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Immunochemical Studies on Blood Groups

XLIX. The I Antigen Complex: Specificity Differences Among anti-I Sera Revealed by Quantitative Precipitin Studies; Partial Structure of the I Determinant Specific for One anti-I Serum¹

From the Departments of Microbiology, Neurology and Human Genetics and Development, Columbia University, the Neurological Institute, Presbyterian Hospital, the Rockefeller University and the New York Blood Center, New York

Abstract

Quantitative precipitin studies with three anti-I sera show them to be distinctly different in specificity as revealed by their reactions with milk fractions, with Le^a substances, with precursor and with cow blood group substances and with the various stages of periodate oxidation and Smith degradation of A, B and H substances. The various I specificities are concealed in interior structures of the blood group A, B, H, Le^a and Le^b substances and may be exposed by stepwise periodate oxidation and Smith degradation of A, B and H substances or by mild acid hydrolysis of B substance. Oligosaccharide inhibition assays showed one anti-I serum (Ma) to be inhibited best by a terminal nonreducing -D-Gal-(1 4)--D-GNAc-(1 6)-structure present in a precursor blood group substance. From quantitative precipitin studies, the specificity of another anti-I serum was entirely different. Evidence suggesting that certain anti-I sera may not contain homogeneous populations of anti-I molecules is presented. The genetic implications of the findings are discussed. Anti-I eluted from OI erythrocytes behaved similarly to the anti-I in the original antiserum. I-anti-I specific precipitates dissolve readily at 37°C and reprecipitate rapidly on colling. The definition of the human I-anti-I system based on hemagglutination reactions in the cold may not have revealed its ture complexity especially with respect to its genetics.

Footnotes

¹ This work was aided by grants from the National Science Foundation (GB-8341) and the National Institute of Allergy and Infectious Diseases (AI-08429), the National Heart Institute (HE-08630 and HE-09011), a General Research Support Grant from the United States Public Health Service and a grant from the Fay-Hunter Estates.

² Lilly International Fellow 1968 to 1969; Fellow of the Arthritis Foundation 1969 to 1971.

³ Helen Hay Whitney Fellow and National Cystic Fibrosis Research Foundation Fellow 1968 to 1971.