scholarly journals Prevalence of Red Blood Cell Major Blood Group Antigens and Phenotypes among Omani Blood Donors

2019 ◽  
Vol 34 (6) ◽  
pp. 496-503
Author(s):  
Arwa Z. Al-Riyami ◽  
Ali Al-Marhoobi ◽  
Saif Al-Hosni ◽  
Sabah Al Mahrooqi ◽  
Michael Schmidt ◽  
...  
Keyword(s):  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Blood Donors ◽  
Blood Group Antigens

scholarly journals Cellular immune responses in red blood cell alloimmunization

Hematology ◽  
2016 ◽  
Vol 2016 (1) ◽  
pp. 452-456 ◽  
Author(s):  
James C. Zimring ◽  
Krystalyn E. Hudson
Keyword(s):  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Cell Biology ◽  
Antigen Processing ◽  
The United States ◽  
Single Amino Acid ◽  
Solid Organ ◽  
Blood Group Antigens ◽  
Transfusion Therapy

Abstract In excess of 340 blood group antigens have now been described that vary between individuals. Thus, any unit of blood that is nonautologous represents a significant dose of alloantigen. Most blood group antigens are proteins, which differ by a single amino acid between donors and recipients. Approximately 1 out of every 70 individuals are transfused each year (in the United States alone), which leads to antibody responses to red blood cell (RBC) alloantigens in some transfusion recipients. When alloantibodies are formed, in many cases, RBCs expressing the antigen in question can no longer be safely transfused. However, despite chronic transfusion, only 3% to 10% of recipients (in general) mount an alloantibody response. In some disease states, rates of alloimmunization are much higher (eg, sickle cell disease). For patients who become alloimmunized to multiple antigens, ongoing transfusion therapy becomes increasingly difficult or, in some cases, impossible. While alloantibodies are the ultimate immune effector of humoral alloimmunization, the cellular underpinnings of the immune system that lead to ultimate alloantibody production are complex, including antigen consumption, antigen processing, antigen presentation, T-cell biology, and B-cell biology. Moreover, these cellular processes differ to some extent with regard to transfused RBCs as compared with other better-studied immune barriers (eg, infectious disease, vaccines, and solid organ transplantation). The current work focuses on illustrating the current paradigm of humoral immunity, with a specific focus on particulars of RBC alloimmunization and recent advances in the understanding thereof.

scholarly journals Comparative Proteomics and Functional Analysis of Red Blood Cell Membrane Proteins in the Rare in(Lu) Blood Type

Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 934-934
Author(s):  
Slim Azouzi ◽  
Mahmoud Mikdar ◽  
Sara El Hoss ◽  
Alexandra Willemetz ◽  
Emilie-fleur Gautier ◽  
...  
Keyword(s):  
Membrane Proteins ◽  
Cell Membrane ◽  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Comparative Proteomics ◽  
26S Proteasome ◽  
Expression Level ◽  
Blood Group Antigens ◽  
Cell Membrane Proteins

Abstract KLF1 is an essential erythroid transcription factor (EKLF) involved both in the ß-globin switch from fetal to adult and in definitive erythropoiesis. KLF1 also activates genes encoding heme biosynthetic enzymes, as well as genes involved in the cell cycle and the synthesis of membrane proteins. Heterozygosity for one or several nucleotide changes in KLF1 may be responsible for the so-called dominant Lu(a-b-) phenotype, also known as In(Lu) for "Inhibitor Lutheran" and characterized by a dramatic reduction in the expression levels of the Lutheran blood group antigens and a slight elevation in hemoglobin F (HbF). Several other blood group antigens are also under the direct control of KLF1, but their number and expression level in In(Lu) red blood cells (RBCs) remain a matter of debate. In addition, mutations in KLF1 in humans lead to anemia, acantocytosis and some of these variants, such as CDA type IV, are characterized by ineffective terminal differentiation and defects in enucleation. Given the major role of KLF1 in erythropoiesis, it would not be surprising that In(Lu) RBCs show abnormal properties. In this work, we performed proteomic studies to quantify membrane proteins in In(Lu) vs control RBCs. Results: using label-free mass spectrometry, we analyzed the expression levels of membrane proteins in 5 In(Lu) and 4 control RBCs. Hierarchical clustering allowed to identify two modulation profiles of protein expression (Figure 1). The first profile (red color) is composed of 49 proteins over-expressed in In(Lu) RBCs, with the majority of them corresponding to the "26S proteasome complex" (PSMA, PSMB, PSMD, and PSME). In addition, we confirmed the overexpression of the 26S proteasome complex in In(Lu) RBCs by western blot analyses. The second profile (green color) includes 23 membrane proteins with a lower expression level in In(Lu) RBCs; these proteins correspond to blood group antigens (e.g. Lu/BCAM, CD44), and to cytoskeletal proteins (e.g. dematin, flotillin). Five proteins carrying blood group systems show a decrease of expression in In(Lu) RBCs over 40%: Chido/Rodgers, Xg, Indian, Duffy and Lutheran: antigens. While our results indicating of decreased expression of Indian and Chido/Rodgers systems are consistent with previous reports, the Duffy expression was unexpectedly found to be decreased by 86%. Since we evidenced an important increase in the proteasome complex, and taking into account that KLF1 is involved in the regulation or erythropoiesis, we, investigated the expression profile of the 26 S proteasome expression during erythropoiesis. We observed an important decrease of all proteins of the proteasome complex during erythropoiesis. Conclusion: from our preliminary results reported in this study, we hypothesized that the increase of the 26S proteasome in the In(Lu) individuals may result from defects in organelle loss and could explain the profound dyserytropoiesis observed in the "nan" mice null for KLF1. Figure 1: Comparative proteomics of red blood cell membrane proteins in In(Lu) blood group type. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

A new role for Pk: finding the 1 in a million

Blood ◽  
2009 ◽  
Vol 113 (20) ◽  
pp. 4826-4827
Author(s):  
Christopher D. Hillyer
Keyword(s):  
Infectious Disease ◽  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Therapeutic Target ◽  
Blood Group Antigens ◽  
Transfusion Medicine ◽  
Potential Therapeutic Target ◽  
Hiv Entry

Blood group antigens can have critical functions beyond the red blood cell. In this issue of Blood, Lund and colleagues demonstrate a role for Pk in HIV entry, providing biologic insight, identifying potential therapeutic target motifs and expanding the intersections of hematology, transfusion medicine, and infectious disease.

CONFIRMATION OF BONE MARROW ENGRAFTMENT BY DEMONSTRATION OF BLOOD GROUP ANTIGENS ON RED BLOOD CELL GHOSTS

1979 ◽  
Vol 28 (3) ◽  
pp. 257-258 ◽  
Author(s):  
KLAUS J. BROSS ◽  
GERHARD M. SCHMIDT ◽  
KARL G. BLUME ◽  
WAYNE E. SPRUCE ◽  
MARK J. FARBSTEIN
Keyword(s):  
Bone Marrow ◽  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Blood Group Antigens ◽  
Bone Marrow Engraftment

scholarly journals Characterization and statistical modeling of glycosylation changes in sickle cell disease

2021 ◽  
Vol 5 (5) ◽  
pp. 1463-1473
Author(s):  
Heather E. Ashwood ◽  
Christopher Ashwood ◽  
Anna P. Schmidt ◽  
Rebekah L. Gundry ◽  
Karin M. Hoffmeister ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Sickle Cell Disease ◽  
Blood Cell ◽  
Red Blood Cells ◽  
Blood Group ◽  
Sickle Cell ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Blood Group Antigens ◽  
Cell Disease

AbstractSickle cell disease is an inherited genetic disorder that causes anemia, pain crises, organ infarction, and infections in 13 million people worldwide. Previous studies have revealed changes in sialic acid levels associated with red blood cell sickling and showed that stressed red blood cells bare surface-exposed clustered terminal mannose structures mediating hemolysis, but detailed glycan structures and anti-glycan antibodies in sickle cell disease remain understudied. Here, we compiled results obtained through lectin arrays, glycan arrays, and mass spectrometry to interrogate red blood cell glycoproteins and glycan-binding proteins found in the plasma of healthy individuals and patients with sickle cell disease and sickle cell trait. Lectin arrays and mass spectrometry revealed an increase in α2,6 sialylation and a decrease in α2,3 sialylation and blood group antigens displayed on red blood cells. Increased binding of proteins to immunogenic asialo and sialyl core 1, Lewis A, and Lewis Y structures was observed in plasma from patients with sickle cell disease, suggesting a heightened anti-glycan immune response. Data modeling affirmed glycan expression and plasma protein binding changes in sickle cell disease but additionally revealed further changes in ABO blood group expression. Our data provide detailed insights into glycan changes associated with sickle cell disease and refer glycans as potential therapeutic targets.

Toxic masculinity in red blood cell units? Testosterone therapy in blood donors revisited

Transfusion ◽  
2021 ◽  
Author(s):  
Kelsey Hazegh ◽  
Bradley D. Anawalt ◽  
Larry J. Dumont ◽  
Tamir Kanias
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Blood Donors ◽  
Testosterone Therapy
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