Agalactosyl IgG (Gal(0) is a glycoform lacking terminal
galactose from the
oligosaccharides situated on the Fc. The percentage of circulating
IgG that is Gal(0) is increased in a a number of
autoimmune diseases, and in certain
chronic infections associated with
autoantibody production. However it is not known whether this represents decreased galactosylation of all
IgG, or an increase in the relative concentration of a subset of agalactosyl
antibodies of specificity relevant to the disease process. Since there is currently no way to separate agalactosyl from galactosylated
IgG, we devised an assay for the relative degree of galactosylation of antibody to
tetanus toxoid (TT), an
antigen irrelevant to the diseases studied, and compared this value with the %Gal(0) of the whole circulating
IgG. In
rheumatoid arthritis (RA) and
tuberculosis (TB), a raised %Gal(0) in serum
IgG was reflected in a parallel rise in the extent to which antibody to TT was agalactosyl. In SLE a rise in %Gal(0) was seen in the presence of very little rise in agalactosyl anti-TT, and in
myasthenia gravis (MG), where serum %Gal(0) is normal, an abnormally low percentage of the anti-TT was agalactosyl. These results imply that in RA and TB a systemic influence is downregulating the galactosylation even of irrelevant
IgG. However in SLE and MG
antibodies of specificities not studied here must be responsible for the %Gal(0) found in serum. It remains to be seen whether these are the
autoantibodies involved in the disease process.