In:
The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 182.12-182.12
Abstract:
The pathogenesis of inflammatory skin disease involves an interaction between immune cells and keratinocytes and Th17-mediated immune response is one of them. Several chemokines (CXCL1, CXCL5, and CXCL8) and antimicrobial peptides (β-defensin [BD1], LL37, S100A8 and S100A9) were transcriptionally upregulated in keratinocyte cell line (HaCaT) upon stimulation with IL-17. IL-17 binds to a heterodimeric receptor consisting of IL-17RA and IL-17RC, and adaptor protein Act1 binds to IL-17RA and mediates IL-17-induced signaling pathways. Because heat shock protein 90 (Hsp90) activity is required for IL-17 signalling via Act-1, we have evaluate the effect of Hsp90 inhibition on keratinocytes on IL-17-mediated cytokine and antimicrobial peptides. HaCaT cells were treated with 100 ng/ml of IL-17 or IL-22 for 24 hrs followed by 1 uM of 17-allylaminogeldanamycin (17-AAG) and collected for the analysis. We found that Hsp90 inhibition by 17-AAG under IL-17 stimulation led to decrease of CXCL1 but increase of CXCL5. In contrast to IL-17 and 17-AAG stimulation of HaCaT cells at 37°C, expression of Act1 and Act1 binding Hsp90 were increased after heat stimulation at 42°C for 30 min. These observation demonstrate the possible immune modulatory effect of the heat on keratinocytes during progression of inflammatory skin disease
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.192.Supp.182.12
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2014
detail.hit.zdb_id:
1475085-5
