Role of Valpha24JalphaQ TCR T Cells in the Pathogenesis of Asthma

特应性疾病是由产生IL-4和IL-5的辅助性T细胞（Th2）的激活失调引起的，因为IL-4的存在有力地增强了幼稚T细胞向Th2细胞的分化，因此寻找能够为幼稚T细胞提供IL-4的细胞群是很重要的。最近，一种独特的T细胞亚群，自然杀伤（NK） T细胞，被证明在激活后产生大量的IL-4，表明它们在Th2细胞分化的起始过程中起调节作用。为了确定NK T细胞是否在人类Th2疾病中发挥作用，我们分析了哮喘和特应性皮炎（AD）患者的NK T细胞。我们对不变的Valpha24JalphaQ CD4^- cd8 ^- T细胞（可能是人类NK T细胞）进行了频率分析，发现哮喘和AD患者的NK T细胞显著减少。此外，我们发现大多数健康人NK T细胞在激活后产生ifn - γ，但不产生IL-4。综上所述，这些结果表明产生IFN-y的NK T细胞的减少可能与哮喘和AD等特应性疾病的发病机制有关。

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 role in human Th2 diseases, we analyzed the NK T cells in patients with asthma and atopic dermatitis (AD). We performed a frequency analysis of the invariant Valpha24JalphaQ CD4^-CD8^- T cells, probable human NK T cells, and found that the NK T cells are significantly decreased in patients with asthma and AD.In addition, we found that the majority of human NK T cells from healthy subjects produce IFN-gamma but not IL-4 upon activation. Taken together, these results suggest that the decrease of NK T cells, which produce IFN-y, may be involved in the pathogenesis of atopic diseases, such as asthma and AD.