Impact of CD31 mismatches on the outcome of hematopoeitic stem cell transplant of HLA-identical sibling.
Graft-versus host disease (GVHD) complicating allogeneic hematopoeitic stem cell transplantation (HSCT) is often attributed to mismatching of minor histocompatibility antigens (mHags), which are poorly defined in humans. CD31 is a candidate human mHag relevant to acute GVHD (aGVHD), but reports disagree about its level of significance. Therefore, we examined the impact of CD31-matching on the outcome of HSCT in different hematological and immunological diseases. About 60 patients receiving HSC from their respective HLA-ABCDR and DQ-identical sibling were studied. DNA was used to study the CD31 allele polymorphism at the codon 125 (LL, LV or VV) in the patient-donor pairs using the principle of allele-specific PCR amplification. Four primer were used; two primers (forward and reverse) for the L allele and another two for the V allele. The CD31 identity was tested for correlation with HSCT outcome measures of aGVHD, chronic GVHD, and relapse. The gene frequency of CD31 alleles (LL, VV and LV) was 28.3, 20 and 51.7%, respectively. CD31 identity was found in 31 pairs (51.7%) versus 29 pairs (48.3%) for nonidentity. The CD31 noncompatibility showed statistical non-significant relation with aGVHD (G 0-I, and G II-IV) and chronic GVHD (De-novo and chronic on acute) (p = 0.59, p = 0.62, p = 036 and p = 0.83, respectively). The CD31 nonidentity had statistical significant relation with aGVHD versus no aGVHD (p = 0.008 and OR = 4.46). The CD31 nonidentity showed statistical significant relation with aGVHD (II-IV) versus no aGVHD (p = 0.012 and OR = 7.14) and also, aGVHD (0-I) versus the no aGVHD (p = 0.03, OR = 3.13, respectively). A statistical significant relation was found between CD31 nonidentity in patient-donor pairs and relapse (p = 0.014 and OR = 4.21). In conclusion, the donor-recipient CD31 nonidentity is a significant risk factor for aGVHD and relapse in HLA-identical sibling.
El-Chennawi
Farha A
FA
Clinical Immunology Unit, Clinical Pathology Department, Mansoura Faculty of Medicine, Mansoura, Egypt.
Kamel
Hosam A
HA
Mosaad
Youssef M
YM
El-Sherbini
Sherif M
SM
El-Billey
Nader A
NA
D000017:ABO Blood-Group System / Q000235:genetics / Q000276:immunology; D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000483:Alleles; D002648:Child; D002675:Child, Preschool; D002908:Chronic Disease; D003062:Codon / Q000235:genetics; D004247:DNA / Q000235:genetics; D005260:Female; D005787:Gene Frequency; D006086:Graft vs Host Disease / Q000453:epidemiology / Q000209:etiology* / Q000276:immunology / Q000517:prevention & control; D006680:HLA Antigens / Q000276:immunology*; D006402:Hematologic Diseases / Q000235:genetics / Q000601:surgery; D019337:Hematologic Neoplasms / Q000601:surgery; D018380:Hematopoietic Stem Cell Transplantation / Q000009:adverse effects*; D006648:Histocompatibility; D006801:Humans; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics / Q000276:immunology*; D012008:Recurrence; D012307:Risk Factors; D035781:Siblings; D014019:Tissue Donors; D019172:Transplantation Conditioning; D016896:Treatment Outcome
D000017:ABO Blood-Group System; D003062:Codon; D006680:HLA Antigens; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D004247:DNA