红细胞分布宽度与炎症性肠病活动度的关系

目的探讨红细胞分布宽度(RDW)是否可以作为评价炎症性肠病(IBD)疾病活动度的指标。方法回顾性分析IBD患者98例,并收集同期65例健康体检者做对照。分别检测IBD组和对照组的RDW、白细胞(WBC)、血小板(PLT)、血红蛋白(Hb)、C反应蛋白(CRP)、血沉(ESR)指标,判断疾病不同阶段RDW的变化趋势,同时分析RDW与各实验室指标的相关性。结果 IBD组RDW值明显高于健康对照组,15.5±1.9vs 13.5±0.7(P<0.01),IBD组活动期患者RDW值明显高于缓解期患者,16.2±1.8vs 14.3±1.2(P<0.01),IBD组的RDW值与ESR、CRP、PLT有显著正相关性,与Hb有显著负相关性(r=0.383、0.421、0.550、-0.554,均P<0.01)。结论 RDW值在IBD组较健康对照组显著升高,RDW值与IBD疾病活动度呈正相关,可以作为区分炎症性肠病活动期与缓解期的指标。     

Expression of blood group antigens on red cell microvesicles

The purpose of this study was to determine whether epitopes of the A, B, D, Fya, M, N, S, s, and K blood group antigens are present on microvesicle membranes shed by red cells during storage. Vesicles were isolated from outdated units of blood having and lacking the specified antigens. Diluted antisera were absorbed with fixed quantities of vesicles from red cells with the test antigen and red cells lacking that antigen (controls). The adsorbed and unadsorbed antisera were titrated and scored by using panel cells from persons known to be heterozygous for all the non-AB antigens. The mean titration scores following adsorption with the vesicles from A, B, D, M+N-, M-N+, S+s-, S-s+, and Fy(a+b-) units were appreciably lower than the control scores (0, 0, 3, 2, 2, 0, 4, and 4 vs. 19, 23, 34, 13, 12, 16, 18, and 29, respectively), which indicated the presence of these epitopes on the membrane of shed vesicles. The results following adsorption with K:1,2 vesicles were equivocal.     

The relationship between immunogenic red blood cell antigens and Human Immunodeficiency Virus infection

Introduction

Evidence suggests that red cell antigens may act as receptors for viruses and bacteria and therefore could be associated with HIV infection. Previous studies have been controversial and therefore the aim of this exploratory study was to analyse the expression of immunogenic red cell antigens in HIV-seropositive individuals and to compare the results to negative donors from South Africa.

ABO blood group antigens of human spermatozoa

ABO blood group antigens on the membrane of human spermatozoa were investigated with the peroxidase-labelled antibody test. Spermatozoa from O secretor were incubated with saliva or seminal plasma of A and B secretors, but the specific peroxidase staining was negative. This result indicates that blood group antigens on human spermatozoa originate from spermatozoon itself, but not from seminal plasma.     

Associations between seroprevalence of Helicobacter pylori and ABO/rhesus blood group antigens in healthy blood donors in southwest Iran

ObjectiveTo investigate correlations between ABO/rhesus (Rh) blood group antigens and anti-Helicobacter pylori and anti-cytotoxin-associated gene A (CagA) seropositivity in blood donors.MethodsA total of 311 blood donors were enrolled. ABO and Rh blood groups were determined using hemagglutination tests. Specific anti-H. pylori IgG and anti-CagA IgG antibodies in sera were quantitated by enzyme-linked immunosorbent assay. Correlations between blood groups and anti-H. pylori and anti-CagA seropositivity were evaluated using the Chi-square test.ResultsO+ was the most frequent blood type (38%, n = 118). Anti-H. pylori IgG seropositivity was observed in 240 (77.2%) blood donors, while anti-CagA IgG seropositivity was observed in 132 (42.5%) blood donors. Although seropositivity rates for both anti-H. pylori and anti-CagA IgG were higher in individuals with blood type O, no statistically significant associations were observed between seropositivity and any ABO/Rh blood groups.ConclusionIndividuals with blood type O may have higher rates of H. pylori seropositivity.     

Generation of transgenic mice with antithetical KEL1 and KEL2 human blood group antigens on red blood cells

BACKGROUND: KEL1, also known as “K,” is one of the most immunogenic red blood cell (RBC) antigens. KEL2, also known as “k,” differs from KEL1 by a single amino acid. Anti‐Kell system antibodies can lead to significant adverse clinical outcomes in humans, including hemolytic complications in alloimmunized transfusion recipients or in infants of alloimmunized mothers. To provide a platform for in‐depth immunologic studies of alloimmunization and subsequent sequelae, we generated transgenic mice expressing the human KEL1 or KEL2 antigens. STUDY DESIGN AND METHODS: Vectors were created in which cDNAs encoding either KEL1 or KEL2 were regulated by an erythroid specific β‐globin promoter and enhancer. Pronuclear microinjections were carried out into a C57BL6 background, and founder pups were identified by polymerase chain reaction and screened for expression by flow cytometry. RBC life span and antigen stability were assessed by dye labeling RBCs, transfusing into agammaglobulinemic (µMT) recipients, and tracking by flow cytometry. RESULTS: The expression of either KEL1 or KEL2 is RBC specific and first occurs on early RBC precursors. Both KEL1 and KEL2 RBCs have a normal circulatory life span and stable antigen expression. Expression of KEL1 or KEL2 does not result in altered levels of murine Kell, and resulting RBCs have normal hematologic variables. CONCLUSION: The KEL1 and KEL2 mice represent the first murine system of RBC immunity with antithetical antigens, allowing a more precise modeling of human RBC immunology in general and also a platform for development of novel therapeutics to prevent or minimize the dangers of RBC alloimmunization to the KEL1 and KEL2 antigens in particular.     

Depressed blood group antigens on red cells from a Mexican donor

Red cells from a Mexican blood donor had depressed H, IF, ID, i, Sda, Sdx, D, LW, Dib, Vel and JMH antigens. A wide range of other blood group antigens had normal activity. The unusual red cell phenotype may be caused by a membrane anomaly that alters orientation of certain cell surface components. The specificities of the depressed red cell antigens in this phenomenon differ from those affected in Melanesians with ovalocytosis or in individuals with the In(Lu) inhibitor gene.     

Learning about genomics and disease from the anucleate human red blood cell

During the differentiation of an erythrocyte, the developing erythroblast shuts down expression of most of its genes but preserves high levels of expression of certain key genes, such as those encoding hemoglobin and critical membrane proteins. In this issue of the JCI, Gallagher et al. show that a specialized type of DNA sequence element known as an insulator protects the expression of ankyrin, a key membrane protein. In several kindreds, mutations in the insulator led to impaired ankyrin expression and congenital hemolytic anemia. This work provides important insights into ways in which epigenetic changes can alter gene expression and thereby lead to human disease.     

Molecular biology of red cell blood group genes

The explosion of new information and technology for probing the fine architecture of gene structure has already brought new insights into the varied phenotypic expression of red cell blood group antigens. Molecular biologic techniques will be increasingly applied to red cell antigens as well as blood group antigens on other blood cells. Not since the introduction of the Coombs reagent has such a powerful method been available with which to increase our understanding of the nature of blood cell antigens.     

The structure and function of the molecules that carry human red blood cell and platelet antigens

A number of molecules on the surface of red blood cells (RBCs) and platelets express antigenic activity. Various biochemical and molecular approaches have been used to determine the structure and possible function that these molecules have for their respective cell types. The existence of variant molecules and null phenotypes and the immunological response to these antigens have aided in the analysis of the structure and function relationships of these molecules. A comparison of the sequence to moieties of known function and the presence of functional domains for many of the molecules allows for a prediction of their function. The proposed function of the molecules that express RBC and platelet antigens includes membrane structure, transporter or channel formation, receptor/ligand signaling or adhesion, enzyme activity, and glycocalyx formation. However, the function of some of these molecules is not known, and many of the variant antigens do not show an obvious functional difference. For unknown reasons, some of these molecules are exceptionally polymorphic and the elucidation of the precise role that these polymorphisms play in structure and function is hindered by limitations in the in vitro and ex vivo analyses and access to precursor cell types. The objective of this review is to define the structure and function of those molecules that express RBC and platelet antigens and the significance, if any, that polymorphisms have for these molecules.     

Human red cell aquaporin CHIP. I. Molecular characterization of ABH and Colton blood group antigens.

Blood group antigens are structural variants in surface carbohydrate or amino acid polymorphisms on extracellular domains of membrane proteins. The red cell water channel-forming integral protein (Aquaporin CHIP) is a homotetramer with only one N-glycosylated subunit, however no CHIP-associated blood group antigens have yet been identified. Immunoblotting, monosaccharide composition analysis, and selective glycosidase digestions revealed that the CHIP-associated oligosaccharide contains ABH determinants and resembles a band 3-type glycan that cannot be cleaved from intact membranes by Peptide:N-glycosidase F. The molecular structure of the Colton antigens was previously unknown, but CHIP was selectively immunoprecipitated with anti-Coa or anti-Co(b). The DNA sequence from Colton-typed individuals predicted that residue 45 is alanine in the Co(a+b-) phenotype and valine in the Co(a-b+) phenotype. The nucleotide polymorphism corresponds to a PflMI endonuclease digestion site in the DNA from Co(a-b+) individuals. These studies have defined antigens within two blood group systems on CHIP: (a) an ABH-bearing polylactosaminoglycan attached to a poorly accessible site in the native membrane; and (b) the Colton antigen polymorphism which may permit the identification of rare individuals with defective water channel expression.     

High-throughput molecular profiling of blood donors for minor red blood cell and platelet antigens

BACKGROUND: ABO and D phenotyping of both blood donors and patients receiving transfusions is routinely performed by blood banks to ensure compatibility. These analyses are performed by antibody-based agglutination assays. Blood is not tested for minor blood group antigens on a regular basis, however, because of cost and time constraints. This can result in alloimmunization of the patient against one to several minor antigens and may complicate future transfusions. STUDY DESIGN AND METHODS: To address this problem, an assay has been generated on the GenomeLab SNPstream genotyping system to test simultaneously polymorphisms linked to 22 different blood antigens with donor's DNA isolated from minute amounts of white blood cells. RESULTS: The results showed that both the error rate of the assay, as measured by the strand concordance rate, and the no-call rate were very low (0.1%). The concordance rate with the actual red blood cell (RBC) and platelet (PLT) serology data varied from 97 to 100 percent. Experimental or database errors as well as rare polymorphisms contributing to antigen conformation could explain the observed differences. These rates, however, are well above requirements because phenotyping and cross-matching will always be performed before transfusion. CONCLUSION: Molecular profiling of blood donors for minor RBC and PLT antigens will give blood banks instant access to many different matched donors through the setup of a centralized data storage system.