A expression in keratinocytes.METHODS:
We used HaCaT keratinocytes as a model system, and determined CpG-induced IL-17A using enzyme-linked immunosorbent assay and Western blot.RESULTS:
When HaCaT keratinocytes were treated with CpG, the expression of several cytokines including IL-17A, tumor necrosis factor-α and CCL20 was markedly increased. Treatment with nuclear factor (NF)-κB inhibitor significantly blocked the CpG-induced IL-17A production, indicating that CpG induced IL-17A expression through the NF-κB signaling pathway. In addition, IL-17A secreted from keratinocytes stimulated the CD4⁺ T cells, resulting in strong induction of IL-22 production.CONCLUSION:
Since IL-22 is an important mediator for psoriatic inflammation, our data suggest that keratinocytes can participate in the pathogenesis of psoriasis via the TLR9-dependent IL-17A production.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Psoriasis
/
Enzyme-Linked Immunosorbent Assay
/
T-Lymphocytes
/
Keratinocytes
/
Blotting, Western
/
Cytokines
/
Interleukin-17
/
Toll-Like Receptor 9
/
Th17 Cells
/
Inflammation
Language:
English
Journal:
Annals of Dermatology
Year:
2016
Type:
Article
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