Measurements have been made of the number of available sites on 10 examples of red cells in which the only abnormality appeared to be a quantitative reduction in the expression of D (weak D cells); these estimates were carried out using three monoclonal anti-D antibodies, Fog-1, Brad-3 and Los-2. The values varied with the monoclonal antibody that was used and fell within the range of 170-1,870 sites/cell. A further 3 examples of weak D cells which had brought about immunisation following transfusion were found to have between 390 and 1,470 sites per red cell. The implications of the D site density on the immunogenicity of weak D cells are discussed. The number of sites on red cells with structurally abnormal D (partial D cells) were also estimated, using the antibody Fog-1. Four of the 5 examples of cells of category IVa (probable phenotype Ror) were found to have a high expression of D (range 29,300-41,300), but the available D sites of categories DVa, DVIa, and DVII were considerably reduced (< 500, < 500 and 2,400-7,500 sites/cell, respectively). As a working hypothesis, it is suggested that there are two types of genetic abnormality leading to an abnormal expression of D. First, a defect in genomic DNA leading only to a quantitative reduction in the number of available D sites; this genomic lesion should be termed 'weak D'. Secondly, genomic defects leading to amino acid sequence abnormalities and structural change in the D polypeptide; these lesions should be collectively known as 'partial D'.

TransfusionVolume 28, Issue 2 p. 197-198 Jk:-3 red cells have a defect in urea transport: a new urea-dependent lysis test Douglas C. J. McDougall FIMLS, MSc, Douglas C. J. McDougall FIMLS, MSc North-East Thames Regional Transfusion Centre Crescent Drive Brentwood Essex, CM15 8DP, EnglandSearch for more papers by this authorMartin McGregor FIMLS, Martin McGregor FIMLS North-East Thames Regional Transfusion Centre Crescent Drive Brentwood Essex, CM15 8DP, EnglandSearch for more papers by this author Douglas C. J. McDougall FIMLS, MSc, Douglas C. J. McDougall FIMLS, MSc North-East Thames Regional Transfusion Centre Crescent Drive Brentwood Essex, CM15 8DP, EnglandSearch for more papers by this authorMartin McGregor FIMLS, Martin McGregor FIMLS North-East Thames Regional Transfusion Centre Crescent Drive Brentwood Essex, CM15 8DP, EnglandSearch for more papers by this author First published: March‐April 1988 https://doi.org/10.1046/j.1537-2995.1988.28288179034.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume28, Issue2March‐April 1988Pages 197-198 RelatedInformation

UCH D4 is a human monoclonal antibody produced by an Epstein-Barr (EB) virus-transformed lymphoblastoid cell line. The antibody is specific for the rhesus D antigen, and is a good laboratory reagent for red blood cell typing. UCH D4 can be purified from the culture supernatant medium with the removal of all detectable DNA and infectious EB virus particles. This purified antibody will be used for in vivo assessment of its ability to prevent Rhesus disease of the newborn.

Abstract. Anti‐Me is an antibody which cross‐reacts with the M and He antigens. It has previously only been found in rabbit serum; the first human example is described.The Henshaw antigen is closely associated with the MNSs system and is found in about 3% of Negroes [1–3] but only rarely in Caucasoids [2]. The original anti‐He was found in a rabbit anti‐M serum by Ikin and Mourant [1] in 1951. Other examples were deliberately produced by the immunisation of rabbits with the blood of Mr. Henshaw [3].The first example of anti‐He in a human serum was found in 1967 by MacDonald et al. [4] in a Caucasoid mother. Although at the time it was not possible to ascertain the racial group of the father, it has since been established that he was a Negro. Other human anti‐He sera have since been found [2].In 1961 Wiener and Rosenfield [5] reported an immune rabbit serum which possessed inseparable anti‐M and anti‐He specificities which they designated anti‐Me. The rabbit which produced the anti‐Me had almost certainly not received Henshaw‐positive cells. The rabbit serum was investigated as a result of a discrepancy found during M‐typing of a Negro involved in a medicolegal case of disputed parentage.The first human example of anti‐Me herein described was found in the serum of Mr. Richards, a 41‐year‐old Caucasoid male with no known transfusion history and has been used at this centre as an anti‐M serum for many years.