The H-2 class II genes and the susceptibility to the development of pulmonary adenoma in mice.

To determine the locus in the H-2 complex that affects susceptibility to the development of pulmonary adenomas in mice, H-2 congenic and recombinant strains of mice with A/Wy, BALB/c, C3H, and B10 backgrounds were subjected to treatment with urethane. The average number and the incidence of adenoma foci were recorded five months after the treatment. In H-2 congenic strains on the A/Wy background, the average number of adenoma foci per mouse was significantly higher in mice of the A/Wy, A/J, and A-Tlab (H-2a) strains than in A.BY (H-2b) mice. In BALB/c and C3H congenic strains, the strains carrying the H-2k haplotype were more susceptible than those carrying the H-2b haplotype. In H-2 congenic strains on the B10 background, the average number and incidence of foci was also higher in haplotypes a, h2, k, and j than in haplotypes b, s, f, d, r, h4, i3, i5, and t4. The average numbers of adenoma foci in (A/J X A.BY)F1 (H-2a/H-2b) and (B10 X B10.A)F1 (H-2b/H-2a) were intermediate between the numbers in the parental strains. In [B10.A(4R) X B10.A (3R)]F1 (H-2h4/H-2i3) and [B10.A(4R) X B10.A(5R)]F1 (H-2h4/H-2i5), the numbers of adenoma foci were higher than in resistant parental recombinants. These patterns of response to urethane matched the patterns of the immune response to lactate dehydrogenase-B (LDH-B) and immunoglobulin gamma 2a (IgG2a) proteins. These differences between mice in their susceptibility to the development of pulmonary adenomas is probably due to the polymorphism of the class II genes in the H-2 complex.