Participation of Inkt Cells in the Early and Late Components of Tc1-Mediated DNFB Contact Sensitivity: Cooperative Role of γδ-T Cells
Participation of Inkt Cells in the Early and Late Components of Tc1-Mediated DNFB Contact Sensitivity: Cooperative Role of γδ-T Cells
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DOI：
10.1111/j.1365-3083.2011.02522.x
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发表时间：
2011-05-01
影响因子：
3.7
通讯作者：
Szczepanik, M.
中科院分区：
文献类型：
--
作者：
Askenase, P. W.;Majewska-Szczepanik, M.;Szczepanik, M.
TNP-Cl（苦基氯）过敏性接触敏感性（CS）的经典24小时应答的先前研究显示CBA小鼠中Th 1细胞的介导，并确定24小时应答的激发需要依赖于iNKT细胞、IL-4和B-1 B细胞的早期2小时CS起始组分。在这里，我们研究了DNFB致敏的BALB/c小鼠中另一种形式的细胞毒性T细胞（Tc 1）CS，并确定也需要类似的CS启动。我们系统地测试了该模型中起始途径的每一步。因此，DNFB Tc 1 CS在iNKT细胞缺陷型CD 1d-/-和J α 18-/-小鼠、IL 4 R α-/-和STAT-6-/-小鼠以及泛B细胞缺陷型JH-/-小鼠中显著受损。此外，由于B-1细胞，Tc 1 DNFB CS起始成分（如Th 1对TNP-Cl的反应）仅在免疫后1天就被激发。总之，我们表明，CS启动也需要在TC 1 CS。此外，我们已经新确定了DNFB诱导的Tc 1 CS的早期和晚期成分的iNKT细胞和γ δ-T细胞的监管支持。总之，iNKT细胞和辅助γ δ-T细胞都参与DNFB诱导的CS的起始和效应阶段。
Prior studies of classical 24 h responses in TNP-Cl (picryl chloride) allergic contact sensitivity (CS), showed mediation by Th1 cells in CBA mice, and established that 24 h elicitation of responses requires an early 2 h CS-initiating component dependent on iNKT cells, IL-4 and B-1 B cells. Here, we studied the other form of cytotoxic T cell (Tc1) CS in DNFB sensitized BALB/c mice and determined that similar CS-initiation also is required. We systematically tested each step of the initiation pathway in this model. Thus, DNFB Tc1 CS was significantly impaired in iNKT cell deficient CD1d-/- and J alpha 18-/- mice, IL4R alpha-/- and STAT-6-/- mice, and also in pan B-cell deficient JH-/- mice. Further, the Tc1 DNFB CS-initiating component, like Th1 response to TNP-Cl, was elicited by only 1-day after immunization, due to B-1 cells. In summary, we show that CS-Initiation also is required in Tc1 CS. Further, we have newly determined regulatory support of both the early and late components of DNFB induced Tc1 CS by iNKT cells and gamma delta-T cells. In summary, both iNKT cells and assisting gamma delta-T cells are involved in initiating and effector phases of DNFB induced CS.