A possible null phenotype in the Cromer blood group complex

Daniels, Geoff; Tohyama, Hiroshi; Uchikawa, Makoto

doi:10.1046/j.1537-2995.1982.22583017458.x

Cited by 64 publications

(42 citation statements)

References 3 publications

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“…In this study, ITF stimulation induced a marked increase in DAF mRNA stability, indicating that posttranscriptional mechanisms mediate ITF-induced up-regulation of the DAF gene. Recent studies have also reported that p38 MAP kinase plays a role in the induction of mRNA stabilization by inflammatory stimuli, e.g., p38 MAP kinase regulates stability of cyclooxygenase-2 and IL-8 mRNAs (38,39). However, the p38 MAP kinase inhibitor SB 203580 did not affect the ITFinduced DAF mRNA stabilization in HT-29 cells.…”

Section: Discussionmentioning

confidence: 97%

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Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Andoh

Kinoshita

Rosenberg

et al. 2001

The Journal of Immunology

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Mucosal damage induces a massive influx of serum complement components into the lumen. The epithelium produces a number of factors that can potentially ameliorate injury including intestinal trefoil factor (ITF), a small protease-resistant peptide produced and secreted onto the mucosal surface by goblet cells, and decay-accelerating factor (DAF), a protein produced by columnar epithelium which protects the host tissue from autologous complement injury. However, coordination of these intrinsic defensive products has not been delineated. DAF protein and mRNA expression were evaluated by immunoblotting and Northern blotting, respectively. NF-κB-DNA binding activity and DAF promoter activity were assessed by an electrophoretic gel mobility shift assay and a reporter gene luciferase assay, respectively. ITF induced a dose- and time-dependent increase in DAF protein and mRNA expression in human (HT-29 and T84) and rat (IEC-6) intestinal epithelial cells. In differentiated T84 cells grown on cell culture inserts, basolateral stimulation with ITF strongly enhanced DAF expression, but apical stimulation had no effects. The C3 deposition induced by complement activation was significantly blocked by the treatment with ITF. In HT-29 cells, ITF increased the stability of DAF mRNA. ITF also enhanced the promoter activity of the DAF gene via NF-κB motif and induced activation of NF-κB-DNA binding activity. ITF promotes protection of epithelial cells from complement activation via up-regulation of DAF expression, contributing to a robust mucosal defense.

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Section: Discussionmentioning

confidence: 97%

“…Recent studies have demonstrated that the p38 mitogen-activated protein (MAP) kinase plays a role in the stabilization of mRNA by inflammatory stimuli (38,39). To evaluate the role of p38 MAP kinase activation in ITF-induced DAF mRNA stabilization, the effects of the p38 MAP kinase inhibitor SB 203580 were assessed.…”

Section: Effects Of Itf On Daf Mrna Stabilitymentioning

confidence: 99%

Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Andoh

Kinoshita

Rosenberg

et al. 2001

The Journal of Immunology

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“…These cells were originally described as lacking a series of blood group antigens known as Cromer-related antigens (Daniels et al, 1982). The Cromer-related antigens were shown to be located on a sialoglycoprotein of Mr 70000 (now known to be DAF), which was absent from Inab phenotype erythrocytes (Spring et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Studies on the defect which causes absence of decay accelerating factor (DAF) from the peripheral blood cells of an individual with the Inab phenotype

Tate

Uchikawa²,

Tanner

et al. 1989

Biochemical Journal

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1. We have studied the peripheral blood cells of an individual with the Inab phenotype who is deficient in decay accelerating factor (DAF). 2. In contrast with the situation in paroxysmal nocturnal haemoglobinuria, membranes from peripheral blood cells of the Inab phenotype individual lack DAF, but retain the other glycosylphosphatidylinositol-linked proteins acetylcholinesterase and LFA-3. 3. Unlike normal Epstein-Barr-virus-transformed lymphoblastoid cell lines (EBV-LCL), DAF was not expressed on EBV-LCL derived from peripheral blood lymphocytes of the Inab individual. 4. No differences in the DAF gene of normal and Inab phenotype individuals could be detected by Southern blotting studies. 5. EBV-LCL derived from the Inab individual had a gross reduction in the level of DAF mRNA compared with normal EBV-LCL. 6. Our results suggest that the DAF gene in the Inab phenotype contains a mutation which affects the transcription or processing of DAF mRNA.

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“…This antibody is Cromer-related since it failed to react with Inab phenotype cells [2], The cells of the antibody maker were subsequently found to be WES+.…”

Section: Introductionmentioning

confidence: 99%

“…Cromer-related antibodies, so called because like antiCra [3] they fail to react with Inab phenotype cells [2], include anti-Tca [4], the possible anti-TcaTcb from a Tc(a-b-c+) individual [5], anti-Dra [6], anti-Esa [7,8] and anti-IFC, the antibody of Inab [2,9] (table I). Two anti bodies, anti-Tcb and anti-Tcc, probably detect the prod ucts of low frequency alleles of 7ca [5,10],…”

Section: Introductionmentioning

confidence: 99%

A ‘New’ Cromer-Related High Frequency Antigen Probably Antithetical to WES

Daniels¹,

Green²,

Darr³

et al. 1987

Vox Sanguinis

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An antibody to a high frequency antigen, made in a WES+ Black antenatal patient (Wash.), failed to react with the red cells of a presumed WES^+ homozygote and is, therefore, probably antithetical to anti-WES. Like anti-WES, it reacted with papain, ficin, trypsin or neuraminidase treated cells but not with α-chymotrypsin or pronase treated cells and was specifically inhibited by concentrated serum. It also reacted more strongly in titration with WES- cells than with WES+ cells. The antibody is Cromer-related as it failed to react with Inab phenotype (IFC-) cells and reacted only weakly with Dr(a-) cells. Wash, cells and those of the other possible WES^+ homozygote are Cr(a+) Tc(a+b-c-) Dr(a+) IFC+ but reacted only very weakly with anti-Es^a.

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A possible null phenotype in the Cromer blood group complex

Cited by 64 publications

References 3 publications

Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Studies on the defect which causes absence of decay accelerating factor (DAF) from the peripheral blood cells of an individual with the Inab phenotype

A ‘New’ Cromer-Related High Frequency Antigen Probably Antithetical to WES

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