title: Interleukin 1 modulates messenger RNA levels of lymphokines and of other molecules associated with T cell activation in the T cell lymphoma LBRM33-1A5.
abstract: We have investigated the mechanism of action of IL 1 on T cell activation. For this purpose, we analyzed the content of specific messenger RNA for lymphokines and other genes that are associated with T cell activation in the murine IL 1-dependent T cell lymphoma LBRM33-1A5. Using cloned genes for IL 2, IL 3, TGF-beta, TY5, IL 2 receptor, Ly-1, c-myc, and p53 as probes in the S1 nuclease protection assay, we compared the amount of specific transcripts among total RNA prepared from unstimulated cells, IL 1 alpha or PHA-stimulated cells, and PHA plus IL 1 alpha-stimulated cells. IL 1 alpha augmented the PHA-induced accumulation of IL 2 mRNA with a magnitude comparable to the amount of IL 2 produced, suggesting that IL 1 alpha modulates IL 2 gene expression at the RNA level. Similar results were obtained with IL 3. We also observed that Ly-1 mRNA appears after PHA treatment and its accumulation was augmented by IL 1 alpha addition. On the basis of the effects of IL 1 alpha and/or PHA treatments on gene expression, we classified these genes into four groups. In all cases, IL 1 alpha seemed to affect mRNA levels quantitatively. These observations support previously described characteristics of this cytokine as a co-stimulator of T cell activation.
mesh_terms: D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000096:biosynthesis* / Q000235:genetics; D008228:Lymphoma, Non-Hodgkin / Q000473:pathology; D009857:Oncogenes / Q000187:drug effects; D010641:Phenotype; D012333:RNA, Messenger / Q000032:analysis*; D013601:T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D008222:Lymphokines; D012333:RNA, Messenger; D003513:Cycloheximide