Modulation effects of human immature and mature dendritic cells on glatiramer acetate specific T cell lines in vitro.
- Author:
Meng-De CAO
1
;
Alessandra SANNA
;
Bao-Guo XIAO
Author Information
1. Department of Microbiology and Immunology, Medical College of Zhengzhou University, Zhengzhou 450052, China. mengdecao@hotmail.com
- Publication Type:Journal Article
- MeSH:
Adult;
Cell Line;
Cytokines;
biosynthesis;
Dendritic Cells;
physiology;
Female;
Glatiramer Acetate;
Humans;
Lymphocyte Activation;
Male;
Middle Aged;
Multiple Sclerosis;
immunology;
Peptides;
immunology;
T-Lymphocytes;
immunology
- From:
Journal of Experimental Hematology
2003;11(4):409-415
- CountryChina
- Language:English
-
Abstract:
A large body of evidence demonstrates that dendritic cells (DC) play a pivotal role in the control of immunity by priming and tolerizing T cells. In multiple sclerosis (MS), autoreactive T cells are proposed to play a pathogenic role by secreting pro-inflammatory cytokines, but comparison studies on the effects of immature and mature dendritic cells on the cytokines profile of antigen-specific T cell lines are lacking. To evaluate the actions of dendritic cell maturation on T cell polarization, the effects of immature and mature dendritic cells derived from MS patients on in vitro proliferative responses, and cytokine production by glatiramer acetate (GA)- specific T cell lines (TCL) derived from MS patients were analyzed. The results demonstrated that it is easy to derive GA-specific TCL from MS patients with high specificity; lipopolysaccharide can efficiently induce DC maturation within 24 hours at a concentration of 5 micro g/ml; mature DC showed higher co-stimulatory capacity of GA-specific TCLs than immature DC. GA-specific TCLs produce dominantly IL-2, IL-4, IFN-gamma and IL-10, but low levels of IL-6. In contrast to immature DC, mature DC enhanced capacity to induce IL-6 and IL-10 secretion, but down-regulate IL-2, IL-4 and IFN-gamma production by GA- specific TCLs. It is concluded that DC maturation status modulating proliferation of TCL and production of cytokines may represent another focus for the study on both immuno-pathogenesis and immunotherapeutic interventions in MS.
