By Emil R. Unanue

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Germain, Kapp, J. A. , J. Exp. Med. 146, 1827 (1977). 4. Pierce, C. W. and Kapp, J. , J. Exp. Med. 148, 1282 (1978). 5. Pierce, C. W. and Kapp J. , in "Ir Genes and la Antigens" (H. 0. ), p. 357. Academic Press, New York, (1978). 6. Pierce, C. W. and Kapp, J. , in "Immunology of Proteins and Peptides I" (M. Z. Stavitsky and A. B. ), p. 419. , New York, (1978). 7. , J. Exp. Med. 142, 460 (1975). 8. Rosenthai, A. S. and Shevach, E. , Contemp. Top. Immunobiol. 5, 47 (1976). 9. Rosenthal, A. , Immunol.

Incubation of M0-depleted responder spleen cells under Mishell-Dutton conditions for two days with J> 10 yg/ml of GAT induces potent GAT-Ts, able to specifically inhibit the primary PFC response of syngeneic spleen cells to soluble GAT. Similar T s can also be induced with unseparated spleen cells and 5 to 10 times higher concentrations of GAT. Such T s fail to suppress the primary PFC response to the related polypeptide antigen GT (as GT-MBSA). These results raise several important issues about M0 function and suppressor cell induction.

These data are quite distinct from those obtained using GAT, which regularly stimulates primary PFC responses when presented on NR-M0. It is unlikely that the results in the GAT model are solely a reflection of antigen transfer to R-M0 since: 1) in the secondary cultures, such transfer to the Fi M0 would lead to responses due to GAT-H-2t> antigen presentation, and such responses are not seen; and 2) NR mice can be primed with and can respond to GAT under the appropriate circumstances in the absence of any R-M0 (see above).

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