Marcinkiewicz J, Chain B M
Department of Immunology, Medical Academy of Cracow, Poland.
Cell Immunol. 1993 Feb;146(2):406-11. doi: 10.1006/cimm.1993.1036.
We have investigated in vitro the ability of T cells from mice primed for contact hypersensitivity to release cytokines of the TH2 subtype, in particular IL-4 and IL-6. We demonstrate that both these cytokines are indeed produced by T cells from the lymph node and spleen of mice immunized by topical application of picryl chloride and restimulated in vitro by TNP-coupled spleen cells. However, the release of IL-4 is limited by the activity of IFN-gamma, a TH1 cytokine which we have previously shown is also produced after contact sensitization. Finally, induction of tolerance to TNP, by intravenous administration of antigen, or transfer of cells from tolerant mice into naive donors prior to sensitization (which suppresses the contact sensitivity reaction in the recipients) leads to a fall in IL-4 production. Thus neither tolerance nor suppression in this system is mediated by the antagonistic activities of TH1- and TH2-type T cells. In contrast, IL-6 production is upregulated during both suppression and tolerance, suggesting that this cytokine may play a part in the negative regulation of contact sensitivity.
我们已经在体外研究了经接触性超敏反应致敏的小鼠T细胞释放TH2亚型细胞因子，特别是白细胞介素-4（IL-4）和白细胞介素-6（IL-6）的能力。我们证明，这两种细胞因子确实是由经皮内注射苦基氯免疫并在体外由三硝基苯（TNP）偶联的脾细胞再次刺激的小鼠淋巴结和脾中的T细胞产生的。然而，IL-4的释放受到干扰素-γ（IFN-γ）活性的限制，IFN-γ是一种TH1细胞因子，我们之前已经证明其在接触致敏后也会产生。最后，通过静脉内给予抗原诱导对TNP的耐受性，或在致敏前将来自耐受小鼠的细胞转移到未致敏的受体中（这会抑制受体中的接触性超敏反应）会导致IL-4产生下降。因此，该系统中的耐受性和抑制作用均不是由TH1型和TH2型T细胞的拮抗活性介导的。相反，在抑制和耐受过程中IL-6的产生均上调，这表明该细胞因子可能在接触性超敏反应的负调节中起作用。
