IL-17 promotes proliferation, inflammation and inhibits apoptosis of HaCaT cells via interacting with the TRAF3 interacting protein 2.

Abstract

The present study aimed to investigate the effects of interleukin-17 (IL-17) on the function of keratinocytes and to further investigate its associated mechanism. Human immortalized epidermal cells (HaCaT) were divided into sham control group (Sham), TRAF3 interacting protein 2 (TRAF3IP2)-knockdown with lentivirus group (si-TRAF3IP2), sham control+IL-17 group (Sham+IL-17) and TRAF3IP2-knockdown with lentivirus+IL-17 group (si-TRAF3IP2+IL-17). MTT and flow cytometry assays demonstrated that IL-17 promoted proliferation and inhibited apoptosis of HaCaT cells, while this effect was reversed following knockdown of TRAF3IP2 with lentiviral vectors. In addition, a marked increase in the levels of IL-6, IL-8, IL-23, TNF-α and VEGF was observed in the Sham+IL-17 group compared with that noted in the Sham group (P<0.05). Furthermore, reverse transcription-quantitative polymerase chain reaction and western blotting indicated that the mRNA and protein expression levels of caspase-3 in the si-TRAF3IP2+IL-17 group were significantly increased compared with those of the Sham+IL-17 group (P<0.05). Taken together, the results indicated that IL-17 promoted proliferation and inflammation and inhibited apoptosis of HaCaT cells by interacting with the TRAF3IP2 adaptor protein, while knockdown of the expression of TRAF3IP2 reduced the effects of IL-17 in HaCaT cells.