Escape from Sensitization to HL-A Antibodies

Human lymphocytes sensitized with HL-A antibodies could not be killed by the addition of complement if the lymphocytes were incubated for periods of 1 to 5 hours at 37° C. This phenomenon was not produced by simple dissociation of the antibodies or by loss of antigens (modulation), but rather is postulated to result from an active release or pinocytosis of HL-A antigens together with the attached antibody. "Escape from sensitization" is followed closely by reformation of antigens, for the cells can readily be resensitized and killed by addition of complement. Loss of sensitization is an active process, since one-day-aged lymphocytes or lymphocytes treated with actinomycin D or puromycin were unable to express this activity. A differential escape rate for different specificities was encountered indicating that HL-A9 was produced more rapidly than several other specificities present on the same lymphocytes. A correlation was noted between the rate of HL-A antigen synthesis by lymphocytes (indicated by escape rate) and the quantity of HL-A antigen in the serum.
Inhibition of lymphocyte cytotoxicity was used to detect the presence of HL-A antigens in serum. Certain specificities, such as HL-A9, were generally present in serum whereas others, such as HL-A8, could not be detected. Cross-inhibition tests with over 100 sera clearly showed an association of inhibition with specificity, although nonspecific inhibition was often observed. Sephadex fractions of sera tested at different concentrations revealed the greatest inhibitory activity in the 19S and 7S fractions.