Detection of a lectin in the blood of cystic fibrosis homozygotes and heterozygotes.

We theorize that cystic fibrosis may be a disease in which a 
plasma factor with lectin-like activity stimulates mucus secretion, causes precipitation of 
mucus glycoproteins, and incidentally affects lymphocytes in culture. To confirm our 
theory, we planned to search for additional lectin-like activities in CF 
serum. Our experiments suggest that the lectin-like substance in CF blood 
requires IgM for its red-blood-cell-agglutination activity. Thus, no difference in agglutination 
titer is observed between CF homozygotes and heterozygotes, because IgM is 
the limiting factor, and IgM concentrations do not differ appreciably in 
such subjects. We suspect that CF homozygotes have a larger pool 
of free lectin in their blood than do heterozygotes, so that 
quantitation of this free lectin pool may distinguish between the two 
phenotypes. Excess free lectin may account for the signs and symptoms 
of CF, whereas lesser amounts may theoretically be advantageous to the 
heterozygote. 