myelin-oligodendrocyte-glycoprotein-(35-55) and Encephalomyelitis

myelin-oligodendrocyte-glycoprotein-(35-55) has been researched along with Encephalomyelitis* in 1 studies

Other Studies

1 other study(ies) available for myelin-oligodendrocyte-glycoprotein-(35-55) and Encephalomyelitis

Article	Year
Estrogen inhibits systemic T cell expression of TNF-alpha and recruitment of TNF-alpha(+) T cells and macrophages into the CNS of mice developing experimental encephalomyelitis. Clinical immunology (Orlando, Fla.), 2002, Volume: 102, Issue:3 Estrogen treatment has been found to have suppressive activity in several models of autoimmunity. To investigate the mechanism of 17 beta-estradiol (E2) suppression of experimental autoimmune encephalomyelitis, we evaluated E2 effects on TNF-alpha expression in the central nervous system (CNS) and spleen of C57BL/6 mice immunized with MOG 35-55/CFA. Kinetic analysis demonstrated that E2 treatment drastically decreased the recruitment of total inflammatory cells as well as TNF-alpha(+) macrophages and T cells into the CNS at disease onset. In contrast, E2 had only moderate effects on the relatively high constitutive TNF-alpha expression by resident CNS microglial cells. E2 treatment also had profound inhibitory effects on expression of TNF-alpha by splenic CD4(+) T cells, including those responsive to MOG 35-55 peptide. We propose that the mechanism of E2 protection may involve both systemic inhibition of TNF-alpha expression and local (CNS) recruitment of inflammatory cells, with modest effects on TNF-alpha expression by resident CNS microglial cells. Topics: Animals; Central Nervous System; Disease Models, Animal; Encephalomyelitis; Estradiol; Female; Flow Cytometry; Glycoproteins; Kinetics; Macrophages; Mice; Mice, Inbred C57BL; Microglia; Myelin-Oligodendrocyte Glycoprotein; Nerve Tissue Proteins; Peptide Fragments; Spleen; T-Lymphocytes; Tumor Necrosis Factor-alpha	2002

Article

Year

Estrogen inhibits systemic T cell expression of TNF-alpha and recruitment of TNF-alpha(+) T cells and macrophages into the CNS of mice developing experimental encephalomyelitis.

Clinical immunology (Orlando, Fla.), 2002, Volume: 102, Issue:3

Estrogen treatment has been found to have suppressive activity in several models of autoimmunity. To investigate the mechanism of 17 beta-estradiol (E2) suppression of experimental autoimmune encephalomyelitis, we evaluated E2 effects on TNF-alpha expression in the central nervous system (CNS) and spleen of C57BL/6 mice immunized with MOG 35-55/CFA. Kinetic analysis demonstrated that E2 treatment drastically decreased the recruitment of total inflammatory cells as well as TNF-alpha(+) macrophages and T cells into the CNS at disease onset. In contrast, E2 had only moderate effects on the relatively high constitutive TNF-alpha expression by resident CNS microglial cells. E2 treatment also had profound inhibitory effects on expression of TNF-alpha by splenic CD4(+) T cells, including those responsive to MOG 35-55 peptide. We propose that the mechanism of E2 protection may involve both systemic inhibition of TNF-alpha expression and local (CNS) recruitment of inflammatory cells, with modest effects on TNF-alpha expression by resident CNS microglial cells.

Topics: Animals; Central Nervous System; Disease Models, Animal; Encephalomyelitis; Estradiol; Female; Flow Cytometry; Glycoproteins; Kinetics; Macrophages; Mice; Mice, Inbred C57BL; Microglia; Myelin-Oligodendrocyte Glycoprotein; Nerve Tissue Proteins; Peptide Fragments; Spleen; T-Lymphocytes; Tumor Necrosis Factor-alpha

2002