A. Saoudi et al., HUMAN-IMMUNOGLOBULIN PREPARATIONS FOR INTRAVENOUS USE PREVENT EXPERIMENTAL AUTOIMMUNE UVEORETINITIS, International immunology, 5(12), 1993, pp. 1559-1567
We have evaluated the effect of human Igs for intravenous use (IVIg) o
n the onset and development of experimental autoimmune uveoretinitis (
EAU), a T cell-dependent autoimmune disease induced in rats by a singl
e immunization with retinal S-antigen (S-Ag). Five consecutive dally i
nfusions of IVIg, starting on the same day as S-Ag immunization, prote
cted (Lewis x Brown - Norway) F1 rats against EAU. The prevention of E
AU was IVIg-specific, i.e. mediated by pooled human IgG from multiple
donors, since neither infusions of BSA nor infusions of pooled Ig from
only two healthy individuals were effective. Treatment with IVIg decr
eased lymphocyte proliferative and antibody responses to S-Ag and the
proliferative response to concanavalin A. Lack of proliferation was no
t dependent upon generation of suppressor cells. Lymph node (LN) cells
from IVIg-treated and S-Ag-immunized animals neither proliferated nor
secreted IL-2 in response to S-Ag but proliferated when co-cultured w
ith LN cells from rats immunized with S-Ag. Our findings are compatibl
e with an induction of a state of functional inactivation/energy of T
lymphocytes by infusions of IVIg. This functional inactivation may be
due to the presence in IVIg of antibodies that bind both in vivo and i
n vitro to rat lymphocytes. Results from the present study suggest a n
ovel mechanism by which IVIg may be beneficial in human autoimmune dis
eases.