BackgroundPigmented villonodular synovitis (PVNS) is a rare condition that involves benign proliferation of the synovial tissue and is characterized by severe joint destruction and high recurrence even after surgical resection. However, poor understanding of the pathogenesis limits its effective therapy.MethodIn this study, gene expression profiles of six patients with PVNS, 11 patients with osteoarthritis (OA), nine patients with rheumatoid arthritis (RA) (E-MTAB-6141), and three healthy subjects (GSE143514) were analyzed using integrating RNA sequencing (RNA-seq) and microarray to investigate the PVNS transcriptome. Gene ontology, string, and cytoscape were used to determine the gene functional enrichment. Cell functional molecules were detected using flow cytometry or immunohistochemical test to identify the cell subset and function. CD14+ cells were isolated and induced to osteoclast to evaluate the monocyte/macrophage function.ResultsThe most obvious local manifestations of PVNS were inflammation, including increased immune cells infiltration and cytokine secretion, and tumor phenotypes. High proportion of inflammatory cells, including T cells, natural killer (NK) cells, NKT cells, and B cells were recruited from the blood. Th17 and monocytes, especially classical monocytes but not nonclassical monocytes, increased in PVNS synovium. An obvious increase in osteoclastogenesis and macrophage activation was observed locally. Elevated expression of MMP9, SIGLEC 15, and RANK were observed in myeloid cell of PVNS than OA. When compared with RA, osteoclast differentiation and myeloid cell activation are PVNS-specific characters, whereas T cell activation is shared by PVNS and RA.ConclusionThe transcriptional expression characteristics of PVNS showed increased immune response, cell migration, and osteoclastogenesis. Osteoclast differentiation is only observed in PVNS but not RA, whereas T-cell activation is common in inflammatory arthritis.

Introduction Immune cells and molecules are considered as clinical biomarkers and potential targets for immunotherapy. Analyses of the composition of peripheral blood cells hold promise for providing a basis for diagnosing and prognosis lung cancer. In this study, we assessed correlations between immune cell subset profiles in peripheral blood and disease prognosis in patients with lung cancer. Methods One hundred and thirteen patients with lung cancer and 99 age‐matched healthy people were enrolled in this study. The percentage and cell count of monocytes, neutrophils, T cells, B cells, natural killer (NK), and NKT cells in peripheral blood were analyzed by flow cytometry or peripheral blood analyzer. Serum cytokines and colony‐stimulating factors were detected by enzyme‐linked immunosorbent assay (ELISA). Results A reduction in antitumor NK cells (p < 0.0001) and an increase in the protumor MDSCs (p < 0.0001) were observed in the lung cancer patients compared with the controls. Monocyte counts were significantly higher in lung cancer patients with histories of smoking (p < 0.05) or drinking (p < 0.01) than in patients with no relevant history or healthy controls. The number of neutrophils and the neutrophil‐to‐lymphocyte ratio (NLR) were particularly higher in patients with liver metastasis (p < 0.01) compared with no metastasis patients or healthy controls. Levels of the monocyte‐derived cytokine interleukin‐6 (p < 0.05), granulocyte colony‐stimulating factor (G‐CSF) (p < 0.0001), and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) (p < 0.0001) were higher in patients than in controls. G‐CSF levels decreased during the remission phase (p < 0.05), and positively correlated with carbohydrate antigen 19–9 (p < 0.05) and gene mutation (p < 0.05). Conclusion Monocyte and neutrophil counts were higher in peripheral blood in lung cancer patients than in controls, especially when patients had histories of smoking, drinking, and liver metastasis. Serum levels of G‐CSF and GM‐CSF were higher in lung cancer patients, and G‐CSF levels positively correlated with disease severity.

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Background: Pigmented villonodular synovitis (PVNS) is a rare condition that involves benign proliferation of the synovial tissue and is characterized by severe joint destruction and high recurrence even after surgical resection. However, poor understanding of the pathogenesis limits its effective therapy.Method: In this study, gene expression profiles of six patients with PVNS and six patients with osteoarthritis (OA) were analyzed using integrating RNA sequencing (RNA-seq) and microarray to investigate the PVNS transcriptome. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, string, and cytoscape were used to determine the gene functional enrichment. Cell surface functional molecules were detected using flow cytometry to identify the cell subset. CD14 positive cells were isolated and induced to differentiate into osteoclast to evaluate the monocyte/macrophage function.Results: RNA-seq and microarray data revealed 195 common differentially expressed genes; expression change trends were consistent in both the methods. The most obvious local manifestations of PVNS were inflammation and tumor phenotypes. Infiltration of a large number of immune cells and increased cytokine secretion induced inflammation. High proportion of CD45+ inflammatory cells, including T cells (CD3+), natural killer cells (CD3-CD56+), NKT cells (CD3+CD56+), and B cells (CD19+), were recruited from the blood. Cell proliferation and migration resulted in manifestation of the tumor phenotype. Tumor checkpoint molecules, such as programmed cell death protein 1, T cell immunoglobulin and mucin domain 3, lymphocyte-activation gene 3, cytotoxic T lymphocyte-associated protein 4, and sialic-acid-binding immunoglobulin-like lectin, were expressed on the surface of CD4+ and CD8+ T cells. In addition, an obvious increase in osteoclastogenesis and macrophage activation were observed locally. Tartrate-resistant acid phosphatase-positive mature osteoclasts that differentiated from CD14+ monocytes were significantly higher in the PVNS synovium than that in OA. Conclusion: The transcriptional expression characteristics of PVNS resulted in increased immune response and cytokine expression, high cell proliferation and migration, and increased osteoclastogenesis and bone injury.