Effect Of Glucocorticoid On CD4～+CD25～+ Regulatory T Cells In Mice With Experimental Autoimmune Encephalomyelitis(EAE)

Multiple sclerosis(MS) is mainly induced by T lymphocytes and characterized by demyelinating lesions accompanying with variable degree of axonal changes in central nerves systems (CNS). In corresponding animal model, experimental autoimmune encephalomyelitis (EAE) is a kind of delayed hypersensitivity autoreactive disease and induced by T helper cells and limited within CNS, which is also taken as an ideal model of human MS. Clinically, glucocorticoid is used as the first choice of curing acute and repeated MS to modify the immune system through multiple pathways.Our research was included in the following three parts:Firstly, MBP was isolated from bovine spine with chloroform-methanol and was injected in BALB / c with Bordetella pertussis bacili to induce EAE and evaluated by scores.Secondly, PBMCs were isolated after glucocorticoid treatment. CD4~+CD25~+FOXP3~+ regulatory T cells and the sera inhibitory cytokines IL-10 was tested..Thirdly, Enriched CD4~+ CD25~+ regulatory T cells from glucocorticoid-treatment groups by FACS were transfused into MBP-treated mice.Our corresponding results were as the following.Firstly, MBP and isolated and induce EAE in BALB / c mice successfully.Secondly, glucocorticoid treatment can delay the pathological process. CD4~+CD25~+FOXP3~+ regulatory T cells numeration was dominantly higher the control and untreated groups. Within the glucocorticoid treatment group, IL-10 was higher than the control and the untreated groups. No difference was found within the control and the untreated group.Thirdly, the isolated CD4~+CD25~+ regulatory T cells can inhibit EAE successfully after transfusion.Our research supplied the powerful evidence for pathogenesis and clinical treatment with glucocorticoid, and which set up base for the potential judgment of pathological process, prognosis and treatment.