No abstract

In psoriasis, a chronic, recurrent, inflammatory skin disease, CD4+T cells and their related cytokines play an important role in its pathogenesis. The role of interleukin (IL)-35, an immunosuppressive cytokine involved in many autoimmune diseases, is unclear in the pathogenesis of psoriasis. This study evaluated IL-35 expression and clinical significance in psoriasis. Protein and mRNA levels of specified markers were measured by enzyme-linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (qRT-PCR), respectively. Results showed that plasma IL-35 concentrations were lower in patients with psoriasis than in healthy individuals (Z = -6.525, P < .0001). Ebi3 and p35 showed lower mRNA levels in peripheral blood mononuclear cells from patients with psoriasis than in healthy individuals (Z = -5.078, P < .0001, Z = -2.609, P = .009, respectively). The areas under the receiver-operating characteristic (ROC) curves of IL-35, Ebi3, and p35 for patients with psoriasis versus the control were 0.86, 0.78, and 0.64, respectively. Pearson correlation analysis showed that plasma IL-35 expression negatively correlated with interferon-gamma, tumor necrosis factor-alpha, levels of IL-23, -17, and -22, or the Psoriasis Activity and Severity Index and positively correlated with levels of transforming growth factor beta and IL-10 levels in patients with psoriasis. Summarily, IL-35 might mediate psoriasis pathogenesis by influencing the expression of Th1/Th17/T -related cytokines and might be a putative target in monitoring or treating psoriasis.

Background/Aims: Long noncoding RNAs (lncRNAs) are important regulators of biological processes and they contribute to the pathological developments of various diseases, including autoimmune diseases. To gain the further understanding, we estimate the expression of lncRNAs in primary immune thrombocytopenia (ITP). Methods: In this study, microarray studies were performed to characterize expression profiles of various lncRNAs and mRNAs in blood samples collected from ITP patients. Quantitative real-time PCR (qRT-PCR) was performed to confirm the results, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and gene ontology analysis were used to provide functional annotations, co-expression network construction (CNC) analysis was made to reveal the relations between lncRNAs and their targeted genes. Results: A total of 1177 and 632 lncRNAs were significantly up-regulated or down-regulated, respectively, in “newly diagnosed ITP” patients versus healthy individuals. In addition, 1182 genes and 737 genes were up-regulated or down-regulated, respectively, in “chronic recurrent ITP” patients versus healthy individuals. In a KEGG analysis, “TNF signaling pathway-Homo sapiens (human)” was a key result. In a gene ontology analysis, “Granulocyte macrophage colony-stimulating factor production (GO: 0032604, ontology: Biological process, P = 1.69577E-05)” and “coreceptor activity (GO: 0015026, ontology: molecular function, P = 4.67594E-06)” were the two most critical results. Data from qRT-PCR and receiver operating characteristic curves further demonstrated that ENST00000440492, ENST00000528366, NR_038920, and ENST00000552576 can efficiently distinguish different stages of ITP, especially NR_038920 and ENST00000528366. In a CNC analysis, four lncRNAs were emphasized, and NR_038920 and ENST00000528366 were both associated with proteins with important roles in autoimmune diseases. Conclusions: These results suggest that lncRNAs act through targeted genes to mediate their functions and to mediate their functions and affect the pathogenesis of ITP.