title: Regulation of inhibitory and activating killer-cell Ig-like receptor expression occurs in T cells after termination of TCR rearrangements.
abstract: A small fraction of T cells expresses killer-cell Ig-like receptors (KIR), a family of MHC class I-specific receptors that can modulate TCR-dependent activation of effector functions. Although KIR(+) cells are enriched within Ag-experienced T cell subsets, the precise relationships between KIR(+) and KIR(-) T cells and the stage of KIR induction on these lymphocytes remain unclear. In this study, we compared KIR(-) and KIR(+) alphabeta T cell clones, sorted by means of the CD158b (KIR2DL2/KIR2DL3/KIR2DS2) specific mAb GL183. We isolated several pairs of CD158b(+) and CD158b(-) alphabeta T cell clones sharing identical productive and nonproductive TCR transcripts. We showed that expression of functional KIR on T cells is regulated after termination of TCR rearrangements. Transcriptional regulation of KIR genes was documented in multiple T cell clones generated from the same donor, and the presence of KIR transcripts was also detected in KIR(-) T cells. These results document a complex regulation of KIR expression in T cells at both pre and posttranscriptional levels, under the control of yet undefined signals provided in vivo.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Unité 463, Institut de Biologie, Nantes, France.
authors.forename: F
authors.initials: F
authors.lastname: Vely
authors.forename: M
authors.initials: M
authors.lastname: Peyrat
authors.forename: C
authors.initials: C
authors.lastname: Couedel
authors.forename: J
authors.initials: J
authors.lastname: Morcet
authors.forename: F
authors.initials: F
authors.lastname: Halary
authors.forename: F
authors.initials: F
authors.lastname: Davodeau
authors.forename: F
authors.initials: F
authors.lastname: Romagne
authors.forename: E
authors.initials: E
authors.lastname: Scotet
authors.forename: X
authors.initials: X
authors.lastname: Saulquin
authors.forename: E
authors.initials: E
authors.lastname: Houssaint
authors.forename: N
authors.initials: N
authors.lastname: Schleinitz
authors.forename: A
authors.initials: A
authors.lastname: Moretta
authors.forename: E
authors.initials: E
authors.lastname: Vivier
authors.forename: M
authors.initials: M
authors.lastname: Bonneville
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D019556:COS Cells; D002454:Cell Differentiation / Q000235:genetics / Q000276:immunology; D002460:Cell Line; D002461:Cell Line, Transformed; D002999:Clone Cells; D005786:Gene Expression Regulation / Q000276:immunology; D015332:Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor; D015333:Gene Rearrangement, beta-Chain T-Cell Antigen Receptor; D004854:Herpesvirus 4, Human / Q000276:immunology; D006801:Humans; D008213:Lymphocyte Activation / Q000235:genetics; D008969:Molecular Sequence Data; D012323:RNA Processing, Post-Transcriptional / Q000276:immunology; D016364:Reading Frames / Q000276:immunology; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000096:biosynthesis / Q000235:genetics*; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000235:genetics; D054340:Receptors, KIR; D054343:Receptors, KIR2DL2; D054344:Receptors, KIR2DL3; D016176:T-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*; D014158:Transcription, Genetic / Q000276:immunology
chemical_list: C515077:KIR2DL2 protein, human; C515078:KIR2DL3 protein, human; D016693:Receptors, Antigen, T-Cell, alpha-beta; D011971:Receptors, Immunologic; D054340:Receptors, KIR; D054343:Receptors, KIR2DL2; D054344:Receptors, KIR2DL3