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Several years ago, we reported that T cells from (responder × nopresponder) F1 hybrids primed to the synthetic terpolymer, L-glutamic acid, L-lysine, L-tyrosine (GLT), 1 to which responses are governed by H-2-1inked Immune response-GLT genes, were restricted in their ability to provide GLT-specific help for 2,4-dinitrophenyl (DNP)-primed B cells from the respective parental mice in response to DNP-GLT (1). Thus, such F1 T cells were able to provide normal helper activity for DNP-specific B cells from responder, but not from nonresponder, donor mice. This finding contrasted sharply with the indiscriminant ability of F1 T cells to interact effectively with partner B cells from either parent when the carrier antigen employed was not one to which responses were governed by a known Ir gene. This observation has subsequently been confirmed by others in studies conducted in mice (2, 3) and guinea pigs (4).These observations were interpreted as an indication that in heterozygous individuals independent subpopulations of interacting T lymphocytes existed, one each corresponding to the respective parental type (1,5,6). Hence, we envisaged that stimulation of a (responder × nonresponder) F1 T-cell population by GLT would sensitize only the population of T cells able to recognize and react with the functional cell-interaction (CI) phenotype of the responder parent; F1 T cells corresponding to the nonresponder parent CI phenotype would not be stimulated by GLT. This situation would therefore be manifested as the defective ability of F1 T cells to interact with nonresponder B cells, irrespective of the antigen specificity of the latter. This original interpretation (1, 5, 6) has been reinforced by the subsequent demonstrations of the existence of independent Wl T-cell subpopulations that are reactive with each respective parental CI phenotype (7-12).

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Immunization of female SJL mice with an emulsion of lyophilized mouse spinal cord, pertussis vaccine, and complete Freund's adjuvant produces a delayed and often relapsing form of experimental allergic encephalomyelitis (DR-EAE). The mice develop initial signs of disease an average of 6 mo after immunization. Relapses occurred 2 wk to 11 mo after the initial illness. Some animals had multiple relapses. Pathologic examination of the brain and spinal cord revealed perivascular infiltration of mononuclear cells with acute demyelination. Areas of subacute and chronic demyelination ("plaques") were also seen. This model produces a clinical course of relapsing-remitting disease with pathologic evidence of both recent and old inflammatory lesions at various levels of the central nervous system. It thus more closely resembles multiple sclerosis than acute EAE.

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