The effect of <i>In(Lu)</i> on some high‐frequency antigens

Daniels, G.L.; Shaw, Marie; Lomas, C; Leak, M. R.; Tippett, P.

doi:10.1046/j.1537-2995.1986.26286152909.x

Cited by 28 publications

(14 citation statements)

References 7 publications

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“…Moulds, unpublished data). Although it was initially reported that ln(Lu) could suppress expression of the Knops antigens 20 , however, later studies indicated that CR1 expression was not controlled by this gene 21–22 …”

Section: Localization Of the Knops Antigens To Cr1mentioning

confidence: 99%

Understanding the Knops Blood Group and its Role in Malaria

Moulds

2002

Vox Sanguinis

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Section: Localization Of the Knops Antigens To Cr1mentioning

confidence: 99%

Understanding the Knops Blood Group and its Role in Malaria

Moulds

2002

Vox Sanguinis

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“…These antibodies are not Lutheran antibodies. The Zn(Lu) gene is known to have a wide range of effects on a number of antigens unrelated to Lutheran [164]. The mechanism underlying this interesting pleiotropic effect remains to be elucidated.…”

Section: Cd44 Glycoproteinmentioning

confidence: 99%

Blood Group‐Active Surface Molecules of the Human Red Blood Cell

Anstee

1990

Vox Sanguinis

120

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Abstract. The surface of the human red blood cell is dominated by a small number of abundant blood group active proteins. The major proteins are the anion transport protein (band 3) which has AB(H) activity, and Glycophorin A which has MN activity. Band 3 and Glycophorin A are of equal abundance in the normal red cell membrane (approximately lo6 copies of each) and the two proteins may associate together as a complex. The glucose transporter (band 4.5) has AB(H) activity and there are about 5 x lo5 copiedred cell. Several polypeptides associate together to form the Rh complex. The major components of this complex (abundance 1-2 x lo5 copieshed cell) are polypeptides of M, 30,000, polypeptides of MI 45,000-100,000 and Glycophorin B. The antigens of the Rh blood group system appear to be associated with the polypeptides of M, 30,000 and those of M, 45,000-100,000 (the latter also express AB(H) activity). Glycophorin B expresses the blood group 'N' antigen and the Ss antigens. Glycophorins C and D carry the Gerbich antigens and, together, these polypeptides comprise approximately lo5 copiedred cell. The complete protein sequence of all the above-mentioned proteins is known, except for the MI 30,000 and M, 45,000-100,000 polypeptides of the Rh complex for which only partial sequences are available, and Glycophorin D, the sequence of which can be inferred from that of Glycophorin C . Several of the minor blood group active proteins at the red cell surface (abundance 4 . 2 x 104/red cell) have been the subject of recent studies. The polypeptide expressing Cromer-related blood group antigens has been identified as decay-accelerating factor and that carrying the Ina/Inb antigens as CD44. The protein sequence of both of these proteins has been deduced form nucleotide sequencing. The polypeptides expressing Kell antigens, Lutheran antigens, Fy antigens, and LW antigens have also been identified and partially characterised.

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“…In(Lu), an autosomal dominant gene, has been reported to downregulate the Knops/McCoy antigens [19], which are localized on the CR1 [20,21] molecule, as well as P1 [22], blood group antigen i, Haemophilus influenzae receptor AnWj [23], the receptor for hyaluronan CD44, which carry the In b blood group antigens [24], Lutheran blood group antigens (Lu), which are located on the B lymphocyte cell adhesion molecule B-CAM coded by a gene located on 19q12-q13 [25], and MER2 blood group antigen. In(Lu) upregulates the expression of the sialyltransferase CDw75, ligand for CD22 [26] ( fig.…”

Section: Introductionmentioning

confidence: 99%

No Quantitative Relationship between CR1 and Lutheran Expression on Erythrocytes: In(Lu) Gene Product Is Not a Common Regulator of CR1 Expression on Erythrocytes

Oudin¹,

LePennec²,

Dervillez³

et al. 1999

Exp Clin Immunogenet

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The density of CR1, the C3b/C4b receptor (CD35), on erythrocytes (E) (CR1/E) is genetically determined. However, the broad distribution of CR1/E within a given genotype suggests that other genetic elements might contribute to the regulation of CR1/E. In some pathological conditions, including systemic lupus erythematosus (SLE), AIDS and hemolytic anemia, CR1 deficiency parallels the severity of the disease. When compared to healthy individuals, an accelerated decrease in CR1/E in these patients has been demonstrated, but other mechanisms interfering with CR1 density regulation during erythropoiesis might also contribute. In exceptional circumstances, CR1/E can be dramatically decreased in healthy individuals by the effect of a regulatory gene, In(Lu), that switches off various surface molecules on E, the structure genes of which are located on four different chromosomes, suggesting a transcription regulatory role for In(Lu) gene products. The hypothesis that products of this gene could physiologically regulate the surface density of all these molecules has been tested by determining Lu^b density on E (Lu^b/E) using quantitative flow cytometry. Lu^b antigenic sites were then compared to CR1/E among healthy individuals of the different CR1 density phenotypes, SLE patients with and without CR1 deficiency, and an exceptional SLE patient totally lacking CR1/E and reticulocytes. No quantitative relationship was found between CR1 and Lu^b expression in either normal or pathological conditions. These data establish that In(Lu) products are not involved in normal or pathological CR1 density regulation.

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The effect of In(Lu) on some high‐frequency antigens

Cited by 28 publications

References 7 publications

Understanding the Knops Blood Group and its Role in Malaria

Understanding the Knops Blood Group and its Role in Malaria

Blood Group‐Active Surface Molecules of the Human Red Blood Cell

No Quantitative Relationship between CR1 and Lutheran Expression on Erythrocytes: In(Lu) Gene Product Is Not a Common Regulator of CR1 Expression on Erythrocytes

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