A panel of commonly used inbred mouse strains was typed for the alleles of the H-1, H-3, H-4, H-7, H-8, H-9, H-12, and H-13 histocompatibility loci using histogenetic techniques. Typing revealed new alleles at all loci with the exception of H-1. Because of the inability to type for the null antigen of the H-1b allele, we could not distinguish between strains possessing H-1b and those possessing ... [Show full abstract] new alleles. The strengths of the non-H-2 antigens varied from the relatively strong H-1c antigen to the extremely weak H-9b antigen. The immune response of 3 F1 groups, CBA/J, DBA/2J, and DBA/1Sn x CR partner, appeared weaker than that of the remaining groups. In general, related strains showed fewer histocompatibility differences than unrelated strains.