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  • Title: [Expression of human fibrinogen-like protein 2/fibroleukin in renal acute allograft rejection and its potential clinical implication].
    Author: Zhang L, Ning Q, Guo H, Zhang WJ, Chen F, Luo XP.
    Journal: Zhonghua Yi Xue Za Zhi; 2004 Mar 17; 84(6):474-7. PubMed ID: 15061965.
    Abstract:
    OBJECTIVE: To investigate the expression of human fibrinogen-like protein 2 (hfgl2)/fibroleukin in renal acute allograft rejection and its correlation with the course of the disease. METHODS: Thirty-one samples of aspiration biopsy of renal acute allograft rejection were collected. Histological sections were stained with hemotoxylin and eosin. Polyclonal antibody against hfgl2 was used to detect the expression of hfgl2 protein by immunohistochemistry. Anti-CD68 and anti-CD8 monoclonal antibodies were used to detect the macrophages activation and lymphocyte respectively in serial sections to identify the cell types that express hfgl2. Anti-fibrinogen monoclonal antibody and thrombus staining were used to detect the fibrin deposition and the formation of thrombus. Double staining with anti-hfgl2 antibody and anti-fibrinogen antibody was performed to clarify the correlation between hfgl2 expression and fibrin deposition. RESULTS: Twenty-nine cases showed hfgl2 expression, mainly displayed in tubule cells, infiltrative cells (macrophages, CD8+ T cells and plasmacytes), and part of the adherent cells or infiltrative cells in tubules and vessels, whereas no hfgl2 protein was detected in glomerulus and endothelium of vessels. Double staining displayed that the fibrin deposition was mainly in the vessels, glomeruli and interstitium, and the lumen of tubule in association with hfgl2 expression. No thrombus was found in all the sections. CONCLUSION: The abnormal expression of hfgl2 in renal acute allograft rejection in human beings activates the thrombosin inside and outside the vessels that causes fibrin deposition and microcirculatory disturbances, thus further exacerbating the pathological injuries of tissues. hfgl2 protein may serve as a new target for therapeutic intervention for acute allograft rejection.
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