An 84-year-old woman with intestinal bleeding had marked reduction of red blood cell antigenicity in the Kell system, and a positive direct antiglobulin test caused by auto-anti-Kpb. KX antigen activity of her cell was increased, an observation which supports the belief that KX marks a precursor structure utilized in the normal Kell biosynthetic pathway. It is postulated that reduced Kell antigenicity was an acquired change that resulted from enzymatic degradation, possibly of bacterial origin.

An IgG autoantibody, named anti-Wj, reacts with all random and most selected red cell samples. It does not agglutinate cells of Lu(a-b-) type caused by the In(Lu) dominant inhibitor gene, but cells of recessive Lu(a-b-) type are reactive. These data establish that synthesis of the Wj antigen is suppressed by the In(Lu) gene, but it is not a part of the Lutheran blood group system. The Wj antigen is not well developed on fetal red cells. This example of auto anti-Wj is a non-complement-binding IgGl protein that did not appear to cause accelerated in vivo destruction of the patient's red cells.

An example is presented of an IgG1, anti-Lu6, that reacted by indirect antiglobulin test and was capable of destroying antigen-positive red cells in vivo. Two methods for the measurement of red cell survival, 51Cr labeling and flow cytometry, gave the same result: 20 percent of the test dose of Lu:6 red cells was destroyed in the first hour after injection and 80 percent in the first 24 hours. The clinical relevance of the antibody was correctly predicted by an in vitro monocyte monolayer assay. The finding that this example of anti-Lu6 was clinically significant should not be taken to mean that all antibodies directed against high-incidence Lutheran and Lutheran system-related antigens will behave similarly. When such antibodies are encountered, in vivo and/or in vitro studies to assess their clinical significance are necessary before rare blood is used for transfusion.