Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Suppressor T cells in syngeneic tumor-bearing mice that inhibited in vitro generation of tumor antigen-specific cytotoxic T lymphocytes were characterized with respect to the kinetics, the nature and the target specificity, using murine malignant glioma (a methylcholanthrene-induced malignant ependymoblastoma, 203-glioma). Suppressor cell activity was assessed by the inhibition of tumor cell killing activity of cytotoxic T lymphocytes, which were prepared from splenic T enriched lymphocytes of mice immunized with 1 X 10(6) mitomycin C (50 micrograms/ml, 45 minutes)-treated 203-glioma cells twice at an interval of 7 days. It was confirmed that suppressor T cells were generated in 203-glioma-bearing mice, and they were tumor antigen-specific as evidenced by the fact that sensitized splenic T lymphocytes from mice bearing other syngeneic EL4 thymoma or allogeneic P 815 mastocytoma or YAC-1 T cell lymphoma did not exhibit the inhibition of the cytotoxic T lymphocyte activity against 203-glioma cells. Significant suppressor cell activity was detected in spleen cells 1 to 5 days after the subcutaneous inoculation of 203-glioma cells with the peak activity on day 3 and it disappeared as early as on day 7, suggesting strongly that the turn-over of suppressor T cells is very quick. Surface markers of suppressor T cells in 203-glioma-bearing mice were checked on day 3 with the results that the suppressor cell activity was eliminated by the treatment with anti-Lyt-2 monoclonal antibody and complement, indicating that the phenotype of suppressor T cells is Lyt-1-.2.3+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Suppressor mechanism in tumor immunology: characteristics of suppressor T-cells in glioma-bearing mice]. 619 6

Recombinant human interleukin-1 (IL-1) alpha and beta were found to activate a latent cytosolic form of the transcription factor NF kappa B in rat C6 glioma. IL-1 beta was 10 times more potent than IL-1 alpha for this activity and both were inhibited by the IL-1 receptor antagonist. The activation was detectable from 20 min and remained sustained for up to 24 h. The electrophoretic mobility of the activated complex was shown to be different from that of the corresponding complexes in another IL-1-responsive cell line, the murine thymoma line EL4.NOB-1. C6 cells, when transiently transfected with five NF kappa B consensus sequence repeats linked to the reporter gene chloramphenicol acetyltransferase (CAT), demonstrated increased CAT activity in response to IL-1 beta treatment. The activation of NF kappa B in glial cells may thus represent an early step in IL-1 signalling in brain and is likely to have consequences for IL-1-induced gene expression in these cells.
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PMID:Interleukin-1 activates transcription factor NF kappa B in glial cells. 837 49

High affinity "peripheral-type" benzodiazepine binding sites were detected in an interleukin-1 (IL-1) responsive murine thymoma cell line EL4.NOB-1. Exposure of these cells to IL-1 over a period of at least 24 hr resulted in down-regulation of the binding sites. This effect was inhibited by the IL-1 receptor antagonist (IL-1RA) which in these cells inhibits IL-1 binding to the type I IL-1 receptor. Phorbol myristate acetate (PMA), another activator of EL4.NOB-1 cells, had an opposite effect to IL-1 in that it increased binding site expression dramatically suggesting different mechanisms of action for these two effectors. IL-1 produced a similar response in the rat glioma cell line C6 whereas PMA was ineffective. Such modulation of the peripheral-type benzodiazepine receptor may provide an insight into its physiological role and its possible participation in IL-1 actions in different cells.
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PMID:Interleukin-1 and phorbol myristate acetate modulate the peripheral-type benzodiazepine receptor in lymphocytes and glial cells. 839 35

It has been shown that leukemia and glioma cells are sensitive to cannabidiol (CBD)-induced apoptosis, whereas primary monocytes and glia cells are relatively insensitive. In the current study, the cellular events and sensitivity to CBD-induced apoptosis between murine thymocytes and EL-4 thymoma cells were compared. Cannabidiol markedly induced apoptosis in a time- and concentration-related manner in both cells. The efficacy of CBD to induce apoptosis was comparable between the 2 types of T cells, whereas CBD induced apoptosis in thymocytes with a slightly greater potency than in EL4 cells. Time-course analyses revealed CBD-mediated apoptosis occurred earlier in EL-4 cells than that in thymocytes. An increased level of cellular reactive oxygen species (ROS) was detected in both cells with the peak response at 2 h post CBD treatment. Concordantly, CBD triggered a gradual diminishment in the cellular thiols. The presence of N-acetyl-L-cysteine (NAC), a precursor of glutathione, markedly attenuated the induction of apoptosis, and restored the diminished levels of cellular thiols. The results demonstrated that both thymocytes and EL-4 thymoma cells were susceptible to CBD-induced apoptosis and that ROS played a critical role in the apoptosis induction.
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PMID:A comparative study on cannabidiol-induced apoptosis in murine thymocytes and EL-4 thymoma cells. 1838 16