title: Frequency of Valpha24+CD161+ natural killer T cells and invariant TCRAV24-AJ18 transcripts in atopic and non-atopic individuals.
abstract: Th2 cells play a central role in type I allergies. However, the source of interleukin-4 which may lead to a Th1/Th2 imbalance is unknown. Valpha24+CD161+ Natural killer T (NKT) cells secrete high amounts of interleukin-4 and/or interferon-gamma and are assumed to participate in the initiation of Th1/Th2 immune responses. Their contribution to the development of Th2-dependent type I allergies is controversial. Our objective in this paper was to determine whether Valpha24+CD161+ NKT cells differ in atopic and non-atopic adults. Venous blood was obtained from thirteen atopic and sixteen healthy adult probands. Valpha24+CD161+ NKT cells were determined in CD4+, CD8(bright/dim) and CD4-CD8- lymphocytes by flow cytometry. At the molecular level, the amounts of T cell receptor (TCR) AV24-AJ18 transcripts were quantified with respect to TCRAV24 chain transcripts alone or to all TCR alpha chain transcripts. To detect potential inserted nucleotides in the N-region, a novel real-time PCR-based technology was applied. Both CD4+ and CD4-CD8- NKT cells were present at higher frequencies than CD8+ NKT cells in all probands. CD8(dim) NKT cell levels were lower in healthy individuals, although not statistically significantly different to the patients. Amounts of AV24-AJ18 transcripts in relation to total TCR alpha-chains and to TCRAV24 alone were equal in both proband groups. N-region diversity was detected in four clones from four different individuals, but altered the amino acid sequence in only one clone of an atopic donor. Analysis of Valpha24+CD161+ NKT cell frequencies at both the cellular and molecular levels failed to reveal significant differences in peripheral blood of atopic and non-atopic probands. If NKT cells contribute to development of type I allergies they must do so at earlier times or in other locations.
authors.affiliation: Childrens Hospital, Ludwig-Maximilians-University, Munich, Germany.
authors.forename: Christine
authors.initials: C
authors.lastname: Prell
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Konstantopoulos
authors.forename: Beatrix
authors.initials: B
authors.lastname: Heinzelmann
authors.forename: Bernhard
authors.initials: B
authors.lastname: Frankenberger
authors.forename: Dietrich
authors.initials: D
authors.lastname: Reinhardt
authors.forename: Dolores J
authors.initials: DJ
authors.lastname: Schendel
authors.forename: Susanne
authors.initials: S
authors.lastname: Krauss-Etschmann
mesh_terms: D000328:Adult; D000954:Antigens, Surface / Q000378:metabolism; D001483:Base Sequence; D016022:Case-Control Studies; D018076:DNA, Complementary / Q000235:genetics; D015332:Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor; D019673:Genes, T-Cell Receptor alpha; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000235:genetics* / Q000276:immunology*; D007371:Interferon-gamma / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000276:immunology*; D037181:Lectins, C-Type / Q000378:metabolism; D055651:NK Cell Lectin-Like Receptor Subfamily B; D010641:Phenotype; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014158:Transcription, Genetic
chemical_list: D000954:Antigens, Surface; D018076:DNA, Complementary; C527203:KLRB1 protein, human; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D015847:Interleukin-4; D007371:Interferon-gamma