OBJECTIVE: Evaluating the serum level of IL-35, IL-36γ and CCL27 cytokines expression in patients with psoriasis and to explore their correlation with disease severity. To explore the role of these cytokines in the pathogenesis of psoriasis vulgaris and to guide clinical practice. METHODS: Thirty patients with psoriasis vulgaris (PV) were treated with routine drug treatment for7 weeks, and 30 healthy controls were used as control group. Peripheral blood of the PV group before and after treatment and control group were detected by double-antibody sandwich ELISA. The expression levels of IL-35, IL-36γ and CCL27 in peripheral blood were analyzed statistically. RESULTS: The expression of IL-35 in the peripheral blood of the pre-PV group (187.54 ± 172.41) was significantly lower than that of the control group (310.52 ± 174.22) and the PV treatment group (417.75 ± 47.07). The level of IL-36γ in peripheral blood of pre-PV group (295.11 ± 27.91) was higher than that of control group (155.40 ± 45.66) and PV treatment group (209.86 ± 27.91). The level of CCL27 in peripheral blood of patients pre-PV treatment (479.06 ± 285.80) was significantly higher than that of the control group (341.53 ± 98.72) and the group after PV treatment (316.56 ± 245.53). There was a negative correlation between IL-35 and IL-36γ levels in serum (r= -0.826, p < .001); IL-36γ was positively correlated with CCL27 level (r = 0.906, p < .001); IL-35 and CCL27 levels were negative correlation (r= -0.810, p < .001). CONCLUSION: IL-36γ and CCL27 may be involved in the pathogenesis of psoriasis as a pro-inflammatory factor. IL-35 may be involved in the pathogenesis of psoriasis as an anti-inflammatory factor.
OBJECTIVE: Evaluating the serum level of IL-35, IL-36γ and CCL27 cytokines expression in patients with psoriasis and to explore their correlation with disease severity. To explore the role of these cytokines in the pathogenesis of psoriasis vulgaris and to guide clinical practice. METHODS: Thirty patients with psoriasis vulgaris (PV) were treated with routine drug treatment for7 weeks, and 30 healthy controls were used as control group. Peripheral blood of the PV group before and after treatment and control group were detected by double-antibody sandwich ELISA. The expression levels of IL-35, IL-36γ and CCL27 in peripheral blood were analyzed statistically. RESULTS: The expression of IL-35 in the peripheral blood of the pre-PV group (187.54 ± 172.41) was significantly lower than that of the control group (310.52 ± 174.22) and the PV treatment group (417.75 ± 47.07). The level of IL-36γ in peripheral blood of pre-PV group (295.11 ± 27.91) was higher than that of control group (155.40 ± 45.66) and PV treatment group (209.86 ± 27.91). The level of CCL27 in peripheral blood of patients pre-PV treatment (479.06 ± 285.80) was significantly higher than that of the control group (341.53 ± 98.72) and the group after PV treatment (316.56 ± 245.53). There was a negative correlation between IL-35 and IL-36γ levels in serum (r= -0.826, p < .001); IL-36γ was positively correlated with CCL27 level (r = 0.906, p < .001); IL-35 and CCL27 levels were negative correlation (r= -0.810, p < .001). CONCLUSION: IL-36γ and CCL27 may be involved in the pathogenesis of psoriasis as a pro-inflammatory factor. IL-35 may be involved in the pathogenesis of psoriasis as an anti-inflammatory factor.