目的:检测HtrA2/Omi,X染色体连锁凋亡抑制剂(X-linked inhibitor of apoptosis,XIAP)和半胱天冬酶-3(Caspase-3)在寻常型银屑病(PV)中的表达。方法:应用免疫组化SABC法检测30例PV皮损与10例正常人皮肤中HtrA2/Omi、XIAP和Caspase-3的表达,并分析HtrA2/Omi、XIAP和Caspase-3表达之间的相关性。结果:PV皮损中XIAP和Caspase-3阳性细胞数明显高于正常皮肤(P<0.01),HtrA2/Omi阳性细胞数与正常皮肤无明显差异(P>0.05)。Caspase-3阳性细胞数和XIAP呈正相关趋势(P<0.05),与HtrA2/Omi表达无明显相关性(P>0.05)。HtrA2/Omi和XIAP的表达无明显相关性(P>0.05)。结论:XIAP和Caspase-3可能在PV的发病中起重要作用。
The expression of the interferon regulatory factor 4 (IRF-4) and the IRF-4-binding protein (IBP) in psoriatic skin lesions was investigated. The expression of IRF-4 and IBP in skin lesions of 20 patients with psoriasis vulgaris were immunohistochemically dectected. Normal skin from 10 healthy people was used as normal control. The study showed that expression of IRF-4 was increased significantly in keratinocytes and inflammatory cells in the lesions of psoriasis vulgaris than that in the normal control. The detection revealed that IBP expression in keratinocytes, lymphocytes, hair follicles, and sebaceous glands in normal skin was significantly lower than that in the lesions of psoriasis vulgaris (P<0.05). Both IRF-4 and IBP might be involved in the pathogenesis of psoriasis vulgaris.
Summary： The deubiquitinating enzyme ubiquitin specific peptidase 15 （USP15） is regarded as a regulator of TGFβ signaling pathway. This process depends on Smad7, the inhibitory factor of the TGFβ signal, and type Ⅰ TGFβ receptor （TβR- Ⅰ ）, one of the receptors of TGFβ. The expression level of USP 15 seems to play vital roles in the pathogenesis of many neoplasms, but so far there has been no report about USP15 in psoriasis. In this study, immunohistochemical staining of USP15, TβR- Ⅰ and Smad7 was performed in 30 paraffin-embedded psoriasis specimens and 10 normal specimens to investigate the expression of USP15, TβR- Ⅰ and Smad7 in psoriasis and to explore the relevance among them. And USP 15 small interfering RNA （USP 15 siRNA） was used to transfect Hacat cells to detect the mRNA expression of TβR- Ⅰ and Smad7. Of 30 cases of psoriasis in active stage, 28, 24 and 26 cases were positive for USP15, TβR- Ⅰ and Smad7 staining, respectively. The positive rates of USP15 and Smad7 were significantly higher in psoriasis specimens than in normal skin specimens （44.1%±26.0% vs. 6.1%±6.6%, 47.2%±27.1% vs. 6.6%±7.1%）, and positive rate of TβR- I （20.3%±22.2%） in psoriasis was lower than that in normal skin specimens （46.7%±18.2%）. There was a significant positive correlation between USP15 and Smad7 expression, and significant negative correlations between USP15 and TβR- Ⅰ expression, and between TβR- Ⅰ and Smad7 expression in psoriasis. After transfection of USP15 siRNA in Hacat ceils, the expression ofTβR- Ⅰ mRNA was up-regulated and that of Smad7 was down-regulated. It is concluded that USP15 may play a role in the pathogenesis of psoriasis through regulating the TβR- Ⅰ/Smad7 pathway and there may be other cell signaling pathways interacting with USP 15 to take part in the development of psoriasis.
Summary： This study examined the correlation of the expression of interleukin-36 （IL-36）, a novel member of interleukin-1 （IL-1） family, with p38 mitogen-activated protein kinase （p38 MAPK） and nu clear factor-kappa B （NF-kB） pathways in psoriasis vulgaris skin lesions. The expression levels of IL-36a, IL-3613, IL-367, phosphorylated p38 MAPK, and NF-id3p65 were detected in the skin tissues of 38 psoriasis patients and 17 healthy control subjects by real-time quantitative reverse transcription po lymerase chain reaction （qRT-PCR） and Western blotting. The cytokine expression levels were com pared between the psoriasis group and the control group. A correlation analysis between cytokine pro teins was performed in the psoriasis group. Results showed that the expression levels of IL-36a, IL-3613, IL-36y, phosphorylated p38 MAPK and NF-rh3p65 in the psoriasis group were Significantly higher than those in the control group （P〈0.001）. In the psoriasis group, the IL-36 cytokine expression was positively correlated with phosphorylated p38 MAPK and NF-kBp65 expression （P〈0.05）. A significant positive correlation was also found between the phosphorylated p38 MAPK and NF-v,.Bp65 expression （P〈0.01）. It was concluded that the increased IL-36 expression is correlated with p38 MAPK and NF-kB pathways in psoriasis vulgaris skin lesions. All the three factors may be jointly involved in the pathogenesis and local inflammatory response of psoriasis.
