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The Study of the Relationship between Transforming Growth Factor-β and Post-Transplant Lymphoproliferative Disorder

Author: DongQiChao
Tutor: LiuJun
School: Shandong University
Course: Department of General Surgery
Keywords: Post-transplant lymphoproliferative disease Transforming growth factor -β EB virus SCID mice
CLC: R55
Type: Master's thesis
Year: 2009
Downloads: 15
Quote: 0
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Abstract

Purpose of lymphoid tissue after transplant proliferative disease is very rare, occur in solid organ transplant or bone marrow transplant, including reactive plasma cell hyperplasia to malignant lymphoma a group of diseases. It is the immunodeficiency lymphoproliferative disease categories in a, compared to the normal population of lymphoid tissue proliferative diseases, there is a great difference in morphology, clinical behavior and prognosis. With the rapid development of the technology of organ transplantation, PTLD incidence also increases. Abroad for such diseases have gained a better person to research but less domestic coverage of such diseases, and so far only a few cases reported. This paper aims to SCID mice lymphoid tissue after transplantation is established animal model of proliferative disease (PTLD), and molded rate a preliminary study was to investigate the transforming growth factor-β (TGF-β) and transplantation based on After the lymphoid tissue proliferative disease (PTLD) in the pathogenesis of important research platform for exploring the pathogenesis and improve the level of clinical diagnosis and treatment of proliferative diseases, transplant lymphoproliferative. This paper by SCID mice to simulate a large number of applications immunosuppressants after organ transplantation caused immunodeficiency (or immune suppression) environment to simulate the human-derived EB virus EB virus infection environmental, anti-TGF-β monoclonal Comparison of antibody and PBS, to explore the relationship of the TGF-β and PTLD incidence. Combined immunodeficient animals (SCID mouse) by intraperitoneal injection of EB virus (EBV)-positive volunteers peripheral blood lymphocytes (huPBL), was measured by IgG to determine the human immune cells in the reconstruction of the mice, when the mice were moribund or anatomy and take out the tumor tissue after death, through the organization of the pathological and immunohistochemical analysis to determine lymph proliferative disease (LPD) produce its cell source to form an animal model of PTLD. Selected after analysis the LPD onset time is short volunteers of the high incidence of blood samples, and then repeat the experiment, to form another group of PTLD model. Then divided into a treatment group (injection of anti-TGF-β monoclonal antibody) and control group (injected with PBS buffer), survival analysis and LPD detection. Results after transplantation volunteers huPBL 8 weeks and 12 weeks SCID mice serum human IgG levels were reached (750.0 ± 13.2) μg / mL (1050.0 ± 14.6) μg / mL. Dying or death, tissue biopsy for large cell lymphoma associated with high mitotic rate, tumor CD20-positive, LMP-1 positive. Each volunteer peripheral blood lymphocytes generated in the mouse body by LPD there is a certain degree of heterogeneity, in the 40 volunteers, 10 patients in the to produce LPD (25%) after 8 weeks, SCID mice median tumor rate of 100%; eight cases at 10-16 weeks LPD (20%), the median into the tumor was 55%; 22 cases in 16 weeks later, still no LPD (55%). ; Re-established in the peripheral blood of volunteers selected EBV () huPBL-SCID model between the treatment group and the control group, the survival time difference (t = 35.78, P <0.05), LPD tumor rate different (P = 0.003 <0.01), and tumor tissue, T, B lymphocytes differences in the horizontal plane, and these differences were statistically significant. Conclusion 1 SCID mice by intraperitoneal injection of EB virus-positive human peripheral blood leukocytes can create transplant lymphoproliferative disease (PTLD) animal models. 2 SCID mice in vivo experiments show that the TGF-β may affect the pathogenesis of PTLD, this effect is related to the characteristics of the TGF-β itself.

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