title: T cell clonal anergy.
abstract: Recent experiments have elucidated two molecular mechanisms that may account for the failure of anergic T cell clones to initiate IL-2 gene transcription following TCR stimulation. First, a block has been identified in the ERK and JNK mitogen-activated protein kinase pathways; the block results from a failure to activate p21ras. It leads to reduced induction of c-Fos and JunB proteins and to a failure to form and phosphorylate the activator protein (AP)-1 heterodimers required for IL-2 gene transcriptional activation. Second, repressor molecules (Nil-2-a and a molecule related to AP-1) have been characterized that dominantly inhibit IL-2 gene transcription.
authors.affiliation: Laboratory of Cellular and Molecular Immunology, National Institutes of Health, Bethesda, MD 20892-0420, USA. rs34r@nih.gov
authors.forename: R H
authors.initials: RH
authors.lastname: Schwartz
mesh_terms: D000818:Animals; D006801:Humans; D007376:Interleukin-2 / Q000235:genetics / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014158:Transcription, Genetic
chemical_list: D007376:Interleukin-2; D011948:Receptors, Antigen, T-Cell