Dissociation of transcription from translation of human IL-1 beta: induction of steady state mRNA by adherence or recombinant C5a in the absence of translation.
Interleukin (IL) 1 is an important mediator of local and systemic disease. Blocking IL-1 using the IL-1 receptor antagonist has reduced the severity of disease in animal models of septic shock, diabetes, graft-vs-host disease, inflammatory bowel disease, and the spontaneous proliferation of leukemia cells. Blocking IL-1 and reduction in the synthesis of IL-1 are important strategies for reducing the progression of inflammatory disease and autoimmune diseases. Nature, however, maintains control over the synthesis of IL-1 by dissociating transcription for translation. In this paper, the basis for the dissociation of IL-1 beta synthesis of mRNA from synthesis of the IL-1 beta protein is reviewed.
Dinarello
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CA
Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts 02111.
D002448:Cell Adhesion; D015936:Complement C5a / Q000737:chemistry / Q000494:pharmacology; D005786:Gene Expression Regulation; D006031:Glycosylation; D006801:Humans; D066298:In Vitro Techniques; D007375:Interleukin-1 / Q000235:genetics* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000502:physiology*; D008070:Lipopolysaccharides / Q000008:administration & dosage; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011971:Receptors, Immunologic / Q000502:physiology; D017472:Receptors, Interleukin-1; D014158:Transcription, Genetic
D007375:Interleukin-1; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D011971:Receptors, Immunologic; D017472:Receptors, Interleukin-1; D015936:Complement C5a