Inherited antigenic differences in human serum beta lipoproteins. A second antiserum.
نویسندگان
چکیده
The sera of patients who have received multiple transfusions may contain antibodies against normal human serum components (1, 2). The first example of such antibodies was reported in a patient (C. de B.) who had received approximately 50 transfusions for the treatment of a refractory anemia of unknown etiology (3). By means of the Ouchterlony double-diffusion technique, it was shown that the antibody formed a precipitin with approximately 55% of normal U. S. white and Negro sera. By twin, family, and population studies (1), it was shown that the presence or absence of the reacting antigen was under genetic control. Individuals with a "dominant" gene designated AgA in single or double dose (genotypes AgA4/AgA, AgA/Ag) were reactors [phenotype Ag(a+)] and those homozygous for the recessive allele Ag nonreactors [Ag(a-)]. The antigen or antigens that react with the antibodies present in the serum of the frequently transfused patient are serum (low-density) ,8-lipoproteins (4). The present paper reports on a second antiserum, the New York antiserum, obtained from a frequently transfused patient with Cooley's anemia. This antiserum reacts with a serum j3lipoprotein, Ag(b+), which is antigenically different from the Ag(a+) antigen first described, and its inheritance appears to be controlled by a different gene.
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ورودعنوان ژورنال:
- The Journal of clinical investigation
دوره 42 شماره
صفحات -
تاریخ انتشار 1963