A patient's serum agglutinated most commercial antibody screening and panel identification red blood cells; however, it did not agglutinate either the cells of ABO compatible donors or washed, saline suspended commercial cells. When suspended in a solution containing 0.1 mg/ml neomycin, all cells, including the patient's, were agglutinated by the patient's serum. Inhibition did not occur by preincubation of either the patient's serum or the test cells with 10 mg/ml neomycin. Serum preincubation with butirosin, kanamycin, or neamine inhibited immediate agglutination in the presence of neomycin. The reactive group is, therefore, included in the neamine fragment. Ultracentrifugation segregated the antibody in the 7S fraction. Following separation by column chromatography, only fractions containing IgA demonstrated antineomycin activity.
Serological studies on a patient whose red cells are polyagglutinable due to T activation have demonstrated concomitant T activity of the separated leukocytes and platelets. Normal leukocytes and platelets are not T active, but activation can be induced in vitro by treatment with neuraminidase or with pneumococcus type III filtrate. Such T-active cells absorb anti-T from Arachis hypogea lectin. Tests on different types of separated leukocytes show that both neutrophils and lymphocytes have latent T antigen receptors. Neuraminidase treatment of platelets does not change their ability to promote clot retraction, to aggregate with ADP, or to take up serotonin.
Examples of both anti-M and anti-N have been reported in patients possessing these antigens; however, in only two instances has anti-M been reported as an autoantibody. This paper describes two additional patients with auto anti-M. In each case the anti-M was shown to be an autoantibody by absorption and elution studies. Optimum reactivity was obtained at 4 C. Column chromatogaphy and 2-mercaptoethanol reduction indicated that the antibody was an IgM globulin. There was no evidence of autoimmune hemolysis in either of these patients.IT IS an extremely rare event for a cold a u t o a g g l u t i n i n t o manifest specificity other than anti-I. Recently, however, two cases of a u t o a n t i -M h a v e been r e p o r t e d in t h e literature. Fletcher and Zmijewskil found an a u t o a n t i -M in t h e serum of a pregnant woman w i t h o u t evidence of hemolytic disease. Tegoli et n1.2 also reported an a u t o a n t i -M in a p a t i e n t following liver transplantation. T w o a d d i t i o n a l p a t i e n t s w i t h a u t o anti-M will be described. Case Report IA 37-year-old white female, who had been pregnant nine times, received two units of blood during an appendectomy and seven units during and after a Caesarean section four years previously. Shortly thereafter, symptoms resulting from anomalous communications between the coronary artery and the pulmonary trunk developcd. She was treated by operative ligation of the abnormal vcssels and received seven units of M negative blood during and after the operation. R e s u l t s T h e patient was typed as Group 0, Rho positive, MNs, U positive, P, positive. T h e patient's hl status was verified with two human and six rabbit anti-M sera. N o mixed field phenomena were observed: thus, the possibilities of chimerism or mosaicism were unlikely.T h e direct antiglobulin test was negative.T h e tests for antibody in the serum prior to the operation were positive only at 4 C. At this temperature all red blood cells in a commercial panel were agglutinated (Table 1). T h e p r e s ence of anti-M was suspected since it was observed that the strongest reactions occurred with homozygous M cells and the weakest with homozygous N cells. T h e patient's serum agglutinated homozygous N cells from an adult but not cord cells, suggesting the possibility of anti-I in addition to anti-M. Furthermore, reactions occurred with MN cord cells, demonstrating that the presence of the I antigen was not necessary for anti-M reactivity. Absorption at 0 C with the patient's ficin-treated cells completely removed the anti-I revealing anti-M. This absorbed serum was then reabsorbed at 0 C with the patient's nonficin-treated cells.
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