title: [Influence of intravenous-immunoglobulin on T lymphocyte subsets, NK cell and some cytokines in mice with experimental viral myocarditis].
abstract: This study sought to gain an insight into the immunological pathogenesis of viral myocarditis and the mechanism of therapeutic action of intravenous-immunoglobulin (IVIG) on the disease, BALB/c mice were randomized into four groups: normal control group; "myocarditis model group", inoculated intraperitoneally with CVB3; "IVIG protection group", injected intraperitoneally with CVB3 and IVIG; and "IVIG treatment groups", injected intraperitoneally with CVB3 and IVIG. The amount of T cell in different T cell subsets and the activities of NK cell, IL-1 and IL-2 were assayed using spleen specimen while peripheral blood was used to measure TNF activity. The results showed: that in comparison with normal control, all spleen T cell subsets decreased in amount in myocarditis model group, so did its NK cell activity while its IL-1, IL-2 and TNF activities increased significantly. When compared with myocarditis model group, however, both IVIG protection group and IVIG treatment group showed significant elevation of NK cell activity and T cell subsets but reduced IL-1, IL-2 and TNF activities with no remarkable change in T cell subsets. The results of suggest that the immunological injury mediated by T cells plays a critical role in the pathogenesis of viral myocarditis. The protective and therapeutic effects of IVIG on the murine CVB3 myocarditis and the related immunological evidence of its actions may indicate the prospect that IVIG will become a potent and safe treatment for viral myocarditis in human.
authors.affiliation: Department of Pediatrics, The Second Affiliated Hospital, WCUMS, Chengdu 610041.
authors.forename: S
authors.initials: S
authors.lastname: Zeng
authors.forename: T
authors.initials: T
authors.lastname: Zhou
authors.forename: Z
authors.initials: Z
authors.lastname: He
authors.forename: Z
authors.initials: Z
authors.lastname: Jin
authors.forename: M
authors.initials: M
authors.lastname: Wang
authors.forename: Z
authors.initials: Z
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Hua
authors.forename: S
authors.initials: S
authors.lastname: Tang
mesh_terms: D000818:Animals; D003384:Coxsackievirus Infections / Q000276:immunology*; D029822:Enterovirus B, Human; D007142:Immunoglobulin gamma-Chains / Q000494:pharmacology*; D007375:Interleukin-1 / Q000276:immunology; D007376:Interleukin-2 / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000276:immunology / Q000821:virology*; D011897:Random Allocation; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D007142:Immunoglobulin gamma-Chains; D007375:Interleukin-1; D007376:Interleukin-2; D014409:Tumor Necrosis Factor-alpha