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Both types of RhnuN cells (amorph and regulator types) lacked the Rh proteins and other proteins, and showed some functional abnormalities. No Rh glycoprotein is immune precipitated by anti-D but it is present in membranes from some RhnuNs as shown by immunoblotting studies with the monoclonal antibody MB-2D10 [30]. The LW protein is missing and some other antibodies only react weakly: anti-U, Duclos, anti-FY5, BRIC 125 (anti-CD47) and the monoclonal antibody 1D8. That so many determinants encoded by genetically independent loci are not fully expressed in RhnuN cells has led to the idea of a protein complex or cluster which involves the Rh proteins, Rh glycoproteins and other proteins [31,32,33]. Since D and CE proteins are integral proteins with about 12 transmembrane domains, it is hypothesised that they and the other proteins interact, perhaps affecting insertion into the membrane. Some of the variation observed in Rh antigens may not depend on mutations in the Rh genes but may reflect alterations in other proteins of the Rh protein complex. D , the most important antigen, has been exhaustively studied. Quantitative and qualitative variation of D is well documented [see 34]. Several other Rh antigens show quantitative and qualitative variation. We have observed variation in C, E, c, e, G, V, VS, Rh17 and Rh29 antigens. Possibly it is a common finding for Rh antigens. Variation of C antigen Table III shows some of the Blood Group Unit’s results of testing samples with rare Rh phenotype against polyclonal anti-C. ComC represents commercial anti-C reagents, all others are single donor antibodies. The first three reagents do not contain any anti-D, the next three contain incomplete anti-D so are not suitable for tests with enzyme treated cells. The different patterns of reaction would make one suspect that these cells carried different variants of C; most variants are also distinguished by their reactions with antibodies to low incidence Rh antigens (Table III). Low incidence antigen JAL (RH48) JAL+ cells have a very weak C antigen, it is most easily detected with commercial reagents (Table III). The antibody in Mrs S Allen’s serum was studied for many years in several laboratories interested in low incidence antigens. There were some hints that it might be an Rh antigen, although Mrs Allen’s husband had been an unremarkable cDe. Eventually several samples expressing the JAL antigen were identified. However, family studies had not proved that JAL was an Rh antigen, although 3 of the propositi had a depressed c antigen and 4 had a depressed C antigen, 2 of whom also had a depressed e antigen [35]. A second immune example of anti-JAL, which caused haemolytic disease of Mrs Pas’ third
DOI link for Both types of RhnuN cells (amorph and regulator types) lacked the Rh proteins and other proteins, and showed some functional abnormalities. No Rh glycoprotein is immune precipitated by anti-D but it is present in membranes from some RhnuNs as shown by immunoblotting studies with the monoclonal antibody MB-2D10 [30]. The LW protein is missing and some other antibodies only react weakly: anti-U, Duclos, anti-FY5, BRIC 125 (anti-CD47) and the monoclonal antibody 1D8. That so many determinants encoded by genetically independent loci are not fully expressed in RhnuN cells has led to the idea of a protein complex or cluster which involves the Rh proteins, Rh glycoproteins and other proteins [31,32,33]. Since D and CE proteins are integral proteins with about 12 transmembrane domains, it is hypothesised that they and the other proteins interact, perhaps affecting insertion into the membrane. Some of the variation observed in Rh antigens may not depend on mutations in the Rh genes but may reflect alterations in other proteins of the Rh protein complex. D , the most important antigen, has been exhaustively studied. Quantitative and qualitative variation of D is well documented [see 34]. Several other Rh antigens show quantitative and qualitative variation. We have observed variation in C, E, c, e, G, V, VS, Rh17 and Rh29 antigens. Possibly it is a common finding for Rh antigens. Variation of C antigen Table III shows some of the Blood Group Unit’s results of testing samples with rare Rh phenotype against polyclonal anti-C. ComC represents commercial anti-C reagents, all others are single donor antibodies. The first three reagents do not contain any anti-D, the next three contain incomplete anti-D so are not suitable for tests with enzyme treated cells. The different patterns of reaction would make one suspect that these cells carried different variants of C; most variants are also distinguished by their reactions with antibodies to low incidence Rh antigens (Table III). Low incidence antigen JAL (RH48) JAL+ cells have a very weak C antigen, it is most easily detected with commercial reagents (Table III). The antibody in Mrs S Allen’s serum was studied for many years in several laboratories interested in low incidence antigens. There were some hints that it might be an Rh antigen, although Mrs Allen’s husband had been an unremarkable cDe. Eventually several samples expressing the JAL antigen were identified. However, family studies had not proved that JAL was an Rh antigen, although 3 of the propositi had a depressed c antigen and 4 had a depressed C antigen, 2 of whom also had a depressed e antigen [35]. A second immune example of anti-JAL, which caused haemolytic disease of Mrs Pas’ third
Both types of RhnuN cells (amorph and regulator types) lacked the Rh proteins and other proteins, and showed some functional abnormalities. No Rh glycoprotein is immune precipitated by anti-D but it is present in membranes from some RhnuNs as shown by immunoblotting studies with the monoclonal antibody MB-2D10 [30]. The LW protein is missing and some other antibodies only react weakly: anti-U, Duclos, anti-FY5, BRIC 125 (anti-CD47) and the monoclonal antibody 1D8. That so many determinants encoded by genetically independent loci are not fully expressed in RhnuN cells has led to the idea of a protein complex or cluster which involves the Rh proteins, Rh glycoproteins and other proteins [31,32,33]. Since D and CE proteins are integral proteins with about 12 transmembrane domains, it is hypothesised that they and the other proteins interact, perhaps affecting insertion into the membrane. Some of the variation observed in Rh antigens may not depend on mutations in the Rh genes but may reflect alterations in other proteins of the Rh protein complex. D , the most important antigen, has been exhaustively studied. Quantitative and qualitative variation of D is well documented [see 34]. Several other Rh antigens show quantitative and qualitative variation. We have observed variation in C, E, c, e, G, V, VS, Rh17 and Rh29 antigens. Possibly it is a common finding for Rh antigens. Variation of C antigen Table III shows some of the Blood Group Unit’s results of testing samples with rare Rh phenotype against polyclonal anti-C. ComC represents commercial anti-C reagents, all others are single donor antibodies. The first three reagents do not contain any anti-D, the next three contain incomplete anti-D so are not suitable for tests with enzyme treated cells. The different patterns of reaction would make one suspect that these cells carried different variants of C; most variants are also distinguished by their reactions with antibodies to low incidence Rh antigens (Table III). Low incidence antigen JAL (RH48) JAL+ cells have a very weak C antigen, it is most easily detected with commercial reagents (Table III). The antibody in Mrs S Allen’s serum was studied for many years in several laboratories interested in low incidence antigens. There were some hints that it might be an Rh antigen, although Mrs Allen’s husband had been an unremarkable cDe. Eventually several samples expressing the JAL antigen were identified. However, family studies had not proved that JAL was an Rh antigen, although 3 of the propositi had a depressed c antigen and 4 had a depressed C antigen, 2 of whom also had a depressed e antigen [35]. A second immune example of anti-JAL, which caused haemolytic disease of Mrs Pas’ third
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