As a promising biomarker, human epididymis protein 4 (HE4) has been widely used for the early detection and differential diagnosis of ovarian cancer. This study evaluated the function of HE4 in the carcinogenesis and progression of ovarian cancer. An enzyme immunometric assay, used to detect HE4 in the serum of ovarian cancer patients, showed that the protein could discriminate between malignant and benign ovarian tumours with high specificity. An exogenous HE4 gene was transfected into ovarian cancer cell lines and an immortalized ovarian epithelial cell line. Compared with the controls, HE4 overexpression significantly promoted cell apoptosis and adhesion. Overexpression of HE4 also led to significant inhibition of cell proliferation, migration and invasiveness in vitro, as well as xenograft tumour formation in vivo. This is the first report to demonstrate the functional importance of HE4 in multiple cellular processes and indicates that HE4 may play a protective role in the progression of ovarian cancer.
Objective Serum soluble CD25 (sCD25) could be used as a biomarker for disease activity in conditions associated with T-cell activation including various autoimmune diseases. This study aimed to explore the role of sCD25 as an indicator of disease activity and organ involvement in patients with systemic lupus erythematosus (SLE). Methods Serum samples were collected from 107 SLE patients and 92 age-matched healthy controls (HCs). All patients were followed up for 24 weeks, and sCD25 was measured by enzyme-linked immunosorbent assay. Clinical and laboratory data were recorded at baseline and then every two weeks until week 24. The Systemic Lupus Erythematosus Disease Activity Index-2000 (SLEDAI)-2K was adopted for assessing disease activity at all visits. Results Serum sCD25 levels were significantly increased in SLE patients compared to those in HCs ( p < 0.001). More patients in the high-sCD25 group had lupus nephritis, arthritis and vasculitis ( p = 0.010, p = 0.023 and p = 0.042, respectively). SLEDAI-2K, erythrocyte sedimentation rate, C-reactive protein and 24-hour urinary protein excretion were all associated with high levels of sCD25 ( p < 0.001, p = 0.002, p = 0.038 and p = 0.029, respectively). During the 24-week follow-up, more patients in the high-sCD25 group developed renal impairment (48% vs 6.2%, p = 0.005), and higher levels of sCD25 ( p = 0.033) were found at the time of onset of renal disease. Conclusions Serum sCD25 is a hallmark of disease activity and a predictor of renal disease in patients with SLE.
BackgroundRheumatoid arthritis (RA) is a prevalent systemic autoimmune disease characterized by the production of autoantibodies1. The tonsil has been demonstrated to be a site of citrullination, and tonsillectomy has been reported to be a potential treatment of RA, suggesting the possibility that the tonsil could be a site of autoimmunity generation in RA2,3. The dysbiosis of gut microbiome and the associated host immune response has been implicated in the initiation and progression of RA4–6. However, there is no in-depth studies on the role of tonsil microbiota in RA. Thus, studies of the characteristics of tonsil microbiome in RA patients, the underlying mechanisms, as well as specific markers for the diagnosis and therapeutic evaluation for RA, are critical for the early diagnosis and prevention of RA.ObjectivesTherefore, we aimed to define the association of RA with tonsil microbiome as well as a microbial and metabolite profile that could predict disease status.Methods16S rRNA gene sequencing was utilized on 220 tonsil swab samples (121 RA patients and 99 healthy controls) as well as 78 fecal samples (68 RA and 10 controls). Analysis of microbial taxa and metabolic pathway were performed to characterise and compare the tonsil microbiome of RA patients and healthy subjectsResultsResults showed that the tonsil harbored a unique microbiome relative to that present in the fecal samples. Patients with RA exhibited different tonsil microbiome from controls. A taxon-level analysis suggested that the relative abundance of 26 microbial clades were significantly altered, with 7 taxa increased and 19 taxa decreased in RA samples. Noticeably, we observed an expansion of rare microbial lineages as well as an alteration in microbial cladogenesis within RA patients. RA tonsil microbiota was associated with smoke, anti-peripheral factor, rheumatoid factors, disease duration and activity. Furthermore, we identified that 86 genes associated with bacterial metabolic pathway were enriched in RA tonsil microbiome.ConclusionsOur results demonstrated that the RA tonsil microbiome differs from that of healthy controls, which correlates with systemic autoimmune changes and may potentially drives initiation of RA.References McInnes IB, and Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011, 365(23): 2205–2219.Kawano M, Okada K, Muramoto H, et al. Simultaneous, clonally identical T cellexpansion in tonsil and synovium in a patient with rheumatoid arthritis and chronic tonsillitis. Arthritis Rheum. 2003, 48(9): 2483–2488.Makrygiannakis D, af Klint E, Lundberg IE, et al. Citrullination is an inflammation-dependent process. Ann Rheum Dis. 2006, 65(9): 1219–1222.Scher JU and Abramson SB. The microbiome and rheumatoid arthritis. Nat Rev Rheumatol, 2011, 7(10): 569–578.Scher JU, Sczesnak A, Longman RS, et al. Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis. Elife, 2013, 2:e01202.Zhang X, Zhang D, Jia H, et al. The oral and gut microbiomes are perturbed in rheumatoid arthritis...
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