Glatiramer acetate increases T- and B -regulatory cells and decreases granulocyte-macrophage colony-stimulating factor (GM-CSF) in an animal model of multiple sclerosis

被引：13

作者：

Aharoni, Rina ^{[1
]}

Eilam, Raya ^{[2
]}

Schottlender, Nofar ^{[1
]}

Radomir, Lihi ^{[1
]}

Leistner-Segal, Sandra ^{[1
]}

Feferman, Tali ^{[1
]}

Hirsch, Dana ^{[2
]}

Sela, Michael ^{[1
]}

Arnon, Ruth ^{[1
]}

机构：

[1] Weizmann Inst Sci, Dept Immunol, Herzel St 234,POB 26, Rehovot, Israel

[2] Weizmann Inst Sci, Dept Life Sci Core Facil, Rehovot, Israel

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2020年 / 345卷

关键词：

Multiple sclerosis; Experimental autoimmune encephalomyelitis; T-regulatory cells (Tregs); B-regulatory cells (Bregs); Granulocyte-macrophage colony-stimulating factor (GM-CSF); Glatiramer acetate (GA); MYELIN BASIC-PROTEIN; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; MICE; INDUCTION; CYTOKINES; THERAPY; TARGET;

D O I：

10.1016/j.jneuroim.2020.577281

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

To identify the mechanisms relevant for the therapeutic effect of glatiramer acetate (GA), we studied T- and B-regulatory cells as well as GM-CSF expression in mice recovered from experimental autoimmune encephalomyelitis (EAE). Selective depletion of Tregs reduced but did not eliminate the ability of GA to ameliorate EAE, indicating a role for additional immune-subsets. The prevalence of Bregs in the periphery and the CNS of EAE-mice increased following GA-treatment. Furthermore, GA downregulated the pathological expression of GM-CSF, on both the protein and mRNA levels. These findings corroborate the broad immunomodulatory mechanism of action of GA in EAE/MS.

引用

页数：15

共 54 条

[1] Glatiramer acetate-specific T cells in the brain express T helper 2/3 cytokines and brain-derived neurotrophic factor in situ [J].