Acitretin therapy for children with PP (monotherapy or combination therapy), all showed a satisfactory therapeutic effect and safety, independent of the short or long-tern therapeutic procedures.

Purpose: The prognostic role of programmed death-ligand 1 (PD-L1) in colorectal cancer remains unclear. We employed a meta-analysis to explore the prognostic value of PD-L1 and to ascertain the relationship between PD-L1 expression and clinicopathological characteristics in CRC patients. Methods: We systematically searched PubMed, Embase and the Cochrane Library until October 2018. Eligible studies about colorectal cancer that pay attention to PD-L1 expression and studies reporting survival information were included. In order to evaluate the prognostic role of PD-L1 for overall survival (OS) and recurrence-free survival (RFS)/disease-free survival (DFS), Hazard ratio (HR) with 95% confidence interval (CI) was used. Odds ratio (OR) with 95% CI was selected to appraise the correlation between PD-L1 with clinicopathological characteristics of colorectal cancer patients. Begg’s funnel plot was used to assess publication bias. Results: Twelve studies involving 4344 patients published from 2013 to 2018 were included in this meta-analysis. Pooled results revealed that PD-L1 overexpression was relevant to shorter OS (HR 1.47, 95% CI =1.01–2.15, p =0.04) and shorter RFS/DFS (HR 1.47, 95% CI =1.01–2.15, p =0.04). Moreover, Patients with high expression of PD-L1 associated with inferior tumor stage (OR=0.57, 95% CI: 0.45, 0.74, p <0.0001) and Vascular invasion-negativity (OR=0.75, 95% CI: 0.6, 0.94, p =0.01). But the expression of PD-L1 is not related to age, sex, tumor location, tumor differentiation, pT stage, pN stage, MSI/MMR status. Conclusion: This meta-analysis revealed that PD-L1 can serve as a significant biomarker for negative prognosis and the adverse clinicopathological features of colorectal cancer and could facilitate the better management of individual patients.

The roles of IL-22 in the pathomechanisms of psoriasis have been well demonstrated. Gap junctional intercellular communication (GJIC) is widely known for its involvement in multiple biological and pathological processes such as growth-related events, cell differentiation, and inflammation. Here, we show that IL-22 significantly decreased GJIC and down-regulated Cx43 expression in HaCaT cells. Cx43 overexpression markedly inhibited the proliferation of and increased GJIC in HaCaT cells, but the silencing of Cx43 exerted the opposite effects. Additionally, Cx43 overexpression effectively rescued the IL-22-induced decrease in GJIC in HaCaT cells. The IL-22-induced down-regulation of Cx43 expression and decrease in GJIC can be significantly blocked by the JNK inhibitor SP600125 and by the overexpression of IL-22RA2 (which specifically binds to IL-22 and inhibits its activity), but not by the NF-κB inhibitor BAY11-7082, in HaCaT cells. Furthermore, the IL-22-induced down-regulation of Cx43 expression mediated by the JNK signaling pathway was confirmed in a mouse model of IL-22-induced psoriasis-like dermatitis. Similarly, Cx43 expression was significantly lower in the lesional skin than in the nonlesional skin of patients with psoriasis. These results suggest that IL-22 decreases GJIC by activating the JNK signaling pathway, which down-regulates Cx43 expression; this process is a possible pathomechanism of keratinocyte hyperproliferation in psoriasis.