Isotype effects of anti-MHC antibodies on inhibition of graft-versus-host splenomegaly in the chicken
W. E. Briles, W. H. McGibbon, and M. R. Irwin, in 1950, identified the genes of the chicken MHC (B complex) which control histocompatibility antigens. Identification of these genes as part of the MHC complex was accomplished in part by means of graftversus- host (GVH) splenomegaly and inhibition of graft-versus-host splenomegaly (GVH-I) by specific anti-B alloantisera. In the course of their testing, several antisera were identified which did not inhibit splenomegaly as expected. These antisera were made by similar donor/recipient combinations and were of the same specificity (anti-B-F24) as antisera that did inhibit splenomegaly. Six alloantisera were separated into IgM and IgG fractions by gel filtration and tested for their ability to inhibit splenomegaly. Of the 6 alloantisera, 2 inhibited splenomegaly, 2 did not inhibit splenomegaly, and the other 2 were not previously tested. The alloantisera and the IgM and IgG fractions were tested for specific antibody titer by agglutination assay and by cellular radioimmunoassay. In those cases where the whole alloantisera was capable of inhibiting splenomegaly, the IgG fraction contained a significant proportion of the total inhibitory activity. The cellular radioimmunoassay titer of these IgG fractions was correspondingly high. In whole alloantisera which did not inhibit splenomegaly, the IgG fractions also did not inhibit splenomegaly and there was a correspondingly low cellular radioimmunoassay titer. The IgM fractions in all six alloantisera showed no significant inhibition, regardless of agglutination or cellular radioimmunoassay titer. In addition to the chicken alloantisera, a mouse monoclonal anti-B-L antibody was tested for ability to inhibit splenomegaly. Despite significant reactivity to lymphocytes, as shown by fluorescent immunoassay, there was no inhibition of splenomegaly.