Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2004 Mar;20(2):129-34
Zhang QH, Cao J, Hu YZ, Huang YH, Lu SY, Wei GZ, Zhao YF.
Department of Physiology, Fourth Military Medical University, Xi'an 710032, China.
To explore the mechanism resulting in the preventive effect of estrogen on experimental autoimmune encephalomyelitis (EAE), which is an animal model for multiple sclerosis (MS), and examine if estrogen can affect the immune response in EAE at dendritic cell(DC) level.
Flow cytometry was used to reveal the surface marker expression.
(3)H-thymidine incorporation was applied to examine the cellular proliferation.
Levels of anti-myelin basic protein(MBP)(68-86) antibody and cytokines were determined by enzyme-linked immunospot and ELISA, respectively.
17beta-estradiol(E2) could dose-dependently accelerate the differentiation process of DCs by up-regulating CD11c, B7-2 and CD40 expressions, but exert no effect on its antigen presentation ability.
MBP-specific T cells cocultured with E2-treated DCs (E2-DC) produced more IL-10 and less IFN-gamma in the supernatant than those without E2 pretreatment(ctr-DC).
In contrast to ctr-DC, E2-DC, if injected i.v. into EAE rats on day 5 post immunization, could initiate antigen nonspecific hyper-responsivity in T cells in terms of enhanced proliferation and cytokine secretion of mononuclear cells in LN, but suppressed antibody secretion from splenocytes.
These results suggest that estrogen can affect the differentiation and function of DCs, which leads T cells switching to Th2 secretion.
This may account partly for the protective effect of estrogen on EAE.