The incidence of the MiIII phenotype among Chinese blood donors in Hong Kong was found to be 6.28%. Eleven individuals apparently homozygous for the MiIII gene were detected by immunoblotting with monoclonal antibodies R1.3 and R18. R1.3 detects an identical epitope on both glycophorins A and B and R18 detects a different epitope on glycophorin A. Immunoblotting with R1.3 showed an absence of bands corresponding to normal glycophorin B. Immunoblotting with R18 showed an absence of a 58 K band, which corresponds to a heterodimer of normal glycophorin B complexing with the MiIII component, found in MiIII heterozygotes. In two families with apparent MiIII homozygous individuals, both parents of the propositi had the MiIII phenotype which implies normal autosomal inheritance of the MiIII gene. In another family, only one parent had the MiIII phenotype and the presence of an Su gene is postulated to explain the immunochemical and serological findings.
The majority of Mi antibodies detected were naturally occurring. This survey proved useful for mass screening of random donors for the procurement of valuable Mi antisera.
During the period 1984-1989, a total of 46 examples of Bv phenotype were encountered out of a total of 567,210 donors, giving an incidence of 1 in 12,330 among the Chinese in Hong Kong. The Bv determinant corresponds to the portion of the B antigen that is present on rabbit red cells, and gives a negative reaction with polyclonal anti-B reagents absorbed with rabbit red cells that still react with B3. Some potent monoclonal anti-B reagents confirm the absence of a B epitope from Bv red cells even by adsorption and elution techniques. The failure of some monoclonal anti-B reagents to detect Bv demonstrates the need to select or blend monoclonal anti-B reagents for use in typing Oriental bloods. Cell-conversion techniques failed to convert O cells to B cells using Bv serum with the appropriate substrate, whereas sera from most of the other B variants were capable of doing so. The Bv phenotype, therefore, represents a distinct category of B subgroups that is easily distinguishable from B3 and other B variants.
The CD45 family of Ag expressed by leukocytes play a key role in lymphocyte activation. In this study, we identify both a restricted pattern of expression of CD45 Ag by human endothelial cells and differences in m.w. of endothelial CD45 compared with lymphocyte CD45. Initially, immunoperoxidase staining of endothelial cells in culture revealed the presence of the CD45RO isoform provided the endothelial cells had been stimulated by IL-1 for several days. No other isoform of CD45 was detected by immunoperoxidase staining of endothelium. Leukocyte common antibodies, reputed to detect all isoforms of CD45, did not detect endothelial CD45RO. A polymerase chain reaction method was then used to demonstrate that the message for the CD45RO isoform was constitutively present, with increased levels after IL-1 stimulation. Western blot confirmed the presence of the RO isoform. No other CD45 isoform was detected, either by PCR amplification for message or by Western blot. There were clear differences between lymphocyte and endothelial CD45. The RO isoform expressed by endothelium has an estimated M(r) of 235,000 in contrast to lymphocyte RO that, on our gels, has an estimated M(r) of 190,000. Given the large surface area of endothelium (approximately 1 km2 in the human), the close apposition of lymphocytes and endothelium in immunologic tissues such as lymph nodes, and the pivotal role CD45 plays in activation, expression of CD45RO by endothelium may have important implications in lymphocyte-endothelial interactions. This is most likely to occur in endothelium after a few days of IL-1 stimulation, e.g., at sites of chronic inflammation, or in the draining lymph node of an inflammatory focus.
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