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Degradation of the Epstein-Barr virus latent membrane protein 1 (LMP1) by the ubiquitin-proteasome pathway - Targeting via ubiquitination of the N-terminal residue

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第31期275卷 23491-23499页

作者： Aviel, S Winberg, G Massucci, M Ciechanover, A Technion Israel Inst Technol Fac Med Dept Biochem IL-31096 Haifa Israel Technion Israel Inst Technol Bruce Rappaport Fac Med Rappaport Family Inst Res Med Sci IL-31096 Haifa Israel Karolinska Inst Ctr Microbiol & Tumor Biol S-17177 Stockholm Sweden

The latent membrane protein 1 (LMP1) of the Epstein-Barr virus is a constitutively active receptor essential for B lymphocyte transformation by the Epstein-Barr virus. It is a short-lived protein, but the proteolytic pathway involved in its degradation is not known. The ubiquitin pathway is a major system for specific protein degradation in eukaryotes. Most plasma membrane substrates of the pathway are internalized upon ubiquitination and delivered for degradation in the lysosome/vacuole. Here we show that LMP1 is a substrate of the ubiquitin pathway and is ubiquitinated both in vitro and in vivo. However, in contrast to other plasma membrane substrates of the ubiquitin system, it is degraded mostly by the proteasome and not by lysosomes. Degradation is independent of the single Lys residue of the protein;a lysine-less mutant LMP1 is degraded in a ubiquitin- and proteasome-dependent manner similar to the wild type protein, Degradation of both wild type and lysine-less protein is sensitive to fusion of a Myc tag to the N terminus of LMP1, In addition, deletion of as few as 12 N-terminal amino acid residues stabilizes the protein, These findings suggest that the first event in LMP1 degradation is attachment of ubiquitin to the N-terminal residue of the protein. We present evidence suggesting that phosphorylation is also required for degradation of LMP1.

关键词：细胞区室化细胞膜/代谢无细胞系统半胱氨酸内肽酶类/代谢半衰期疱疹病毒4型人淋巴组织增殖性疾病/病因学赖氨酸/遗传学多酶复合物/代谢突变癌基因蛋白质类病毒性/代谢磷酰化蛋白酶体内肽酶复合物蛋白质加工转译后肿瘤细胞培养的泛素类/代谢病毒基质蛋白质类/代谢

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Expression of p16/INK4a in posttransplantation lymphoproliferative disorders

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AMERICAN JOURNAL OF PATHOLOGY 2000年第5期156卷 1573-1579页

作者： Martin, A Baran-Marzak, F El Mansouri, S Legendre, C Leblond, V Charlotte, F Davi, F Canioni, D Raphaël, M Univ Avicenne Ctr Hosp Serv Anat & Cytol Pathol Bobigny France Univ Avicenne Ctr Hosp Unite Propre Enseignement Super Equipe Acceuil 1625 Paris France Univ Paris Unite Format Rech Sante Med Biol Humaine Paris France Univ Pitie Salpetriere Ctr Hosp Serv Hematol Paris France Univ Pitie Salpetriere Ctr Hosp Serv Anat & Cytol Pathol Paris France Univ Pitie Salpetriere Ctr Hosp Serv Hematol Biol Paris France Hop Necker Enfants Malad Serv Anat & Cytol Pathol Paris France

It was recently demonstrated that classification of posttransplantation lymphoproliferative disorders (PT-LPDs) into morphological and molecular categories is clinically relevant. It was also reported that PT-LPD not associated with Epstein-Barr virus (EBV) had a more aggressive course than most lesions associated with EBV, Because the cyclin-dependent kinase inhibitor p16/INK4a has been reported to be frequently inactivated in high-grade lymphomas, we evaluated 17 PT-LPD to determine whether p16/ INK4a expression could be correlated to morphology, EBV detection, and a Ki-67 labeling index. We demonstrated that tumors with no p16/INK4a expression (n = 8) had a predominantly monomorphic appearance, and most were EBV negative (respectively, 7/8 and 5/8), whereas lesions with p16/INK4a expression (n = 9) were mostly polymorphic PT-LPD (6/9) (p = 0.049) and associated with EBV (9/9) (P = 0.015). In particular, strong p16/INK4a expression was observed in atypical immunoblasts and Reed-Sternberg-like cells. Furthermore, the proliferation index was significantly higher in tumors lacking p16/ INK4a expression than in other lesions (P = 0.0008). In conclusion, down-regulation of p16/INK4a was mostly observed in PT-LPD lesions known to follow more aggressive courses: monomorphic tumors and EBV-negative PT-neoplasms. Conversely, overexpression of p16/INK4a was associated with EBV-positive PT-LPD. While p16/INK4a might play a role in the proliferative rate of LP-LPD, further investigations are needed to assess the clinical relevance of p16/INK4a expression in predicting the evolution of tumors and to explain how EBV could favor p16/INK4a protein accumulation in lesions.

关键词：印迹法 DNA 载体蛋白质类/分析载体蛋白质类/遗传学克隆细胞周期素依赖激酶抑制剂p16 DNA/遗传学 DNA/代谢 DNA甲基化 DNA 病毒/遗传学爱泼斯坦巴尔病毒感染/病毒学基因表达调控疱疹病毒4型人/遗传学免疫组织化学 Ki-67抗原/分析淋巴组织增殖性疾病/病因学淋巴组织增殖性疾病/代谢淋巴组织增殖性疾病/病理学成年人老年人女(雌)性人类男(雄)性中年人

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Isolated intestinal transplantation for intestinal failure

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AMERICAN JOURNAL OF GASTROENTEROLOGY 2000年第6期95卷 1506-1515页

作者： Sudan, DL Kaufman, SS Shaw, BW Fox, IJ McCashland, TM Schafer, DF Radio, SJ Hinrichs, SH Vanderhoof, JA Langnas, AN Univ Nebraska Med Ctr Dept Surg Omaha NE 68198 USA Univ Nebraska Med Ctr Dept Pediat Omaha NE 68198 USA Univ Nebraska Med Ctr Dept Internal Med Omaha NE 68198 USA Univ Nebraska Med Ctr Dept Pathol Omaha NE 68198 USA

OBJECTIVE: Parenteral nutrition sustains life in patients with intestinal failure. However, some experience life-threatening complications from parenteral nutrition, and in these individuals intestinal transplantation may be Lifesaving. METHODS: This is a retrospective review of 28 consecutive isolated small bowel transplants performed in eight adults and 20 children between December 1993 and June 1998 at the University of Nebraska Medical Center. RESULTS: The I-yr patient and graft survivals were 93% and 71%, respectively. The causes of graft loss were hyperacute rejection (n = 1), acute rejection (n = 5), vascular thrombosis (n = 1). and patient death (n = 1). The median length of time required until full enteral nutrition was 27 days. All 28 patients have experienced acute rejection of their small bowel grafts and rejection led to graft failure in five. Jaundice and/or hepatic fibrosis was present preoperatively in 17 of the 28 recipients and hyperbilirubinemia was completely reversed in all patients with functional grafts within 4 months of transplantation. Three patients developed posttransplant lymphoproliferative disease (11%). Three recipients developed cytomegalovirus enteritis and all were successfully treated. CONCLUSIONS: Patient survival after intestinal transplantation is comparable to parenteral nutrition for patients with intestinal failure. Better immunosuppressive regimens are needed to decrease the risk of graft loss from acute rejection. The incidence of posttransplant lymphoproliferative disorder is higher after intestinal transplantation than after other solid organ transplants and the risk of cytomegalovirus enteritis is low with the use of cytomegalovirus seronegative donors. Liver dysfunction in the absence of established cirrhosis can be reversed. (Am J Gastroenterol 2000;95: 1506-1515. (C) 2000 by Am. Cell. of Gastroenterology).

关键词：血型抗原血型鉴定和交叉配血肠道营养移植物排斥移植物存活肠疾病/外科学肠/病理生理学肠/移植肝/病理生理学淋巴组织增殖性疾病/病因学年患病率手术后并发症再手术回顾性研究时间因素青少年成年人女(雌)性人类男(雄)性中年人

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Interleukin-18, interferon-γ, IP-10, and Mig expression in Epstein-Barr virus-induced infectious mononucleosis and posttransplant lymphoproliferative disease

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AMERICAN JOURNAL OF PATHOLOGY 1999年第1期155卷 257-265页

作者： Setsuda, J Teruya-Feldstein, J Harris, NL Ferry, JA Sorbara, L Gupta, G Jaffe, ES Tosato, G NCI Hematopathol Sect Pathol Lab NIH Bethesda MD 20892 USA Harvard Univ Massachusetts Gen Hosp Sch Med Dept Pathol Boston MA USA US FDA Ctr Biol Evaluat & Res Bethesda MD USA

T cell immunodeficiency plays an important role in the pathogenesis of posttransplant lymphoproliferative disease (PTLD) by permitting the unbridled expansion of Epstein-Barr virus (EBV)-infected B lymphocytes. However, factors other than T cell function may contribute to PTLD pathogenesis because PTLD infrequently develops even in the context of severe T cell immunodeficiency, and athymic mice that are T-cell-immunodeficient can reject EBV-immortalized cells. Here we report that PTLD tissues express significantly lower levels of IL-18, interferon-gamma (IFN-gamma), Mig, and RANTES compared to lymphoid tissues diagnosed with acute EBV-induced infectious mononucleosis, as assessed by semiquantitative RT-PCR analysis. Other cytokines and chemokines are expressed at similar levels. Immunohistochemistry confirmed that PTLD tissues contain less IL-18 and Mig protein than tissues with infectious mononucleosis. IL-18, primarily a monocyte product, promotes the secretion of IFN-gamma, which stimulates Mig and RANTES expression. Both IL-18 and Mig display antitumor activity in mice involving inhibition of angiogenesis, These results document greater expression of IL-18, IFN-gamma, Mig, and RANTES in lymphoid tissues with acute EBV-induced infectious mononucleosis compared to tissues with PTLD and raise the possibility that these mediators participate in critical host responses to EBV infection.

关键词：趋化因子CCL5/代谢趋化因子CXCL10 趋化因子CXCL9 趋化因子 CXC/代谢爱泼斯坦巴尔病毒感染/代谢免疫组织化学传染性单核细胞增多症/代谢胞间信号肽类和蛋白质类白细胞介素18/代谢淋巴组织增殖性疾病/病因学淋巴组织增殖性疾病/代谢器官移植手术后并发症逆转录聚合酶链反应青少年成年人儿童儿童学龄前女(雌)性人类男(雄)性中年人

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Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in Bcr-Abl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder

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MOLECULAR AND CELLULAR BIOLOGY 2000年第4期20卷 1149-1161页

作者： Hao, SX Ren, RB Brandeis Univ Rosenstiel Basic Med Sci Res Ctr Dept Biol Waltham MA 02454 USA

Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplastic transformation of a hematopoietic stem cell. The majority of cases of CML are associated with the (9;22) chromosome translocation that generates the bcr-abl chimeric gene. Alpha interferon (IFN-alpha) treatment induces hematological remission and prolongs life in 75% of CML patients in the chronic phase. It has been shown that mice deficient in interferon consensus sequence binding protein (ICSBP), a member of the interferon regulatory factor family, manifest a CML-like syndrome. We have shown that expression of Bcr-Abl in bone marrow (BM) cells from 5-fluorouracil (5-FU)-treated mice by retroviral transduction efficiently induces a myeloproliferative disease in mice resembling human CML. To directly test whether icsbp can function as a tumor suppressor gene, we examined the effect of ICSBP on Bcr-Abl-induced CML-like disease using this murine model for CML. We found that expression of the ICSBP protein was significantly decreased in Bcr-Abl-induced CML-like disease. Forced coexpression of ICSBP inhibited the Bcr-Abl-induced colony formation of BM cells from 5-FU-treated mice in vitro and Bcr-Abl-induced CML-like disease in vivo. Interestingly, coexpression of ICSBP and Bcr-Abl induced a transient B-lymphoproliferative disorder in the murine model of Bcr-Abl-induced CML-like disease. Overexpression of ICSBP consistently promotes rather than inhibits Bcr Abl-induced B lymphoproliferation in a murine model where BM cells from non-5-FU-treated donors were used, indicating that ICSBP has a specific antitumor activity toward myeloid neoplasms. We also found that overexpression of ICSBP negatively regulated normal hematopoiesis. These data provide direct evidence that ICSBP can act as a tumor suppressor that regulates normal and neoplastic proliferation of hematopoietic cells.

关键词：抗代谢药抗肿瘤/药理学 B淋巴细胞/病理学碱基序列骨髓移植集落形成单位测定共有序列 DNA引物/遗传学疾病模型动物减量调节氟尿嘧啶/药理学基因 abl 血细胞生成/遗传学干扰素调节因子类干扰素类/代谢白血病髓系慢性 BCR-ABL阳性/遗传学白血病髓系慢性 BCR-ABL阳性/代谢白血病髓系慢性 BCR-ABL阳性/病理学淋巴组织增殖性疾病/病因学淋巴组织增殖性疾病/遗传学小鼠近交BALBC 骨髓增殖性疾病/遗传学骨髓增殖性疾病/预防和控制阻遏蛋白质类/遗传学阻遏蛋白质类/代谢易位遗传动物人类男(雄)性小鼠

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Rapid reconstitution of Epstein-Barr virus-specific T lymphocytes following allogeneic stem cell transplantation

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BLOOD 2000年第8期96卷 2814-2821页

作者： Marshall, NA Howe, JG Formica, R Krause, D Wagner, JE Berliner, N Crouch, J Pilip, I Cooper, D Blazar, BR Seropian, S Pamer, EG Yale Univ Sch Med Sect Infect Dis New Haven CT USA Yale Univ Sch Med Sect Med Oncol New Haven CT USA Yale Univ Sch Med Sect Hematol New Haven CT USA Yale Univ Sch Med Nephrol Sect New Haven CT USA Yale Univ Sch Med Dept Med New Haven CT 06510 USA Yale Univ Sch Med Dept Immunobiol New Haven CT 06510 USA Yale Univ Sch Med Dept Lab Med New Haven CT 06510 USA Univ Minnesota Ctr Canc Dept Pediat Div Blood & Marrow Transplantat Minneapolis MN 55455 USA

Epstein-Barr virus (EBV)-specific CD8 T lymphocytes are present at remarkably high frequencies in healthy EBV+ individuals and provide protection from EBV-associated lymphoproliferative diseases. Allogeneic peripheral blood stem cell transplantation (allo-PBSCT) is a commonly used therapy in which T-cell surveillance for EBV is temporarily disrupted. Herein, human leukocyte antigen (HLA) class I tetramers were used to investigate the reestablishment of the EBV-specific CD8 T-cell repertoire in patients following allo-PBSCT. CD8(+) T cells specific for lytic and latent cycle-derived EBV peptides rapidly repopulate the periphery of matched sibling allo-PSSCT patients. The relative frequencies of T cells specific for different EBV peptides in transplantation recipients closely reflect those of their respective donors. Investigation of patients at monthly intervals following unmanipulated allo-PBSCT demonstrated that the frequency of EBV-specific T cells correlates with the number of EBV genome copies in the peripheral blood and that expansion of EBV-specific T-cell populations occurs even in the setting of immunosuppressive therapy. In contrast, patients undergoing T-cell-depleted or unrelated cord blood transplantation have undetectable EBV-specific T cells, even in the presence of Epstein-Barr viremia, The protective shield provided by EBV-specific CD8 T cells is rapidly established following unmanipulated matched sibling allo-PBSCT and demonstrates that HLA class I tetramers complexed with viral peptides can provide direct and rapid assessment of pathogen-specific immunity in this and other vulnerable patient populations. (C) 2000 by The American Society of Hematology.

关键词：抗原呈递抗原病毒/免疫学生物聚合物 CD8阳性T淋巴细胞/细胞学 CD8阳性T淋巴细胞/免疫学爱泼斯坦巴尔病毒感染/免疫学可行性研究移植物存活 HLA-A2抗原/免疫学 HLA-B7抗原/免疫学 HLA-B8抗原/免疫学血液肿瘤/治疗造血干细胞移植疱疹病毒4型人/免疫学疱疹病毒4型人/分离和提纯组织相容性试验肾移植淋巴组织增殖性疾病/病因学淋巴组织增殖性疾病/预防和控制淋巴组织增殖性疾病/病毒学大分子物质 T淋巴细胞亚群/细胞学 T淋巴细胞亚群/免疫学组织供者移植预处理移植同种/免疫学病毒载量 β2微球蛋白/免疫学成年人儿童女(雌)性人类男(雄)性中年人

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SH2D1A mutation analysis for diagnosis of XLP in typical and atypical patients

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HUMAN GENETICS 1999年第5期105卷 501-505页

作者： Yin, L Ferrand, V Lavoué, MF Hayoz, D Philippe, N Souillet, G Seri, M Giacchino, R Castagnola, E Hodgson, S Sylla, BS Romeo, G Int Agcy Res Canc F-69372 Lyon 08 France CHU Vaudois Div Hypertens & Med Vasc CH-1011 Lausanne Switzerland Hop Debrousse Serv Hematol F-69322 Lyon 01 France Ist Giannina Gaslini Mol Genet Lab I-16148 Genoa Quarto Italy Ospitale G Gaslini Div Malattie Infett I-16148 Genoa Quarto Italy Guys Hosp Div Med & Mol Genet London SE1 9RT England

X-linked lymphoproliferative disease (XLP) is a rare inherited immunodeficiency to Epstein-Barr virus (EBV). The gene responsible for XLP has recently been identified as the four-exon SH2D1A gene encoding a 128-amino-acid protein that contains an SH2-domain. Functional studies indicate the SH2D1A protein acts as a regulator of at least two signal transduction pathways initiated by the cell surface molecules SLAM and 2B4, respectively, and possibly related to the host immune response to EBV infection. We have carried out a systematic mutation study of the SH2D1A gene in our series of 19 typical and 8 atypical XLP patients by polymerase chain reaction (PCR), reverse transcription/PCR, and sequencing, and have reconstructed the haplotypes of the patients. Four out of the 13 mutations detected are previously unreported. The identification of SH2D1A mutations in carriers from all three XLP families screened and the detection of mutations in two out of eight atypical patients indicates the usefulness of a DNA-based diagnosis for XLP disease.

关键词：载体蛋白质类/遗传学 DNA突变分析双核苷酸重复外显子基因连锁单倍型细胞内信号肽和蛋白质类淋巴组织增殖性疾病/诊断淋巴组织增殖性疾病/病因学淋巴组织增殖性疾病/遗传学突变系谱 RNA 信使/遗传学 RNA 信使/代谢逆转录聚合酶链反应信号传导/遗传学 X染色体/遗传学 src同源域/遗传学女(雌)性人类男(雄)性

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Endoscopic diagnosis of lymphoproliferative disease after solid organ transplantation

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JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION 1999年第4期28卷 375-376页

作者： Kocoshis, SA Univ Pittsburgh Childrens Hosp Pittsburgh Sch Med Pittsburgh PA 15213 USA

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IMMUNOLOGICALLY DIAGNOSED MALIGNANCY IN SJOGRENS PSEUDOLYMPHOMA

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AMERICAN JOURNAL OF MEDICINE 1978年第3期65卷 424-429页

作者： FAGUET, GB WEBB, HH AGEE, JF RICKS, WB SHARBAUGH, AH DWIGHT D EISENHOWER ARMY MED CTR DEPT MED FT GORDON GA USA

Studies of lymphocyte markers in a patient with Sjogren''s syndrome who exhibited histologically benign lymphoproliferation in the lung revealed a malignant cell clone. T [thymus-derived] and B [bone marrow-derived] cells were quantitated according to their ability to form spontaneous rosettes with sheep erythrocytes and to fluoresce with fluorescein-conjugated antiserums, respectively. Circulating lymphocytes were 66% T cells (N = 58 .+-. 2%) and 14% B cells (N = 22 .+-. 1%), the latter exhibiting normal polyclonal distribution of membrane immunoglobulins. Lymphocyte suspensions obtained from fresh lymph node and biopsy specimens from a lymphoid lung nodule revealed 95% and 88% B cells, with 1 percent and 2% T cells, respectively. When cryostat-frozen sections from both tissues were reacted with each of the heavy and light chain-specific antiserums, most cells demonstrated the presence of intracytoplasmic .mu. kappa immunoglobulin exclusively. Twenty-two months later, a clinically and histologically classic lymphoma developed. Repeat marker studies performed on cells freshly isolated and frozen sections from the histologically malignant lymph node revealed persistence of the monoclonal marker on most cells.

关键词： B淋巴细胞/免疫学免疫球蛋白κ链/分析肺/病理学肺肿瘤/诊断肺肿瘤/病因学肺肿瘤/病理学淋巴细胞活化淋巴瘤/诊断淋巴瘤/病因学淋巴瘤/病理学淋巴组织增殖性疾病/诊断淋巴组织增殖性疾病/病因学淋巴组织增殖性疾病/病理学受体抗原 B细胞/分析玫瑰花结形成干燥综合征/并发症干燥综合征/病理学 T淋巴细胞/免疫学人类男(雄)性中年人

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Activation and adoptive transfer of Epstein-Barr virus-specific cytotoxic T cells in solid organ transplant patients with posttransplant lymphoproliferative disease

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第18期96卷 10391-10396页

作者： Khanna, R Bell, S Sherritt, M Galbraith, A Burrows, SR Rafter, L Clarke, B Slaughter, R Falk, MC Douglass, J Williams, T Elliott, SL Moss, DJ Queensland Inst Med Res Epstein Barr Virus Unit Brisbane Qld 4006 Australia Univ Queensland Joint Oncol Program Brisbane Qld 4006 Australia Prince Charles Hosp Queensland Heart & Lung Transplant Unit Brisbane Qld 4032 Australia Princess Alexandra Hosp Brisbane Qld 4102 Australia Alfred Hosp Dept Allergy & Clin Immunol Prahran Vic 3181 Australia Alfred Hosp Dept Resp Med Prahran Vic 3181 Australia Monash Univ Prahran Vic 3181 Australia

The treatment of Epstein-Barr virus (EBV)associated lymphoproliferative disease (PTLD) in EBV seronegative solid organ transplant recipients who acquire their EBV infection after engraftment poses a considerable challenge because of underlying immunosuppression that inhibits the virus-specific cytotoxic T cell (CTL) response in vivo. We have developed a protocol for activating autologous EBV-specific CTL lines from these patients and show their potential use for immunotherapy against PTLD in solid organ transplant patients. Peripheral blood mononuclear cells from a panel of solid organ transplant recipients with and without active PTLD were used to assess EBV-specific memory CTL responses. The activation protocol involved cocultivation of peripheral blood mononuclear cells with an autologous lymphoblastoid cell line under conditions that favored expansion of virus-specific CTL and hindered the proliferation of allospecific T cells. These CTL consistently showed (i) strong EBV-specificity, including reactivity through defined epitopes in spite of concurrent immunosuppressive therapy, and (ii) no alloreactivity toward donor alloantigens. More importantly, adoptive transfer of these autologous CTLs into a single patient with active PTLD was coincident with a very significant regression of the PTLD, These results demonstrate that a potent EBV-specific memory response can be expanded from solid organ recipients who have acquired their primary EBV infection under high levels of immunosuppressive therapy and that these T cells may have therapeutic potential against PTLD.

关键词：过继转移细胞系细胞系转化心脏移植/免疫学疱疹病毒4型人/免疫学肾移植/免疫学肺移植/免疫学淋巴细胞活化淋巴组织增殖性疾病/病因学淋巴组织增殖性疾病/免疫学淋巴组织增殖性疾病/治疗胰腺移植/免疫学手术后并发症/免疫学 T淋巴细胞细胞毒性/免疫学 T淋巴细胞细胞毒性/病毒学移植免疫学成年人女(雌)性人类男(雄)性中年人

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