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INTRODUCTION: Minor histocompatibility antigen HA-1 (MiHAg-HA-1) disparity between a patient and his or her human leukocyte antigen (HLA) genoidentical donor has been widely associated with an increased risk of graft-versus-host disease following allogeneic hematopoietic stem cell transplantation. OBJECTIVE: To examine the effect of HA-1 disparity on the incidence of both acute and chronic graft-versus-host disease in Tunisian recipients of hematopoietic stem cells. METHODS: A total of 60 patients and their 60 respective sibling hematopoietic stem cell donors were enrolled in this study. All patients prophylactically received cyclosporine A and/or methotrexate for graft-versus-host disease. An HA-1 genotyping assay was performed with the SSP-PCR method, and HLA-A*0201- and/or HLA-A*0206-positive samples were identified using the Luminex HLA typing method. RESULTS: The Luminex HLA typing assay showed that 54 patients were positive for either the HLA-A*0201 or HLA-A*0206 alleles. Among these cases, six pairs were mismatched for MiHAg-HA-1. Both acute and chronic graft-versus-host disease occurred in four mismatched patients (Fisher's p-values were 0.044 and 0.170, respectively). A univariate logistic regression model analysis showed that only acute graft-versus-host disease may be affected by recipient MiHAg-HA-1 disparity (p: 0.041, OR: 6.727), while chronic graft-versus-host disease correlates with both age and recipient/donor sex mismatch (p: 0.014, OR: 8.556 and p: 0.033, OR: 8.664, respectively). CONCLUSION: Our findings support previously reported data suggesting a significant association between HA-1 disparity and the risk of acute graft-versus-host disease following hematopoietic stem cell transplantation.

Background & Aims: This study extends our previously reported observations that various immunological factors are associated with the occurrence of histologically proven recurrent hepatitis C. The two specific issues investigated were to confirm the associations of MHC alleles and donor/recipient mismatch with the occurrence of recurrent hepatitis C in an independent cohort of newly transplanted patients and to look for immunologic and nonimmunologic variables affecting the severity of the recurrent disease. Methods: Two separate cohorts of consecutive patients were studied: a look-back cohort (LC) of 120 patients and a cohort for studying the disease progression (CSDP) of 190 patients. Protocol liver biopsies were obtained at least 1, 3, 5, 7, and 10 years after liver transplantation (LT). Results: A fully mismatched donor/recipient pair at the DRB1 locus was confirmed to be associated with both the recurrence of histologic hepatitis in the LC (59% vs 23%, P = .0002) and its progression beyond stage 3 in the CSPD (71.4% vs 39.3%, P = .0003). Relevant immunologic and nonimmunologic variables were included into a multivariate Cox proportional model and three variables, namely, donor age, full HLA-DRB1 donor-recipient mismatch, and HLA B14, resulted in independent risk factors for the development of severe fibrosis. Conclusion: This study provides evidence that DRB1 donor-recipient mismatch affects both the occurrence and progression of recurrent hepatitis C disease. This information is clinically relevant as it may help to better allocate organs and to recognize patients at risk for progression so that specific interventions can be implemented. © 2006 by the American Gastroenterological Association Institute

We describe here two novel DRB1 alleles, officially named *040405 and *1190. DRB1*040405 differs from DRB1*0404 for one point mutation at codon 72 with no coding changes. DRB1*1190 is identical to DRB1*110101 except for a nucleotide substitution at codon 24 which causes an aminoacidic mutation from valine to methionine. Over time we have been witnessing the identification of a great number of new HLA alleles. DRB1 allelic variability is mostly present in the second exon and more that 760 alleles have been so far identified. Here, we report the description of two novel DRB1 alleles, named *040405 and *1190, and identified in two Caucasoid subjects.

Here, we have described the characterization of two novel human leukocyte antigen-B (HLA-B) alleles. The new alleles, HLA-B*0732 and HLA-B*5809, were identified in Italian Caucasian individuals. B*0732 differs from HLA-B*0708 by one nucleotidic change at position 412 (from G to A) in exon 3, leading to an amino acidic substitution from Asp (GAC) to Asn (AAC) at codon 114. The sequence of B*5809 is identical to that of HLA-B*5801, except for a point mutation at position 583 in exon 3, where a T is substituted by a C. This change leads to an amino acidic substitution from Tyr (TAC) to His (CAC) at codon 171.

We report the identification of a novel DRB3*02 using sequence-based typing (SBT). This new allele, officially named DRB3*0217, was detected while performing HLA high resolution typing of a bone marrow recipient and his siblings. DNA sequencing demonstrated the presence of a nucleotide substitution in exon 2 at position 199 where a C was substituted by a T. This point mutation at codon 67 (CTC--TTC) has resulted in an amino acid substitution from Leucine to Phenylalanine.