A. Achiron et al., Suppression of experimental autoimmune encephalomyelitis by intravenously administered polyclonal immunoglobulins, J AUTOIMMUN, 15(3), 2000, pp. 323-330
Experimental autoimmune encephalomyelitis (EAB) was induced in Lewis rats e
ither by active immunization with myelin basic protein (MBP) or by adoptive
transfer using anti-MBP specific CD4(+) T cells. Treatment with human poly
clonal immunoglobulins (IgG) effectively suppressed active EAE. Time-depend
ent experiments demonstrated that the effect of IgG was manifested only whe
n treatment was given immediately after immunization; administration from d
ay 7 after disease induction did not suppress the disease. in the adoptive
transfer model of EAE, IgG had no effect in vivo. However, pretreatment in
vitro of the antigen-specific T-cells with IgG inhibited their ability to m
ediate adoptive EAE, as it did in active EAE. Similarly, in vitro IgG pretr
eatment of the antigen-specific T-cells suppressed the proliferative respon
se to MBP. Fluorescent Activated Cell Sorter (FACS) analysis demonstrated t
he binding of IgG to activated T-cell lines that was inhibited by soluble F
e molecules. The differential effects of IgG on active EAE and on the adopt
ive transfer of EAE suggest that IgG in vivo can suppress disease by acting
during the early phase of the immune response which involves naive T cells
. The inhibition of T-cell proliferation and adoptive transfer of EAE by in
cubation of T cells in vitro appears to require higher concentrations of Ig
G than those obtained in vivo. (C) 2000 Academic Press.