Cytokines, cellular & molecular therapy最新文献_第7页

Adoptive T-cell immunotherapy of cancer. 癌症的过继性t细胞免疫治疗。

Cytokines, cellular & molecular therapy Pub Date : 1999-06-01

Q Li, A E Chang

引用次数: 0

Generation of autologous immunity to acute myeloid leukaemia and maintenance of complete remission following interferon-alpha treatment. 急性髓系白血病自体免疫的产生和干扰素治疗后完全缓解的维持。

Cytokines, cellular & molecular therapy Pub Date : 1999-06-01

M W Lowdell, R Craston, H G Prentice

引用次数: 0

The therapeutic potential of erythropoietin receptor transgenes. 促红细胞生成素受体转基因的治疗潜力。

Cytokines, cellular & molecular therapy Pub Date : 1999-06-01

S L Kirby

{"title":"The therapeutic potential of erythropoietin receptor transgenes.","authors":"S L Kirby","doi":"","DOIUrl":"","url":null,"abstract":"Allogeneic bone marrow transplantation is an effective curative therapy for both malignant and heritable diseases. The use of genetically altered autologous hematopoietic stem cells (HSC) is being increasingly investigated as a treatment for a variety of non-malignant but significantly morbid diseases, including hemoglobinopathies, immunodeficiencies and autoimmune diseases. Other hematopoietic cells capable of proliferation, such as antigen-specific T cells and dendritic cells, have also been used for adoptive immunotherapy. Genetic procedures to modify these various therapeutic cells so that they can be selectively amplified either in vitro or in vivo could enhance their efficacy. For example, HSC that contain a gene that confers a survival, selection or growth advantage may enhance their engraftment. Such enhancement could be expected to reduce graft failures and the intensity of the required conditioning regimen, thereby decreasing the toxicities of transplantation. In this review, the functions of cytokine receptor transgenes coding for erythropoietin receptors (EpoR) are analyzed. The characteristics of these transgenic cells and animals are discussed with regard to the possible therapeutic use of EpoR transgenes in the transplantation of hematopoietic cells.","PeriodicalId":79485,"journal":{"name":"Cytokines, cellular & molecular therapy","volume":"5 2","pages":"97-104"},"PeriodicalIF":0.0,"publicationDate":"1999-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21377652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CD30L-ETA': a new recombinant immunotoxin based on the CD30 ligand for possible use against human lymphoma. CD30L-ETA'：一种基于 CD30 配体的新型重组免疫毒素，可用于对抗人类淋巴瘤。

Cytokines, cellular & molecular therapy Pub Date : 1999-06-01

S Barth, B Matthey, M Huhn, V Diehl, A Engert

{"title":"CD30L-ETA': a new recombinant immunotoxin based on the CD30 ligand for possible use against human lymphoma.","authors":"S Barth, B Matthey, M Huhn, V Diehl, A Engert","doi":"","DOIUrl":"","url":null,"abstract":"Recombinant DNA technology makes it possible to genetically fuse V genes or cytokines to toxin domains, resulting in immunotherapeutics for selective destruction of tumor cells. Since recombinant immunotoxins can be easily manipulated in terms of affinity or cytotoxic potency and produced in large quantities, we have developed a new CD30 ligand-based fusion toxin (CD30L-ETA'). Human CD30L cDNA was ligated into a pET-based expression plasmid and thereby fused to a modified Pseudomonas aeruginosa exotoxin A (ETA') lacking its cell-binding domain I. After IPTG-indiced expression in E. coli strain BL21(DE3), the 60 kDa His-tagged fusion protein (CD30L-ETA') was isolated from inclusion bodies. Denatured protein was renatured in the presence of 0.4 M arginine and a glutathione redox system. Refolded protein was purified and concentrated by ion-exchange chromatography on a HiTrap Q column. The binding properties of CD30L-ETA' were evaluated by competitive ELISA, immunohistochemical staining, and FACS analysis on CD30-expressing cells. The in vitro toxicity of the fusion protein was then tested on the CD30+ Hodgkin-derived cell line L540cy and the Burkitt's lymphoma cell line BL38. CD30L-ETA' exhibited specific cytotoxicity against L540cy cells (IC50 = 24 ng/ml) as determined by [3H]leucine uptake assays. This is the first report on the specificity and cytotoxic potency of a chimeric CD30L fusion toxin against Hodgkin's disease-derived cells.","PeriodicalId":79485,"journal":{"name":"Cytokines, cellular & molecular therapy","volume":"5 2","pages":"69-78"},"PeriodicalIF":0.0,"publicationDate":"1999-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21377710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular analysis of resistance to interferon in patients with laryngeal papillomatosis. 喉乳头状瘤患者干扰素耐药性的分子分析。

Cytokines, cellular & molecular therapy Pub Date : 1999-06-01

R Garciá-Millián, A Santos, S E Perea, R González-Cabañas, C Valenzuela, M Araña

{"title":"Molecular analysis of resistance to interferon in patients with laryngeal papillomatosis.","authors":"R Garciá-Millián, A Santos, S E Perea, R González-Cabañas, C Valenzuela, M Araña","doi":"","DOIUrl":"","url":null,"abstract":"Although interferon (IFN)-alpha has been used successfully as an adjuvant therapy in laryngeal papillomatosis, some patients are resistant to this treatment. In order to know which patients will benefit from the therapy, we have tried to find a relationship between the IFN response and the viral and host parameters in the lesion. Detection of viral type and copy numbers by polymerase chain reaction (PCR) showed that all patients infected with human papillomavirus (HPV)-11 were sensitive to the treatment, in contrast to those infected with HPV-6. These differences could be explained in part by the inability of HPV-11 E7 to inhibit the induction of an IFN-responsive element, whereas HPV-6 E7 almost completely inhibited the activity of this promoter in transient transfection experiments. Local immune status in the lesion showed that all HPV-11-infected patients had detectable levels of interleukin (IL)-15 and IFN-gamma mRNA, in contrast to HPV-6-infected patients, in whom mRNA for these cytokines was almost absent. Viral copy numbers and levels of IL-4 mRNA could not be correlated with IFN response. Only one patient resistant to recombinant IFN-alpha2b and negative for HPV DNA presented high titers of neutralizing anti-IFN-alpha2b antibodies. This patient became sensitive when natural IFN-alpha was administered. These results suggest that response to IFN may be a complex phenomenon resulting from the interaction between viral and host elements.","PeriodicalId":79485,"journal":{"name":"Cytokines, cellular & molecular therapy","volume":"5 2","pages":"79-85"},"PeriodicalIF":0.0,"publicationDate":"1999-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21377711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acute myeloblastic leukaemia: graft-versus-host and graft-versus-leukaemia responses to autologous IL-2 activated lymphocytes in rapid and slow disease. 急性髓母细胞白血病:移植物抗宿主和移植物抗白血病对自身IL-2活化淋巴细胞在快速和缓慢疾病中的反应

Cytokines, cellular & molecular therapy Pub Date : 1999-03-01

B J Boughton, A W Simpson

引用次数: 0

Cytokines (IFNs, TNF-alpha, IL-2 and IL-12) and animal models of cancer. 细胞因子(ifn, tnf - α， IL-2和IL-12)和癌症动物模型。

Cytokines, cellular & molecular therapy Pub Date : 1999-03-01

F Burke

引用次数: 0

TNF-alpha in acute cardiac transplant rejection. 急性心脏移植排斥反应中的tnf - α。

Cytokines, cellular & molecular therapy Pub Date : 1999-03-01

M Azzawi, P S Hasleton, I V Hutchinson

{"title":"TNF-alpha in acute cardiac transplant rejection.","authors":"M Azzawi, P S Hasleton, I V Hutchinson","doi":"","DOIUrl":"","url":null,"abstract":"Acute cardiac allograft rejection is an immune-mediated response, hallmarked by cellular infiltration and myocyte damage in the transplanted heart. Cardiac biopsy sampling has been the 'gold' standard for routinely monitoring episodes of acute rejection. As cardiac biopsy is invasive, attention has focused on other non-invasive methods, such as serum analysis, for monitoring purposes. Tumour necrosis factor alpha (TNF-alpha) is a lymphocyte- and macrophage-derived cytokine that is pleiotropic in its actions. Its proinflammatory functions suggest that it may play an important role in initiating and orchestrating the rejection response. Studies demonstrating a correlation in the expression of TNF-alpha with the severity of the rejection episode have placed TNF-alpha as a prime candidate marker of rejection, and have prompted further study to elucidate these findings. This review discusses the limitations of the methodologies used to identify TNF-alpha, and how intragraft expression of TNF-alpha is not reflected in the serum. Furthermore, we describe how other stimuli besides the rejection response can affect TNF-alpha production, arguing against its use as a 'rejection-specific' marker. Nevertheless, genetic studies suggest that TNF-alpha may influence transplant outcome, and offer a new tool for studying the role of TNF-alpha in acute transplant rejection","PeriodicalId":79485,"journal":{"name":"Cytokines, cellular & molecular therapy","volume":"5 1","pages":"41-9"},"PeriodicalIF":0.0,"publicationDate":"1999-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21256776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Upregulation of antitumor immunity by IL-12 gene-transfected AK-5 tumor cells in vivo. IL-12基因转染AK-5肿瘤细胞对体内抗肿瘤免疫的上调作用。

Cytokines, cellular & molecular therapy Pub Date : 1999-03-01

K S Nandakumar, K Lakshmi Rao, B V Pardhasaradhi, A Khar

{"title":"Upregulation of antitumor immunity by IL-12 gene-transfected AK-5 tumor cells in vivo.","authors":"K S Nandakumar, K Lakshmi Rao, B V Pardhasaradhi, A Khar","doi":"","DOIUrl":"","url":null,"abstract":"We have earlier demonstrated a significant role for IL-12 in the regression of a rat histiocytic tumor, AK-5. In order to analyze further the antitumor immunity induced by interleukin (IL)-12, we have established IL-12-secreting tumor cell clones by gene transfection. Significant enhancement in the lytic potential of splenocytes by the culture supernatants containing IL-12 demonstrated retention of biological activity by the tumor-cell-derived cytokine. Athymic nude mice transplanted subcutaneously with tumor cells engineered to secret IL-12 showed a significant reduction in tumor size, with enhanced antibody-dependent cellular cytotoxicity. Analysis of the serum samples from animals injected with the IL-12 gene-transfected AK-5 cells on different days revealed a significant increase in circulatory IL-12, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and antitumor antibodies, all of which contributed to the reduction in tumor mass. The enhanced proliferative capacity of splenocytes from these animals indicated the presence of highly activated immune cells in vivo. Similarly, intraperitoneal transplantation of IL-12 gene-transfected tumor cells in syngeneic Wistar rats induced a significant increase in cellular cytotoxicity, with a concomitant reduction in circulatory IL-12 (p40) protein. Administration of antibodies to IL-12 and IFN-gamma reduced the expression of the costimulatory molecules B7.1 and B7.2 and the cytolytic effectors granzyme B and Fas-L, suggesting their involvement in IFN-gamma-dependent antitumor immune response induced by IL-12. The present study thus demonstrates that IL-12 gene therapy could be among the promising approaches for an effective cancer therapy.","PeriodicalId":79485,"journal":{"name":"Cytokines, cellular & molecular therapy","volume":"5 1","pages":"7-14"},"PeriodicalIF":0.0,"publicationDate":"1999-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21256773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antisense strategy in hematological malignancies. 血液系统恶性肿瘤的反义策略。

Cytokines, cellular & molecular therapy Pub Date : 1999-03-01

K Warzocha

{"title":"Antisense strategy in hematological malignancies.","authors":"K Warzocha","doi":"","DOIUrl":"","url":null,"abstract":"Standard cytotoxic chemotherapy for neoplastic disease is fraught with systemic toxicity. The ratio of the toxic dose to the therapeutic dose is relatively low, which reflects the large number of cellular targets affected by the chemotherapeutic agent as well as its inability to distinguish between normal and malignant cells. The discovery of oncogenes and tumor suppressor genes involved in the process of transformation of normal cells into malignant cells has opened new areas of research in oncology, aimed at discovering drugs that could selectively inhibit their biological effects. This therapeutic modality, called an antisense strategy, has become a powerful tool for selectively reducing the expression of target genes in vitro, and there is increasing interest in the possibility of using the same technology in vivo for therapeutic purposes. In oncohematology, a number of trials have been initiated with antisense oligonucleotides directed against molecular targets, including the bcl-2, c-myc, bcr-abl, c-myb or p53 oncogenes and tumor suppressor genes. The experience gained from these studies will be applicable to the next generation of antisense compounds, which may include oligonucleotides with novel backbones or other structural modifications, as well as for expansion of the use of antisense oligonucleotides in combination approaches for the treatment of hematological malignancies.","PeriodicalId":79485,"journal":{"name":"Cytokines, cellular & molecular therapy","volume":"5 1","pages":"15-23"},"PeriodicalIF":0.0,"publicationDate":"1999-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21256774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0