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Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease. MicroRNAs (miRNAs) are a group of endogenous small non­coding RNAs that regulate target genes, and play a critical role in many biological processes. However, the underlying mechanism of specific miRNA, miR­130a­3p, in AS remains largely unknown. Therefore, the present study aimed to explore the underlying mechanism of miR­130a­3p in the development of AS. In the present study, it was revealed that miR­130a­3p was downregulated in T cells from HLA­B27­positive AS patients compared with the HLA­B27­negative healthy controls. Next, bioinformatics software TargetScan 7.2 was used to predict the target genes of miR­130a­3p, and a luciferase reporter assay indicated that HOXB1 was the direct target gene of miR­130a­3p. Furthermore, it was determined that HOXB1 expression was upregulated in T cells from HLA­B27­positive AS patients. In addition, the results of the present study indicated that miR­130a­3p inhibitor significantly inhibited cell proliferation ability and induced cell apoptosis of Jurkat T cells, while the miR­130a­3p mimic promoted proliferation ability and inhibited cell apoptosis of Jurkat T cells. Notably, all the effects of the miR­130a­3p mimic on Jurkat T cells were reversed by HOXB1­plasmid. Collectively, our data indicated that miR­130a­3p was decreased in T cells from AS patients and it could regulate T­cell survival by targeting HOXB1.

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Lupus nephritis (LN) is a polygenic disease caused by an interaction between hereditary and environmental factors. Numerous gene copy number variations have been identified to contribute to this disease. Previously, immunoglobulin (Ig)G Fcγ receptor 3B (FCGR3B) copy number variation (CNV) was reported to be associated with LN in the Caucasian population. However, the effect of FCGR3B CNV on LN in the Chinese population remains unknown. The present study aimed to investigate whether CNVs of FCGR3B are associated with LN in the Henan Chinese population. FCGR3B CNVs were determined in 142 LN patients and 328 healthy controls. A modified methodology based on competitive polymerase chain reaction, a Multiplex AccuCopy™ kit was used to detect FCGR3B copy number. Clinical and laboratory data was collected retrospectively from medical records. To evaluate associations between FCGR3B CNVs and LN susceptibility, the present study calculated the odds ratios using a logistic regression analysis. The current study identified that the distribution of FCGR3B copy number was significantly different between LN and healthy controls (P=0.031). A low copy number (<2) of FCGR3B was significantly enriched in LN patients (P=0.042), and was a risk factor for LN (odds ratio=2.059; 95% confidence interval, 1.081-3.921; P=0.028). However, a high copy number (>2) had no effect on LN. There were no associations between FCGR3B CNV and clinical phenotypes of LN. The results from the present study demonstrate that a low copy number of FCGR3B is a risk factor for LN in a Chinese population.