Analysis of the role of STAT6 signaling in the induction of CHS

接触性超敏反应（CHS）被认为主要与辅助性t细胞（Th） 1的激活有关。然而，也有证据表明Th2细胞或Th2细胞因子在CHS的发展中起作用。为了分析Th2细胞因子、IL-4和IL-13的功能贡献，将STAT6缺陷（STAT6-/-）和野生型对照（wt）小鼠（C57BL/6）分别用5% TNCB、0.5% DNFB或5% Oxa接触致敏，然后观察任何皮肤反应。与wt小鼠相比，STAT6-/-小鼠的耳部肿胀明显减少，峰值反应延迟。组织学分析显示，与wt小鼠相比，STAT6-/-小鼠皮肤中嗜酸性粒细胞和中性粒细胞的浸润在24小时后显著减少。STAT6-/-小鼠的皮肤组织和TNBS修饰脾细胞刺激的T细胞上清液中Th2细胞因子（IL-4、IL-5）的表达以及攻毒后的IgE和IgG1反应也显著降低，而IFN γ的表达在STAT6-/-小鼠和wt小鼠中相同。此外，过继转移实验显示，注射致敏wt小鼠的淋巴结细胞后，STAT6-/-小鼠诱导了接触性超敏反应。我们的数据表明，STAT6信号在CHS的i诱导阶段起着关键作用。

Contact hypersensitivity (CHS) is thought to be mainly associated with the activation of T-helper (Th) 1 cells. However, there is also evidence that Th2 cells or Th2 cytokines play a role in the development of CHS.In order to analyze the functional contribution of Th2 cvtokines, IL-4 and IL-13, STAT6 deficient (STAT6-/-) and wild-type control (wt) mice (C57BL/6) were contact sensitized with 5% TNCB, 0.5 % DNFB or 5% Oxa, and then any skin reactions were examined. Ear swelling was significantly reduced with a delayed peak response in STAT6-/- mice as compared with wt mice.A histological analysis revealed that the infiltration of both eosinophils and neutrophils in the skin challenged after 24 h in STAT6-/- mice decreasead substantially in comparison with that in wt mice. The expression of Th2 cytokines (IL-4, IL-5 ) in TNCB-challenged skin tissues and the supernatants from T cells stimulated by TNBS -modified spleen cells as well as the IgE and IgG1 response after challenge were also profoundly reduced in STAT6-/- mice, whereas the expression of IFN γ was the same in STAT6-/- mice and wt mice after challenge. Furthermore, Adoptive transfer experiments revealed that STAT6-/- mice induced the contact hypersensitivity after injection of lymph node cells obtained from sensitized wt mice.Our data suggest that the STAT6 signal palys a critical role in the i nductionphase of CHS.