title: Differentially induced expression of C-type lectins in activated lymphocytes.
abstract: The human NK gene complex encodes for the leucocyte C-type lectins, CD69, AICL (activation-induced C-type lectin), LLT1 (lectin-like transcript), CD161/NKR-P1A, CD94, and for NKG-2 molecules. These gene products have been implicated in the regulation of the function of natural killer (NK) cells and other lymphocytes. In this study the expression of C-type lectins during the early activation of PMA-stimulated peripheral blood lymphocytes was examined. To investigate the influence of de novo protein synthesis on activation-dependent expression of C-type lectins, cells were cultured in presence of cycloheximide (CHX) and mRNA levels were analyzed by semi-quantitative reverse transcription-polymerase chain reaction. Upregulated levels of CD69, AICL, and LLT1, but less pronounced changes of CD161/NKR-P1A and CD94 mRNA were found at early time points of cellular activation. CD69 was superinduced by CHX at the nuclear precursor transcript and the mRNA level suggesting that regulation of transcriptional activity and mRNA stability contribute to extent of CD69 mRNA accumulation. CHX treatment resulted also in an overexpression of AICL, LLT1, and CD161/NKR-P1A mRNAs. Conversely, CHX blocked CD94 mRNA expression in PMA-stimulated cells, demonstrating that this process is dependent on new protein synthesis. Expression kinetics in context with susceptibility to CHX indicate that the mechanisms responsible for upregulated CD69, AICL, and LLT1 expression are distinct from those which control CD161/NKR-P1A or CD94 expression. J. Cell. Biochem. Suppl. 36: 201-208, 2001.
authors.affiliation: Faculty of Biosciences, Pharmaceutics and Psychology, University of Leipzig, Talstrasse 33, D-04103 Leipzig, Germany. eichwolf@uni-leipzig.de
authors.forename: W
authors.initials: W
authors.lastname: Eichler
authors.forename: P
authors.initials: P
authors.lastname: Ruschpler
authors.forename: M
authors.initials: M
authors.lastname: Wobus
authors.forename: K
authors.initials: K
authors.lastname: Drössler
mesh_terms: D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000235:genetics / Q000378:metabolism; D000954:Antigens, Surface / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D006801:Humans; D037102:Lectins / Q000235:genetics / Q000378:metabolism*; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D055651:NK Cell Lectin-Like Receptor Subfamily B; D051920:NK Cell Lectin-Like Receptor Subfamily D; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000954:Antigens, Surface; D003513:Cycloheximide; D037102:Lectins; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D055651:NK Cell Lectin-Like Receptor Subfamily B; D051920:NK Cell Lectin-Like Receptor Subfamily D; D011500:Protein Synthesis Inhibitors; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D000099192:CD69 Antigens; C104778:CLEC2B protein, human; C400041:CLEC2D protein, human; C527203:KLRB1 protein, human; C497869:KLRD1 protein, human