Lymphokine and cytokine research最新文献_第5页

TNF-alpha-induced antiproliferation is not dependent on the autocrine action of TGF-beta 1 in a thyroid cancer cell line. 在甲状腺癌细胞系中，tnf α诱导的抗增殖不依赖于tgf - β 1的自分泌作用。

Lymphokine and cytokine research Pub Date : 1994-04-01

X P Pang, M Yoshimura, J Wang, S M Dubinett

{"title":"TNF-alpha-induced antiproliferation is not dependent on the autocrine action of TGF-beta 1 in a thyroid cancer cell line.","authors":"X P Pang, M Yoshimura, J Wang, S M Dubinett","doi":"","DOIUrl":"","url":null,"abstract":"The autocrine inhibitory action of transforming growth factor-beta 1 (TGF-beta 1) may play an important role in maintaining the normal state of thyroid follicular epithelial cells. Deficiency of this regulatory mechanism has been implicated in the pathogenesis of nontoxic nodular goiter and thyroid epithelial cell cancer. Tumor necrosis factor-alpha (TNF-alpha) has an antiproliferative action in a human papillary thyroid carcinoma cell line, NP-PTC cells, through a receptor-mediated mechanism. In the present work, we studied the antiproliferative action of TNF-alpha and TGF-beta 1 in NP-PTC cells. TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1. Both TNF-alpha and TGF-beta 1 inhibited the proliferation of NP-PTC cells. A neutralizing antibody specific to human TGF-beta 1 blocked the antiproliferative action of TGF-beta 1 on NP-PTC cells, but it failed to block TNF-alpha-induced antiproliferation. Further, TNF-alpha and TGF-beta 1 acted synergistically to inhibit NP-PTC cell proliferation. The results show that both TNF-alpha and TGF-beta 1 inhibit the proliferation of NP-PTC cells. However, the actions of TGF-beta 1 and TNF-alpha differ in NP-PTC cells; TNF-alpha activates nuclear factor kappa B (NF-kappa B) and TGF-beta 1 does not. Although TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1, the antiproliferative action of TNF-alpha is not dependent on the autocrine action of TGF-beta 1 in NP-PTC cells.","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 2","pages":"93-7"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19054683","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

TNF-alpha potentiation of the lymphokine-activated killer response of murine thymus cells. tnf - α增强小鼠胸腺细胞淋巴因子激活的杀伤反应。

Lymphokine and cytokine research Pub Date : 1994-04-01

P Ujházy, D Maccubbin, C Eppolito, E Mihich, M J Ehrke

{"title":"TNF-alpha potentiation of the lymphokine-activated killer response of murine thymus cells.","authors":"P Ujházy, D Maccubbin, C Eppolito, E Mihich, M J Ehrke","doi":"","DOIUrl":"","url":null,"abstract":"The role of tumor necrosis factor (TNF-alpha) on in vitro generation of lymphokine-activated killer (LAK) cells from murine thymocytes was investigated and compared to that on generation of LAK from splenocytes. TNF-alpha increased the potential of interleukin-2 (IL-2) at suboptimal concentrations to generate LAK activity in thymocytes even more than in splenocytes. In parallel, augmented [3H]thymidine uptake by thymocytes and splenocytes was seen. However, no net increase in viable cell number was observed. LAK effector cells from TNF-alpha plus IL-2 cultures responded with an increased [3H]thymidine uptake to restimulation by IL-2 alone. These results suggest that TNF-alpha + IL-2 may be inducing the expansion of a small subset of cells. NK1.1+ cells are a very minor subset of thymocytes, nevertheless phenotype analysis showed that in thymocytes, IL-2 + TNF-alpha generates NK1.1+ CD8- LAK effectors in contrast to NK1.1- CD8+ cells found with IL-2 alone. This result is consistent with the finding in the proliferation studies. The fact that thymocytes are stimulated by the TNF-alpha + IL-2 combination to proliferate as well as to develop a phenotypically distinct effector supports the role of TNF-alpha in intra- and extrathymic regulation.","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 2","pages":"99-106"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19054684","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

Simultaneous analysis of multiple cytokine receptor mRNAs by RNase protection assay in LPS-induced endotoxemia. 通过 RNase 保护测定法同时分析 LPS 诱导的内毒素血症中的多种细胞因子受体 mRNA。

Lymphokine and cytokine research Pub Date : 1994-04-01

A K Stalder, I L Campbell

{"title":"Simultaneous analysis of multiple cytokine receptor mRNAs by RNase protection assay in LPS-induced endotoxemia.","authors":"A K Stalder, I L Campbell","doi":"","DOIUrl":"","url":null,"abstract":"In order to examine the regulation of cytokine receptor gene expression an RNase protection assay (RPA) was developed that allows the simultaneous and semiquantitative measurement of mRNAs encoding for the IL-1 p60 and p80, TNF p55 and p75, IFN-gamma, and IL-6 receptors. Titration experiments revealed that this method was very sensitive allowing the detection of the target cytokine receptor mRNAs down to at least 0.01 microgram of spleen poly(A)+ RNA. The cytokine receptor RPA was used to examine the expression of the receptor genes in various organs from normal mice and mice that had been injected with LPS. In normal mice expression of the IL-1R p80, TNFR p55 and p75, IFN-gamma, and IL-6R but not the IL-1R p60 transcripts was readily detectable in spleen, liver, kidney, and brain. Following LPS treatment, there was an induction of the IL-1R p60 mRNA in all organs and an up-regulation of the IL-1R p80, TNFR p55 and p75, IFN-gamma, and IL-6 receptor mRNAs particularly in spleen, liver, and kidney. Interorgan differences were observed in the regulation of these receptor mRNAs, indicating an organ-specific response to the LPS challenge. Our findings indicate the cytokine receptor RPA is a powerful and versatile tool for the simultaneous analysis of multiple cytokine receptor mRNAs in tissue samples. This technique will prove valuable in further evaluating the coordinated regulation of the expression of these genes, which are pivotal in the biology of cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 2","pages":"107-12"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19054781","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

Enhanced expression of HLA-A,B,C and inducibility of TAP-1, TAP-2, and HLA-A,B,C by interferon-gamma in a multidrug-resistant small cell lung cancer line. 干扰素- γ在多药耐药小细胞肺癌细胞系中增强HLA-A、B、C的表达和诱导TAP-1、TAP-2和HLA-A、B、C的表达

Lymphokine and cytokine research Pub Date : 1994-04-01

B Fisk, C G Ioannides, S Aggarwal, J T Wharton, C A O'Brian, N Restifo, B S Glisson

{"title":"Enhanced expression of HLA-A,B,C and inducibility of TAP-1, TAP-2, and HLA-A,B,C by interferon-gamma in a multidrug-resistant small cell lung cancer line.","authors":"B Fisk, C G Ioannides, S Aggarwal, J T Wharton, C A O'Brian, N Restifo, B S Glisson","doi":"","DOIUrl":"","url":null,"abstract":"Recent evidence suggests that deficient HLA Class I expression in SCLC lines may be due, in part, to down-regulation of TAP-1 and TAP-2 expression, and, thus, deficient antigen processing. Given the capability of the multidrug transporter mediating MDR, P-gp, to transport peptides, we hypothesized that P-gp may substitute for TAP-1/TAP-2 and enhance antigen processing in SCLC. To investigate this, we studied the H69 line (parent SCLC) and VPR-2 (MDR subline selected in etoposide, P-gp +). HLA-A,B,C expression was significantly increased in VPR-2 cells relative to H69, and was much more inducible with IFN-gamma. TAP-1 and TAP-2 were expressed at low levels in both lines. Differential induction of TAP-1 expression with IFN-gamma exposure was observed, with a dramatic increase in VPR-2 cells, and no change in H69. TAP-2 expression was enhanced in both lines with IFN-gamma, but to a greater degree in VPR-2. VPR-2 cells were resistant to LAK killing relative to H69, and were minimally sensitized with IFN-gamma. In contrast, IFN-gamma enhanced susceptibility of H69 to LAK killing 3-fold. The direct correlation between enhancement of HLA-A,B,C expression by IFN-gamma and the differential inducibility of TAP-1 and TAP-2 expression in P-gp-SCLC lines is novel. Relative LAK sensitivity of H69 and its increase by IFN-gamma may have clinical implications.","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 2","pages":"125-31"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19054783","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

TNF cytotoxicity: effects of HER-2/neu expression and inhibitors of ADP-ribosylation. TNF细胞毒性:HER-2/neu表达和adp -核糖基化抑制剂的影响。

Lymphokine and cytokine research Pub Date : 1994-04-01

P Tang, M C Hung, J Klostergaard

引用次数: 0

Interference of circulating azathioprine but not methotrexate or sulfasalazine with measurements of interleukin-6 bioactivity. 循环硫唑嘌呤对白细胞介素-6生物活性测量的干扰，而甲氨蝶呤或柳氮磺胺嘧啶对白细胞介素-6生物活性的干扰。

Lymphokine and cytokine research Pub Date : 1994-04-01

P Barrera, A M Boerbooms, R W Sauerwein, P N Demacker, L B van de Putte, J W van der Meer

{"title":"Interference of circulating azathioprine but not methotrexate or sulfasalazine with measurements of interleukin-6 bioactivity.","authors":"P Barrera, A M Boerbooms, R W Sauerwein, P N Demacker, L B van de Putte, J W van der Meer","doi":"","DOIUrl":"","url":null,"abstract":"Bioassays are currently used to measure the presence of functionally active cytokines in biological fluids. These assays may be influenced by the presence of other substances, either cytokine specific or not, in such fluids. In the present study, we analyzed whether some currently used disease-modifying antirheumatic drugs (DMARDs) could interfere with the measurements of circulating interleukin-6 (IL-6) bioactivity in the B9 hybridoma assay. When sera from healthy controls and patients treated with various DMARDs, such as azathioprine (AZA), methotrexate (MTX), intramuscular gold, and sulfasalazine (SASP), were tested in the IL-6 bioassay, an inhibitory effect was observed only with sera from patients treated with AZA. Addition of exogenous AZA, 6-mercaptopurine (6-MP), and MTX to the IL-6 bioassay resulted in a dose-dependent inhibition of the B9 cell proliferation induced by IL-6, AZA being most potent on a molar basis. Concentrations of AZA and 6-MP compatible with serum concentrations achieved in RA patients were able to inhibit the bioassay, but this was not the case for MTX. Exogenous SASP and its metabolites did not modify the IL-6-induced B9 cell proliferation. This study shows that circulating AZA (or its metabolites) exert an inhibitory effect in the IL-6 bioassay. This method is therefore not suitable to measure IL-6 concentrations in patients treated with AZA. Interference of drugs must be ruled out when bioassays are used to evaluate cytokine levels in biological fluids.","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 2","pages":"155-9"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18914384","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

Interferon-alpha 2 counteracts interleukin-1 alpha-stimulated expression of urokinase-type plasminogen activator in human foreskin microvascular endothelial cells in vitro. 干扰素- α 2抵消白细胞介素-1 α刺激的尿激酶型纤溶酶原激活物在体外人包皮微血管内皮细胞中的表达。

Lymphokine and cytokine research Pub Date : 1994-04-01

J Wojta, H Zoellner, M Gallicchio, E L Filonzi, J A Hamilton, K McGrath

{"title":"Interferon-alpha 2 counteracts interleukin-1 alpha-stimulated expression of urokinase-type plasminogen activator in human foreskin microvascular endothelial cells in vitro.","authors":"J Wojta, H Zoellner, M Gallicchio, E L Filonzi, J A Hamilton, K McGrath","doi":"","DOIUrl":"","url":null,"abstract":"We investigated the effect of interferon-alpha 2 (IFN-alpha 2) on interleukin-1 alpha (IL-1 alpha)-induced up-regulation of urokinase type plasminogen activator (u-PA) expression in human foreskin microvascular endothelial cells (HFMEC) and human umbilical vein endothelial cells (HUVEC) in vitro. When IFN-alpha 2 and IL-1 alpha were added to the cells simultaneously, IFN-alpha 2 inhibited IL-1 alpha-induced up-regulation of u-PA antigen in a dose- and time-dependent fashion in HFMEC, whereas in HUVEC no effect of IFN-alpha 2 on IL-1 alpha-induced u-PA was seen. IL-1 alpha-induced up-regulation of PAI-1 antigen in HFMEC was not counteracted by IFN-alpha 2. When IFN-alpha 2 was added to HFMEC 1 or 2 h after IL-1 alpha a significant inhibition in u-PA synthesis was seen, whereas when IFN-alpha 2 was added to the cells 8 h after IL-1 alpha no effect on the induction of u-PA synthesis by IL-1 alpha was seen. IFN-alpha 2 also inhibited significantly the IL-1 alpha stimulated up-regulation of specific u-PA mRNA expression. In conclusion, our data show that IFN-alpha 2 can counteract the IL-1 alpha-induced up-regulation of u-PA in a similar way as IFN-gamma. This effect, which seems to be specific for microvascular endothelial cells, could contribute to the modulation of endothelial cell-mediated extravascular proteolysis in processes such as wound healing, neovascularisation, and endothelial cell migration.","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 2","pages":"133-8"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19054784","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

Modulation of the cytotoxic activity of tumor necrosis factor by protein tyrosine kinase and protein tyrosine phosphatase inhibitors. 蛋白酪氨酸激酶和蛋白酪氨酸磷酸酶抑制剂对肿瘤坏死因子细胞毒活性的调节。

Lymphokine and cytokine research Pub Date : 1994-04-01

S Mishra, R Mathur, A W Hamburger

{"title":"Modulation of the cytotoxic activity of tumor necrosis factor by protein tyrosine kinase and protein tyrosine phosphatase inhibitors.","authors":"S Mishra, R Mathur, A W Hamburger","doi":"","DOIUrl":"","url":null,"abstract":"The mechanism by which tumor necrosis factor (TNF) inhibits cell growth is not known. The importance of tyrosine phosphorylation in mediating the cytotoxicity of TNF has been suggested from previous studies. In this report, we investigated the effects of both tyrosine kinase (TK) and protein tyrosine phosphatase (PTP) inhibitors on the cytotoxic effects of TNF. TNF-induced changes in cellular PTPase activity were also examined. Incubation of tumor cells with genistein or tyrphostin, known TK inhibitors, protected against TNF cytotoxicity in a dose-dependent manner. Protection by TK inhibitors was observed at early time points after the start of TNF incubation. Preincubation of tumor cells with sodium orthovanadate, a known PTPase inhibitor, also protected against TNF cytotoxicity only at early time points after addition of TNF. Activation of total cellular PTPase activity by TNF was observed at early times of TNF incubation only in TNF-sensitive cell lines. Immunoblot analysis revealed that TNF enhanced tyrosyl phosphorylation of the epidermal growth factor receptor (EGFR) only in TNF-sensitive cell lines. No other substrates were tyr-phosphorylated after addition of TNF. The results suggest that both cellular PTKs and PTPases play a significant role in orchestrating the early events in the cytotoxic response of TNF. The nature and types of PTKs and PTPases involved in this process need further investigation.","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 2","pages":"77-83"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19054681","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

Antiproliferative lymphokine production by human peripheral blood lymphocytes and lymph node lymphocytes detected by a modified double layer soft agarose clonogenic assay. 改良双层软琼脂糖克隆实验检测人外周血淋巴细胞和淋巴结淋巴细胞的抗增殖淋巴因子产生。

Lymphokine and cytokine research Pub Date : 1994-02-01

T Saito, M Okadome, K Sugihara, M Sano, T Kamura, H Nakano

{"title":"Antiproliferative lymphokine production by human peripheral blood lymphocytes and lymph node lymphocytes detected by a modified double layer soft agarose clonogenic assay.","authors":"T Saito, M Okadome, K Sugihara, M Sano, T Kamura, H Nakano","doi":"","DOIUrl":"","url":null,"abstract":"The double layer soft agarose clonogenic assay using colony formation of target cells as an endpoint was adapted for the detection of antiproliferative lymphokine production from peripheral blood lymphocytes (PBL) and lymph node lymphocytes (LNL). The colony formation of cervical cancer cell lines, HeLa, CAC-1, and TMCC, in the upper layers was significantly inhibited by the inclusion of either PBL or LNL pretreated with PHA in the lower layers. Without stimulation by PHA, neither resident PBL nor LNL exhibited antiproliferative activity on the tumor cells in the upper layers. The antiproliferative activity against target cells increased in relation to the density of lymphocytes in the lower layers, and was dependent on protein synthesis by lymphocytes. Since the cell to cell contact between the effector cells and target cells is not possible in this assay, the reduction of colony formation should be attributed to soluble factor(s) that were secreted from the lymphocytes. Additionally, an antibody against IFN-gamma neutralized most of the antiproliferative activity, and equivalent levels of IFN-gamma were found to be present in the supernatant of PBL and LNL lower layers by a radioimmunoassay. The double layer soft agarose assay system should thus serve as a useful method for studying antiproliferative lymphokine production by lymphocytes.","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"13 1","pages":"55-62"},"PeriodicalIF":0.0,"publicationDate":"1994-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19177202","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

In situ detection of cytokine messenger RNAs in the eccrine sweat gland of normal human skin. 正常人皮肤分泌汗腺细胞因子信使rna的原位检测。

Lymphokine and cytokine research Pub Date : 1994-02-01

K D Boehm, J K Yun, C Garner, K P Strohl, C A Elmets

引用次数: 0