title: CD4-CD8- T cells bearing invariant Valpha24JalphaQ TCR alpha-chain are decreased in patients with atopic diseases.
abstract: Atopic disorders are caused by disregulated activation of T helper 2 (Th2) cells that produce IL-4 and IL-5. Because the presence of IL-4 potently augments the differentiation of naive T cells into Th2 cells, it is important to seek the cell population which provides IL-4 for naive T cells. Recently, a unique subpopulation of T cells, natural killer (NK) T cells, has been shown to produce a large amount of IL-4 upon activation, suggesting their regulatory role in initiation of Th2 cell differentiation. To determine whether NK T cells play a regulatory role in human Th2 cell-mediated atopic diseases, we analysed the frequency of invariant Valpha24JalphaQ CD4-CD8- double-negative (DN) T cells, human NK T cells, in patients with atopic asthma and atopic dermatitis. We also studied cytokine production from Valpha24+ Vbeta11+ DN T cells, which comprise most of Valpha24JalphaQ DN T cells. We found that the invariant Valpha24JalphaQ DN T cells were greatly diminished in patients with asthma and atopic dermatitis. On the other hand, there was no significant difference in Valpha24+ CD4+ T cells possessing invariant Valpha24JalphaQ TCR between healthy subjects and atopic patients. We also found that Valpha24+ Vbeta11+ DN T cells from healthy subjects predominantly produced interferon-gamma (IFN-gamma) but not IL-4 upon activation. These results suggest that NK T cells may not be essential for human atopic disease and that the disappearance of NK T cells, most of which produce IFN-gamma, may be involved in the pathogenesis of atopic diseases.
authors.affiliation: Department of Internal Medicine II, Chiba University School of Medicine, Chiba, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Oishi
authors.forename: A
authors.initials: A
authors.lastname: Sakamoto
authors.forename: K
authors.initials: K
authors.lastname: Kurasawa
authors.forename: H
authors.initials: H
authors.lastname: Nakajima
authors.forename: A
authors.initials: A
authors.lastname: Nakao
authors.forename: N
authors.initials: N
authors.lastname: Nakagawa
authors.forename: E
authors.initials: E
authors.lastname: Tanabe
authors.forename: Y
authors.initials: Y
authors.lastname: Saito
authors.forename: I
authors.initials: I
authors.lastname: Iwamoto
mesh_terms: D000293:Adolescent; D000328:Adult; D015704:CD4 Antigens / Q000276:immunology; D016827:CD8 Antigens / Q000276:immunology; D002454:Cell Differentiation; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000473:pathology; D007135:Immunoglobulin Variable Region / Q000276:immunology; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology
chemical_list: D015704:CD4 Antigens; D016827:CD8 Antigens; D007135:Immunoglobulin Variable Region; D016693:Receptors, Antigen, T-Cell, alpha-beta