NB was supported by grant Molecular and Cell Biology of RAS Presidium.
Monoclonal anti-A activity against the FORS1 (Forssman) antigen
Version of Record online: 13 JUL 2014
© 2014 AABB
Volume 55, Issue 1, pages 129–136, January 2015
How to Cite
Barr, K., Korchagina, E., Popova, I., Bovin, N. and Henry, S. (2015), Monoclonal anti-A activity against the FORS1 (Forssman) antigen. Transfusion, 55: 129–136. doi: 10.1111/trf.12773
- Issue online: 13 JAN 2015
- Version of Record online: 13 JUL 2014
- Manuscript Accepted: 28 MAY 2014
- Manuscript Revised: 21 MAY 2014
- Manuscript Received: 18 MAR 2014
- Molecular and Cell Biology of RAS Presidium
The FORS blood group system (originally recognized as the Apae phenotype) was discovered by sporadic activity against polyclonal anti-A reagents and activity against the lectin Helix pomatia. The extent of monoclonal anti-A reagent activity against the FORS1 antigen is serologically and immunochemically incomplete.
Study Design and Methods
In the absence of natural FORS1-positive red blood cells (RBCs), kodecytes were created with synthetic disaccharide and pentasaccharide Forssman function-spacer-lipid (FSL) constructs, Fsdi-kodecytes, and FORS1-kodecytes, respectively. FSL constructs were also applied to solid surfaces and used in solid-phase enzyme immunoassays. A range of characterized monoclonal anti-A and anti-B reagents were then serologically and immunochemically characterized against these Forssman antigens. Polyclonal human anti-A, anti-B, the lectin H. pomatia serologic reagents; and canine RBCs were used as serologic controls.
None of 19 different monoclonal anti-A reagents were able to detect the pentasaccharide Forssman on FORS1-kodecytes, while three reagents were able to detect disaccharide Forssman on Fsdi-kodecytes. Most anti-A reagents were immunochemically reactive with both the di- and the pentasaccharide Forssman antigens in the solid-phase assays. Historic polyclonal human anti-A and the lectin H. pomatia reacted strongly with the FORS1-kodecytes, correlating with the discovery of the Apae phenotype and supporting the use of FORS1-kodecytes as FORS1 surrogates.
Monoclonal anti-A reagents, despite showing reactivity against the FORS1 antigen in solid-phase assays are unlikely to cause the agglutination of FORS1 antigen–positive RBCs.