The putative I-Jk- strain AKR/J synthesizes I-Jk+ molecules: implications for Jt gene control of I-J expression.

At present, the genetic basis for control of murine I-J determinants is unknown. On one hand, it is clear that polymorphism in I-J molecules is controlled by genes mapping in the I region of the H-2 gene complex on chromosome 17. On the other hand, molecular genetic studies provide evidence that I-J molecules are not encoded by I region genes. Although formal proof of the latter must await isolation and characterization of I-J structural genes, these observations are compatible with the concept that I-J molecules are encoded by non-H-2 genes, but the expression of these non-H-2 genes is regulated or influenced by I region genes. Recent studies by Hayes et al. provide evidence for non-H-2 control of the cell surface expression of I-Jk determinants in strain AKR/J. This strain typed I-Jk-, as judged by complement dependent cytolysis with monoclonal I-Jk antibodies. Studies with recombinant inbred and congenic strains suggested that the I-Jk- phenotype in strain AKR/J was controlled by a gene (Jt) mapping on chromosome 4. Based on these observations and studies with F1 hybrids and numerous other strains, Hayes et al. concluded that interaction between the Jt gene and an H-2 gene on chromosome 17 (probably E beta or E alpha) regulates the production and expression of I-Jk molecules, and hypothesized that I-Jk epitopes may reside on Jt modified Class II molecules or on the Jt gene product.(ABSTRACT TRUNCATED AT 250 WORDS)