Hofstetter Harald H, Karulin Alexey Y, Forsthuber Thomas G, Ott Patrick A, Tary-Lehmann Magdalena, Lehmann Paul V
Department of Pathology, Case Western Reserve University, Cleveland OH 44106-4943, USA.
J Neuroimmunol. 2005 Dec 30;170(1-2):105-14. doi: 10.1016/j.jneuroim.2005.09.004. Epub 2005 Oct 27.
Experimental allergic encephalomyelitis (EAE) is an animal model of multiple sclerosis. While EAE is mediated by the cytokines produced by specific T cells, the cytokine signature of these effector cells is unresolved. We tested CD4 cells from MOG peptide 35-55 immunized C57BL/6 mice for their peptide induced cytokine production on antigen presenting cells of the respective cytokine knockout mice, or wild type mice. IL-4 and IL-6 production was seen on wild type antigen presenting cells, suggesting that IL-4 and IL-6 are not T cell products. In contrast, IFN-gamma, IL-2 and IL-3 were found to be produced by the MOG specific CD4 cells. Understanding the cognate vs. bystander cytokine production in EAE might help dissect the contribution of cytokines to the pathogenesis of the disease.
实验性自身免疫性脑脊髓炎(EAE)是多发性硬化症的动物模型。虽然EAE由特定T细胞产生的细胞因子介导,但这些效应细胞的细胞因子特征尚未明确。我们检测了用髓鞘少突胶质细胞糖蛋白(MOG)肽35 - 55免疫的C57BL/6小鼠的CD4细胞,观察其在相应细胞因子基因敲除小鼠或野生型小鼠的抗原呈递细胞上诱导肽产生细胞因子的情况。在野生型抗原呈递细胞上观察到白细胞介素-4(IL-4)和白细胞介素-6(IL-6)的产生,这表明IL-4和IL-6不是T细胞产物。相反,发现干扰素-γ(IFN-γ)、IL-2和IL-3是由MOG特异性CD4细胞产生的。了解EAE中同源与旁观者细胞因子的产生可能有助于剖析细胞因子在该疾病发病机制中的作用。