4 research outputs found

    Treatment with anti-JAM-C antibody delays onset of K/BxN serum transfer-induced arthritis

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    <p><b>Copyright information:</b></p><p>Taken from "Expression and function of junctional adhesion molecule-C in human and experimental arthritis"</p><p>http://arthritis-research.com/content/9/4/R65</p><p>Arthritis Research & Therapy 2007;9(4):R65-R65.</p><p>Published online 5 Jul 2007</p><p>PMCID:PMC2206366.</p><p></p> Incidence of K/BxN serum transfer-induced arthritis is shown for anti-JAM-C antibody-treated (= 10, black symbols) and isotype-matched control antibody-treated (= 10, open symbols) mice. Results are expressed as the percentage of arthritic mice per group. Incidence of arthritis was significantly lower in anti-JAM-C antibody-treated mice as compared to isotype-matched antibody-treated controls on day 3. *< 0.05 versus control mice, as assessed by chi-square test. Severity of K/BxN serum transfer-induced arthritis. Arthritis was evaluated by clinical assessment of arthritis severity scores for anti-JAM-C antibody-treated (= 10, black symbols) and isotype-matched control antibody-treated (= 10, open symbols) mice. Results shown represent the mean ± standard error of the mean (SEM) for each group of mice. There were no significant differences between the groups. Histological assessment of arthritis. Representative sections are shown for anti-JAM-C antibody-treated (upper panels) and isotype-matched control antibody-treated (lower panels) mice 13 days after serum transfer. Original magnifications × 40 (left panel) (scale bar = 125 μm) and × 100 (right panel) (scale bar = 50 μm). Histological scores for synovial thickness, exudates, and edema 13 days after serum transfer. Results shown represent the mean ± SEM for anti-JAM-C antibody-treated (= 10, black columns) and isotype-matched control antibody-treated (= 10, open columns) mice. No significant differences were observed between the groups. Ab, antibody; JAM-C, junctional adhesion molecule-C

    Expression of junctional adhesion molecule-C (JAM-C) in mouse arthritic synovium and synovial fibroblasts

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    <p><b>Copyright information:</b></p><p>Taken from "Expression and function of junctional adhesion molecule-C in human and experimental arthritis"</p><p>http://arthritis-research.com/content/9/4/R65</p><p>Arthritis Research & Therapy 2007;9(4):R65-R65.</p><p>Published online 5 Jul 2007</p><p>PMCID:PMC2206366.</p><p></p> Expression of JAM-C was examined by immunohistochemistry in knee joints of mice with antigen-induced arthritis (AIA) and in paws of mice with K/BxN serum transfer-induced arthritis . The left panels show expression of JAM-C in the synovial lining layer (upper panel) and associated with blood vessels in the sublining (lower panel). The right panels show negative control sections incubated with preimmune serum. Original magnification × 400 (scale bar = 20 μm). Reverse transcriptase-polymerase chain reaction (PCR) analysis of mRNA expression in mouse synovial tissue samples and in cultured mouse synovial fibroblasts. A representative agarose gel electrophoresis of PCR products is shown. AIA1 and AIA2, antigen-induced arthritis synovial tissue; bp, base pairs; HO, polymerase chain reaction negative control; K/BxN1 and K/BxN2, K/BxN serum transfer-induced arthritis synovial tissue; mSF1 and mSF2, two different mouse synovial fibroblast cultures isolated from antigen-induced arthritis synovial tissue; RTneg, non reverse-transcribed sample

    Expression of junctional adhesion molecule-C (JAM-C) in human arthritic synovium

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    <p><b>Copyright information:</b></p><p>Taken from "Expression and function of junctional adhesion molecule-C in human and experimental arthritis"</p><p>http://arthritis-research.com/content/9/4/R65</p><p>Arthritis Research & Therapy 2007;9(4):R65-R65.</p><p>Published online 5 Jul 2007</p><p>PMCID:PMC2206366.</p><p></p> Expression of JAM-C was examined by immunohistochemistry in human osteoarthritis (OA) and rheumatoid arthritis (RA) synovial tissue. The panels labeled 1 show the original magnification (× 100). The panels labeled 2 show expression of JAM-C in the synovial lining layer (magnification × 400), and panels labeled 3 show JAM-C associated with blood vessels in the sublining (magnification × 400). The panels labeled 4 show negative control sections incubated with preimmune serum. Scale bars = 60 μm (panels 1 and 4) and 15 μm (panels 2 and 3). Quantification of JAM-C expression in OA and RA synovial tissues. JAM-C immunohistochemical synovial tissue sections from four different OA and RA patients were scanned, and the surface of immunoreactive areas was determined and expressed as the percentage of the surface of the image examined. Results are expressed as the mean ± standard error of the mean. *< 0.001 OA versus RA as assessed using the Wilcoxon rank sum test. Reverse transcriptase-polymerase chain reaction (PCR) analysis of mRNA expression in human synovial tissue samples and in cultured human synovial fibroblasts. A representative agarose gel electrophoresis of PCR products is shown. bp, base pairs; HO, polymerase chain reaction negative control; hSF1 and hSF2, human rheumatoid arthritis synovial fibroblast cultures from two different patients used after the third passage; OA, osteoarthritis synovial tissue; RA, rheumatoid arthritis synovial tissue; RT neg, non-reverse-transcribed sample

    Treatment with anti-JAM-C antibody decreases neutrophil infiltration into the joints during antigen-induced arthritis

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    <p><b>Copyright information:</b></p><p>Taken from "Expression and function of junctional adhesion molecule-C in human and experimental arthritis"</p><p>http://arthritis-research.com/content/9/4/R65</p><p>Arthritis Research & Therapy 2007;9(4):R65-R65.</p><p>Published online 5 Jul 2007</p><p>PMCID:PMC2206366.</p><p></p> Infiltration of neutrophils , lymphocytes , and macrophages into the synovium was detected by immunohistochemistry using anti-MPO, anti-CD3, and anti-MAC-2 antibodies, respectively. The left panels show representative knee joint sections of control and anti-JAM-C antibody-treated mice. Original magnification × 400 (scale bar = 25 μm). In the right panels, leukocyte infiltration per field was evaluated by semi-quantitative scoring for anti-JAM-C antibody-treated (= 6, black columns) and isotype-matched control antibody-treated (= 5, open columns) mice. There was a significant decrease in synovial neutrophil infiltration in anti-JAM-C antibody-treated mice as compared to isotype-matched antibody-treated controls. *< 0.05 versus control mice, as assessed by analysis of variance. Ab, antibody; JAM-C, junctional adhesion molecule-C
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