Abstract

THE HLA complex consists of many closely linked genes which code for a variety of characters, particularly the expression of cell surface antigens found on lymphocytes (HLA-A, B, C, DR antigens) or erythrocytes (Chido and Rodgers blood groups) and polymorphic variation of certain complement components (Bf, C2, C4). We1 have recently suggested that the polymorphism of the fourth component of human complement (C4), detected by immunofixation electrophoresis, is controlled by two genes linked to HLA and not by codominant alleles at a single locus as previously described2,3. One C4 variant, designated F, is controlled by one locus with alleles determining the presence (F+) or absence (f0) of four fast-moving anodal bands of C4 while the second variant, S, is controlled by a second locus with alleles determining the presence (S+) or absence (s0) of four slow-moving cathodal bands. We noted that C4 F individuals homozygous for the s0 allele and lacking the four cathodal bands were always Chido (Cha) negative, whereas individuals homozygous for the f0 allele and lacking the four anodal bands of C4 (C4 S) were always Rodgers (Rga) negative. This intriguing observation led us to study the relationship of Chido and Rodgers red cell antigens, which are also found in serum and C4. We show here that Chido and Rodgers are distinct antigenic components of human C4, a finding which provides a biological explanation as to why these unique red cell antigens are controlled by genes of the HLA complex.

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