Free Content CD4−CD8− T cells bearing invariant Vα24JαQ TCR α-chain are decreased in patients with atopic diseases

Authors: Oishi, Y.1; Sakamoto, A.1; Kurasawa, K.1; Nakajima, H.1; Nakao, A.1; Nakagawa, N.1; Tanabe, E.1; Saito, Y.1; Iwamoto, I.1

Source: Clinical & Experimental Immunology, Volume 119, Number 3, March 2000 , pp. 404-411(8)

Publisher: Blackwell Publishing

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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 Vα24JαQ 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 Vα24+ Vβ11+ DN T cells, which comprise most of Vα24JαQ DN T cells. We found that the invariant Vα24JαQ DN T cells were greatly diminished in patients with asthma and atopic dermatitis. On the other hand, there was no significant difference in Vα24+ CD4+ T cells possessing invariant Vα24JαQ TCR between healthy subjects and atopic patients. We also found that Vα24+ Vβ11+ DN T cells from healthy subjects predominantly produced interferon-gamma (IFN-γ) 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-γ, may be involved in the pathogenesis of atopic diseases.

Keywords: Vα24JαQ TCR α-chain; natural killer T cells; atopic diseases; interferon-gamma

Document Type: Research article

DOI: 10.1046/j.1365-2249.2000.01157.x

Affiliations: 1: Department of Internal Medicine II, Chiba University School of Medicine, Chiba, Japan

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