The molecular backgrounds of variants encountered in Afro-Caribbean black individuals and associated with the production of clinically significant antibodies against high-incidence antigens (anti-RH18, anti-RH34) and against Rhe epitopes were determined. We showed that RH:؊18 phenotypes are produced by 3 distinct RHCE alleles: ceEK carrying 48G>C (

These results strongly suggest that protein RBC intrinsic immunogenicity depends on the distribution of DRB1* restriction molecules.

Aberrant hepatic expression of HLA molecules has been shown to be present in primary biliary cirrhosis and may play a determining role in the pathogenesis of the disease. We have studied the effect of the long-term administration of ursodeoxycholic acid on hepatic HLA expression. Nine untreated patients with primary biliary cirrhosis, eight patients treated for at least a year with ursodeoxycholic acid and eight control subjects without hepatobiliary disease were compared. HLA expression was studied on liver biopsy sections using a direct immunofluorescence technique with specific monoclonal antibodies directed against class I or class II HLA molecules. Aberrant biliary HLA class II expression was not modified by chronic administration of ursodeoxycholic acid. In contrast, aberrant hepatocyte HLA class I expression was markedly reduced. Reduction in HLA class I expression may lead to decreased cytotoxic T cell-dependent lobular necrosis, which is thought to contribute to the progression of primary biliary cirrhosis to advanced stages. These findings suggest that the beneficial effect of ursodeoxycholic acid treatment in primary biliary cirrhosis could result not only from a reduction in the intrahepatic accumulation of cytotoxic bile acids but also from a reduction in immunological injury.

The study showed the heterogeneity of the molecular background of the weak C, VS+, hr(B)-, Hr(B)- phenotype in the black population. The screening of blood donors in this population for hr(B)- or Hr(B)- phenotype should implement the molecular characterization of Rh genes.

This is the first documented case of fatal HDFN due to anti-Jr(a). Therefore, we recommend close monitoring of pregnant women with a high-titer anti-Jr(a), especially those with an incompatible transfusion history and/or multiple pregnancies. This case report provides new arguments about the clinical significance of anti-Jr(a) in the transfusion setting.

The expression of CD45 and IgE cell surface antigens on human leucocytes was studied by flow cytometry. More than 80% of sorted cells that expressed low CD45 (CD45dim) and high IgE (IgEbright) antigen site density were identified as basophils. Immunomagnetic depletion of the CD45d'"-IgEbT'ght cell subset by a biotin-coupled anti-IgE antibody and streptavidin-coated magnetic beads was greater than 90%, and more than 80% of cells binding significant numbers of beads exhibited the morphological characteristics of basophils. Interestingly, when the cell staining was performed in the presence of calcium and magnesium, we observed a significant increase of CD45 and an equivalent decrease of IgE cell surface expression, as well as an IgE concentration dependent diminution of the number of CD45d'"-IgEbnght cells.

The challenge in clinical red blood cell (RBC) transfusion of patients with sickle cell disease, notably, would be to provide not only phenotypically matched, but also genetically matched, RBC units regarding RhCE variants.

A complete anti-D investigation in individuals with a D variant (weak D or partial D identified by molecular analysis) should be systematically performed before any valid conclusion on the nature of the antibody. Transfusing weak D Type 1 or weak D Type 2 patients with D+ RBC units should be recommended. Weak D Type 1 or weak D Type 2 pregnant women do not need anti-D immunoprophylaxis.