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H-2 Gene Control of Resistance to P815-X2 Mastocytoma¹

Section of Medical Oncology, Departments of Medicine and Microbiology-Immunology and the Cancer Center, Northwestern University Medical School, Chicago, Illinois 60611

Some, but not all, mutations at H-2 loci can alter, in either direction, histocompatible tumor resistance in the model system of P815-X2 mastocytoma (DBA/2 origin) transplanted into DBA/2J or (C57BL/6 x DBA/2J)F₁ mice. This hybrid effect has been shown previously to depend on the immune system. We have examined eight mutants at H-2K^b (bm1, bm4, bm6, bm7, bm8, bm10, bm11, and bm16, two at H-2D^b (bm13 and bm14), and one I-A^b mutant (bm12). When one parent is an H-2^b mutant (C57BL/6 mutant), the hybrid progeny (C57BL/6 mutant x DBA/2J)F₁ may have increased (bm7 and bm8) or decreased (bm10, bm11, bm12, and bm16) survival times when compared to (C57BL/6 x DBA/2J)F₁ controls. Hybrids from bm1, bm4, bm6 (all H-2K^b), and bm13 and bm14 (both H-2D^b) mutants showed no differences in survival. Several of the mutant molecules differ from those of the parental strain by only one or two amino acids. Apparently, these small changes in H-2 antigens are capable of altering resistance to a histocompatible tumor to produce an immune response gene-like effect.

The availability of H-2 mutant strains and detailed data on the molecular nature of the gene products make the model presented in this report a particularly useful system to study.

¹ Supported in part by Grants CA 27599, CA 27955, and AI 16919 from the NIH.

² To whom requests for reprints should be addressed.

Received 2/16/83. Accepted 8/31/83.