Does the Adhesion Molecule CD31 Act as a Minor Histocompatibility Antigen?

Costa, Letícia da; Charron, Dominique; Loiseau, Pascale

doi:10.1182/blood.v90.3.1332.1332_1332_1332

Cited by 3 publications

(4 citation statements)

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“…Concerning CD31 (codon 125), our study confirmed the conclusion by Behar et al (1996) that mismatch of codon 125 polymorphysm is a risk factor for severe aGVHD; in particular, in both these series aGVHD occurred in nearly 70% of incompatible transplantation pairs and in about 20–30% of compatible ones. Also in the case series of Nichols et al (1996) and Da Costa et al (1997) severe aGVHD was observed more frequently in CD31 (codon 125) incompatible than in compatible pairs, but the difference was not statistically significant. However, if we pool all data together, 26% of patients with severe aGVHD had received BMT from a CD31 (codon 125)‐incompatible donor, whereas only 14% with no or mild aGVHD were transplanted from a CD31 (codon 125)‐incompatible donor.…”

Section: Discussionmentioning

confidence: 72%

“…In the meantime, Behar et al (1996) identified an amino acid polymorphism (leucine/valine at codon 125) of CD31 (also known as platelet endothelial cell adhesion molecule‐PECAM) and reported that in 46 BMT from an HLA‐identical sibling the risk of aGVHD was higher when donor–recipient pairs were mismatched at this residue (Behar et al , 1996). However, Nichols et al (1996) and Da Costa et al (1997) were unable to confirm this association. In order to gain further information on this subject, CD31‐codon 125 polymorphism was also investigated in our donor–recipient pairs.…”

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confidence: 91%

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Incompatibility for CD31 and human platelet antigens and acute graft‐versus‐host disease after bone marrow transplantation

Balduini¹,

Noris²,

Giorgiani³

et al. 1999

Br J Haematol

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Bone marrow transplantation (BMT) is often complicated by acute graft‐versus‐host disease (aGVHD). In patients transplanted with an HLA‐matched donor the occurrence of this complication is believed to be favoured by disparities at the minor histocompatibility antigens (mHA). However, few of these polymorphic molecules have been identified. We sought to determine whether donor/recipient incompatibility for HPA‐1, HPA‐2, HPA‐3, HPA‐5 or CD31 (codon 125) antigens represented a risk factor for aGVHD and genotyped these antigens in 70 bone marrow donors and their HLA‐identical recipients. All patients were children who received BMT for haematological malignancies at a single institution according to well‐defined therapy protocols. Statistical analysis showed that incompatibility for CD31 (codon 125) was a risk factor for grade II–IV aGVHD in the overall patient population, whereas HPA‐3 incompatibility predicted aGVHD occurrence in HLA‐A2 patients only. The magnitude of the aGVHD risk was directly related to the number of HPA/CD31 incompatibilities. No correlation was found between non‐identity for HPA/CD31 and aGVHD. Since incompatibility but not non‐identity for CD31 or HPA‐3 was a risk factor for aGVHD, we suggest that allelic variants of these molecules can serve as mHA in BMT recipients from HLA‐identical donors.

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Section: Discussionmentioning

confidence: 72%

mentioning

confidence: 91%

Incompatibility for CD31 and human platelet antigens and acute graft‐versus‐host disease after bone marrow transplantation

Balduini¹,

Noris²,

Giorgiani³

et al. 1999

Br J Haematol

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“…The correlation between a single amino acid substitution and GvHD has been described for the adhesion molecule CD31 (20). This finding could not be confirmed by others (21,22). Whether CD31-derived peptides can be presented to T cells, induce an immune response, and thus act as a "classical" mHag is not known.…”

Section: Discussionmentioning

confidence: 89%

Genomic identification of the minor histocompatibility antigen HA‐1 locus by allele‐specific PCR

et al. 1998

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Graft-versus-host disease (GvHD) can be a major complication of allogeneic bone marrow transplantation even in recipients of HLA genotype-identical transplants. Disparities in minor histocompatibility antigens (mHags) between donor and recipient are a potential risk for the development of GvHD. A mismatch for the mHag HA-1 can cause GvHD in adult recipients of allogeneic bone marrow from HLA-identical donors. The mHag HA-1, first identified by HLA-A*0201-restricted cytotoxic T cells (CTLs), was recently chemically characterized as a nonapeptide. On the cDNA level, the HA-1 locus has two alleles, HA-1H and HA-1R, which differ in two nucleotides, resulting in a single amino acid substitution. Here we report on the genomic structure of the HA-1 locus. Isolation and sequencing of cosmid DNA encoding the HA-1 peptide sequence revealed that the HA-1 alleles are encoded by two exons. Two different primer sets were designed, each consisting of allele-specific primers and a common primer, and both sets containing intronic sequences. We performed genomic DNA typing of three families consisting of 24 HLA-A*0201-positive individuals. The predicted allele-specific products correlated in all cases with the mHag classification by CTLs and by RT-PCR. We demonstrate for the first time the genomic identification of the mHag HA-1 locus. Prospective genomic typing for the HA-1 alleles will improve donor selection and identify HLA-A*0201-positive recipients with a high risk for HA-1-induced GvHD.

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“…14,15 However, in other studies with large patient cohorts these findings were not supported. 16,17 Carbimazole (1-carbethoxy-3-methyl-2-thioimidazole) is a thioamide that is used for the treatment of hyperthyroidism (not available in the United States). Hemocytopenias caused by this drug are regarded as rare events and are usually attributed to bone marrow suppression.…”

Section: Introductionmentioning

confidence: 99%

Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a target glycoprotein in drug-induced thrombocytopenia

Kroll

Sun

2000

Blood

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Drug-induced immune thrombocytopenia (DITP) is a serious complication of drug treatment. Previous studies demonstrated that most drug-dependent antibodies (DDAbs) react with the platelet membrane glycoprotein (GP) complexes IIb/IIIa and Ib/IX/V. We analyzed the sera from 5 patients who presented with DITP after intake of carbimazole. Notably, thrombocytopenia induced by carbimazole was relatively mild in comparison to patients with DITP induced by quinidine. The sera reacted with platelets in an immunoassay on addition of the drug. In immunoprecipitation experiments with biotin-labeled platelets and endothelial cells, reactivity with the platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) could be demonstrated, whereas neither GPIIb/IIIa nor GPIb/IX was precipitated in the presence of the drug. These results could be confirmed by GP-specific immunoassay (MAIPA) using monoclonal antibodies (mabs) against PECAM-1. In addition, the binding of DDAbs could be abolished by preincubation with soluble recombinant PECAM-1. Carbimazole-dependent antibodies showed similar reactivity with platelets carrying the Leu125 and Val125 PECAM-1 isoforms, indicating that this polymorphic structure, which is located in the first extracellular domain, is not responsible for the epitope formation. Binding studies with biotin-labeled mutants of PECAM-1 and analysis of sera with mabs against different epitopes on PECAM-1 in MAIPA assay suggested that carbimazole-dependent antibodies prominently bound to the second immunoglobulin homology domain of the molecule. Analysis of 20 sera from patients with quinidine-induced thrombocytopenia by MAIPA assay revealed evidence that DDAbs against PECAM-1 are involved in addition to anti-GPIb/IX and anti-GPIIb/IIIa. We conclude that PECAM-1 is an important target GP in DITP.

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Does the Adhesion Molecule CD31 Act as a Minor Histocompatibility Antigen?

Cited by 3 publications

References 3 publications

Incompatibility for CD31 and human platelet antigens and acute graft‐versus‐host disease after bone marrow transplantation

Incompatibility for CD31 and human platelet antigens and acute graft‐versus‐host disease after bone marrow transplantation

Genomic identification of the minor histocompatibility antigen HA‐1 locus by allele‐specific PCR

Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a target glycoprotein in drug-induced thrombocytopenia

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