Abstract

Allergic encephalomyelitis (AE) is widely accepted as a promising model system for incisive studies of auto-immunity (1,2). All evidence suggests that the disease results from an immune response called forth by injected nervous tissue emulsified in Friend's adjuvant and directed against unique antigenic constituents in the nervous system of the sensitized host. Still unsettled, however, is the nature of the immune response and precisely how it interacts with its “target”— the neuraxis(3,4). The strongest evidence that sensitized cells, rather than circulating antibodies, are the immunological instruments of tissue injury has been the successful transfer of AE in rats and other animals by means of sensitized lymphoid cells, in contrast to the lack of transfer with immune serum(5–8). In previous AE-transfer studies reported from this laboratory, the donor lymphoid cells were injected into the recipient rats via the intravenous route(3–5,9). The purpose of this paper is to describe transfer of the disease in rats using the intracerebral route. In circumventing the undefined role of the blood-brain-barrier and insuring immediate and direct contact between donor cells and “target” the intracerebral route offers an additional and particularly advantageous system for the study of AE. Methods. Donor rats and cell suspensions. Rats of the Lewis strain were employed as donors. This is a highly inbred and isohistogenic strain based on skin grafting criteria (10). The donors were sensitized by intracutaneous injection of 0.7 ml (0.1 ml in each of 7 sites) of a standard guinea pig spinal cord-adjuvant inoculum as described previously(5,9). The donors were sacrificed 9 days after sensitization—a time previously found to be optimal for intravenous transfer of AE within the Lewis rat strain(4). Lymph nodes draining injection sites (cervical, paratracheal, axillary and pectoral) were processed following previously described methods (5,9).

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