The
Ehrlich ascites tumor, which has been subjected to prolonged selection for growth in allogeneic hosts, possesses powerful mechanisms for the suppression of
antigens normally found on the cell surface. It has previously been shown (1, 2) that when cells in which
surface antigens are fully expressed are fused with Ehrlich cells, the suppressive mechanisms of the latter continue to operate and the new
surface antigens introduced into the hybrid cell by the other partner are also suppressed. In the present paper we describe the properties of hybrids in which one parent cell was the TA3
ascites carcinoma. There are two sublines of this
carcinoma which originally arose as a spontaneous mammary
carcinoma in a strain A mouse. The TA3/St line has a high concentration of H-2(a)
antigens and shows a strain-specific
transplantation behavior; the TA3/Ha subline has a drastically reduced
antigen concentration and readily transgresses histoincompatibility barriers. The immunoresistant TA3/Ha subline arose spontaneously without having been subjected to any known immunological selection pressure. Hybridization of TA3/Ha cells with normal diploid ACA fibroblasts reestablished full expression of H-2(a)
antigens in nine independently derived hybrid clones. Full reestablishment of both D- and K-end components of the H-2(a) complex could be demonstrated. In some hybrid clones the concentration of H-2(a)
antigens was found to be comparable to that seen in (A x ACA)F(1) fibroblasts, whereas in others a higher concentration was observed, even exceeding, in some cases, the levels found in the TA3/St line. The H-2(f) complex, contributed by the ACA parent cell, was fully expressed in eight of the nine hybrid clones studied.
Antigen suppression thus behaves as a recessive character in the TA3/Ha hybrids, whereas in the Ehrlich hybrids
antigen suppression is dominant.