Anti-HrB and anti-hrb revisited.

BACKGROUND: Since their description in the 1970s, anti-Hr(B) (antibody against a high-prevalence Rh antigen) and anti-hr(B) (anti-e-like antibody) are still a subject of debate about representing two aspects of a global immune response or being two independent antibodies. STUDY DESIGN AND METHODS: The aim of this study was to evaluate the immune response against the antigens of Rh system of 30 individuals presenting a hr(B)(RH31)- phenotype. Genomic analysis of RH genes was performed in all individuals. RESULTS: Among the 30 individuals, 27 had a Hr(B)(RH34)- phenotype. No immunization against Rh antigens was found in 16 individuals. Three individuals made anti-D only, whereas six individuals made anti-Hr(B) (four with anti-hr(B) and two without anti-hr(B)) and two individuals made anti-hr(B) without anti-Hr(B). Among the 30 individuals, three had a Hr(B)+ phenotype. No immunization against Rh antigens was found in one individual, whereas two individuals made anti-hr(B); the genomic analysis of selected individuals showed the presence of a (C)ce(s) haplotype, either Type 1 or Type 2, and a DIII Type 5 ce(s) haplotype, in the homozygous state, in compound heterozygosity with each other or in heterozygosity with a DcE haplotype. Genomic data were in accordance with serologic data. CONCLUSION: Our data provide the evidence that anti-Hr(B) and anti-hr(B) are independent antibodies, defining two different specificities. These antibodies may be produced by individuals expressing variants of RhCE protein. Serologic and molecular data indicate that e antigen encoded by the (C)ce(s) haplotype is a partial antigen. In individuals carrying a (C)ce(s) haplotype, the risk and the type of alloimmunization to Rh antigens are related to the second Rh haplotype.

Adenovirus-mediated fibroblast growth factor 1 expression in the lung induces epithelial cell proliferation: consequences to hyperoxic lung injury in rats.

High concentrations of oxygen can induce pulmonary toxicity and cause injury to alveolar epithelial and endothelial cells. The present study was performed to determine whether the potent epithelial and endothelial fibroblast growth factor 1 (FGF-1) protected against hyperoxia-induced lung injury. Recombinant adenovirus carrying the gene encoding human secreted FGF-1 (Ad. FGF1) increased the proliferation of lung epithelial cells in vitro. Ad.FGF1 or control vector with an empty expression cassette (Ad.V152) was administered intratracheally to Wistar rats. With Ad.FGF1 (10(9), 5 x 10(9), 10(10), or 5 x 10(10) viral particles [VP]), FGF-1 protein was found in bronchoalveolar lavage fluid 4 days postinfection at levels proportional to the viral dose and was detected in plasma after doses of 10(10) VP or more were administered. Histological examination of the lungs showed intense proliferation and apoptosis of alveolar and bronchial epithelial cells, with few inflammatory cells. The alveolar architecture returned to normal within 17 days. Rats pretreated with Ad.FGF1 (10(9) or 5 x 10(9) VP) 2 days before exposure to hyperoxia (95% O2) survived, whereas rats pretreated with Ad.V152 died within 3 days. In conclusion, adenovirus-mediated FGF-1 overexpression in the lungs causes epithelial cell proliferation and has beneficial effects in hyperoxic lung injury.