DOCSLIB.ORG

Conditions Causing Weak Expression of Kell System Antigens

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Conditions Causing Weak Expression of Kell System Antigens Review: conditions causing weak expression of Kell system antigens R. ØYEN, G.R. HALVERSON, AND M.E. REID Key Words: Kell system, KEL gene, weakened Kell Kpa Cis-Modifying Phenotype antigens Kell system antigens (other than Kpa) on Kp(a+b–) RBCs may be weaker than on RBCs of common Kell type Background a 1 due to the cis-modifying effect of the Kp allele. This phe- Since the discovery of anti-K in 1946, the Kell blood 9 2 nomenon was first noted decades ago by Allen et al., group system has grown to include 22 antigens. The sys- who found that K+k+Kp(a+b+) RBCs were weakly reac- tem has five sets of alleles that produce antithetical anti- tive with some examples of anti-k. We have seen numer- gens, one or two of low-incidence and the others of ous examples of anti-k that react 2+ with RBCs of high-incidence. In addition, eight antigens of high-inci- common Kell phenotype but are nonreactive (by direct dence and three of low-incidence have been recognized testing) with a K+k+Kp(a+b+) RBC sample that is rou- (Table 1). The system also includes a null phenotype, Ko, tinely included on our in-house panel. Kell system anti- in which the red blood cells (RBCs) are devoid of all Kell gens, including the Kpa antigen, are expressed weakly on system antigens, and a Kellmod phenotype, in which all RBCs from Kpa/Ko individuals.9–11 In fact, the cis-modi- Kell antigens are expressed weakly. fying effect of Kpa is most evident in Kpa/Ko individu- The occurrence of low-incidence Kell system antigens 10 a als but is also evident for the k antigen if the partner differs considerably in different ethnic groups: K, Kp , and chromosome carries K. Since the RBCs of most Kp(a+) K17 are found mainly in Caucasians; Jsa in blacks; and Ula 3 people also type as Kp(b+), the antigens produced by the in Finns and Japanese. K23, K24, and K25 have been iden- Kpb allele mask the cis-modifying effect of the Kpa allele. tified in one family each, all Caucasian. A single Kell gene The cis-modifying effect of Kpa varies from one individu- (KEL) has not encoded more than one low-incidence anti- al to another and it is difficult to demonstrate on RBCs gen. For example, a gene that produces K has never pro- a a a a a 3 from Kp /Kp people. None of the genes encoding other duced Kp , Js , Ul , K17, K23, K24, or K25. Since now it Kell system antigens has shown a similar cis-modifying is known that polymorphism in the Kell blood group sys- 4–6 effect. Unlike other RBCs that have a weak expression of tem is the result of point mutations, the presence of Kell blood group system antigens, the Kx antigen is not more than one low-incidence Kell system antigen on a sin- enhanced on Kp(a+b–) RBCs. gle chromosome is statistically an unlikely event. In fact, The cis-modifying effect has not been described with this status is similar to the situation with low-incidence anti- Kpc, the other low-incidence antithetical antigen to Kpb. gens in Lutheran and Cromer blood group systems. c c This may be because Kp is rare and K+Kp(c+) or Kp /Ko Kell blood group antigens are inactivated by treatment RBCs have not been found. of RBCs with disulfide reagents such as dithiothreitol (DTT) and aminoethylisothiouronium bromide (AET), due to disruption of the multiple disulfide bonds.7 The Table 1. Antigens in the Kell blood group system remarkable susceptibility of Jsa and Jsb antigens to such Allelic High-incidence Low-incidence Obsolete treatment, as compared to other Kell antigens,8 is proba- K(K1)/k(K2) Ku(K5) Ula(K10) Kw(K8) Kpa(K3)/Kpb(K4)/Kpc(K21) K12 K23 K9* bly due to the location of the amino acid substitution asso- Jsa(K6)/Jsb(K7) K13 K25(VLAN) K15* ciated with this polymorphism, which is within a cluster K11/K17 K16 5 K14/K24 K18 of cysteine residues. K19 This paper will review causes of weak expression of K20 antigens in the Kell blood group system, compare their K22 *K9(KL) has been replaced by K15(Kx) and K20(Km). Since K15 is not part relative strengths, and discuss how this information can of the Kell blood group system, it has been given system status by the ISBT be used in antibody identification studies. working party: 019(XK). IMMUNOHEMATOLOGY, VOLUME 13, NUMBER 3, 1997 75 R. ØYENETAL. K:–13 Phenotype linked XK gene was responsible for the observed weak- The original propositus and his sister are the only indi- ening of the Kell system antigens.3 There is no known viduals identified with RBCs of the K:–13 phenotype. family in which the McLeod phenotype has been passed Their RBCs have a decreased expression of common anti- from father to son. In one family, a normal K+k+ man and gens in the Kell system. It is not known if this decrease is a K–k+ McLeod carrier female have two McLeod pheno- due to a cis-modifying effect as is seen with the Kp(a+b–) type sons, one K+wk+w and the other K–k+w.19 These phenotype, since the low-incidence allele to K13 has not data indicate that the Kell genes are normal in the McLeod been discovered. It became apparent during family stud- phenotype but expression of the antigens is modified. ies that the two K:–13 individuals may have inherited the If immunized to allogenic RBCs, non-CGD McLeod indi- Ko gene as judged by tests with anti-Kx. Titration studies viduals produce anti-Km and CGD McLeod individuals pro- using RBCs from presumed K:13/Ko family members did duce anti-Kx+Km. Anti-Km reacts with all RBCs of common 12 not exhibit weakening of Kell system antigens. Kell type but not with those of either McLeod or Ko phe- Individuals with RBCs of common Kell/Ko type cannot be notype. Anti-Kx+Km reacts with all RBCs except those with identified by quantitative studies if the Kpb gene is pres- McLeod phenotype (of CGD and non-CGD types).15,20 13–15 ent. Therefore, it is unlikely that the weak expression Thus, crossmatch-compatible McLeod or Ko RBCs may be of Kell antigens observed in the K:–13 phenotype is a con- used to transfuse immunized non-CGD McLeod individuals, sequence of the Ko allele. while only McLeod RBCs will be compatible with serum from immunized CGD McLeod individuals. Kmod Phenotypes Anti-Kx+Km is required to identify conclusively Kmod is an umbrella term used to describe RBCs that McLeod phenotype RBCs. This antibody, which is only have a permanent decreased expression of Kell system made by individuals with the CGD-type of McLeod, is in antigens.16 The degree of Kell system antigen depression short supply and thus detection of McLeod phenotype of Kmod RBCs varies from individual to individual (rang- RBCs mainly relies on observed weakening of Kell anti- ing from nonreactive to 1+ on direct testing) but appears gens on the individual’s RBCs by hemagglutination. Since to be a permanent feature of an individual’s own RBCs. different Kell system antibodies vary in their ability to RBCs from Kmod individuals from the same family show a detect weakened expression of the corresponding anti- similar degree of depression.17 The antigen depression gen of RBCs with the McLeod phenotype, we recom- may be so severe that adsorption and elution using potent mend that suitable sera be preselected for this purpose. Kell system antibodies may be needed to differentiate In our experience, anti-K14 (polyclonal and monoclonal) Kmod RBCs from Ko phenotype RBCs. Indeed, some is the most effective specificity. Flow cytometry using examples originally thought to be of the Ko phenotype anti-K14 demonstrates the weakening of this antigen on have been reclassified as Kmod. The Kx antigen is RBCs from McLeod phenotype males and clearly shows 21,22 enhanced on Kmod phenotype RBCs, a feature that dis- the two RBC populations in McLeod carrier females. tinguishes the phenotype from the McLeod phenotype. McLeod carrier females have two populations of RBCs: Individuals with the Kmod phenotype, if immunized, one is of the McLeod type and the other is of common Kell produce an antibody similar to anti-Ku (called anti- type. The proportion of McLeod RBCs to common Kell RBCs Ku–like), an antibody that is nonreactive against Ko RBCs varies in different females but is consistent within a female 21 and autologous RBCs (Table 2). The antibodies from Kmod over time and in different females in the same family. individuals are not mutually compatible when crosstest- 18 a ed against other Kmod RBCs. Kp cis-modifying in conjunction with McLeod Severe depression of Kell antigens has been reported McLeod Phenotype in one family in which the propositus appeared to have 23 RBCs of the McLeod phenotype (both chronic granu- RBCs of the Ko phenotype. However, his RBCs had a lomatous disease [CGD] and non-CGD types) show very weak expression of the Kx antigen. His son’s RBCs marked weakening of all Kell system antigens and lack the typed Kp(a+b+)Kx+ and his two daughters’ RBCs typed Kx antigen (Table 2). The phenotype was initially con- Kp(a+wb+w)Kxw. Molecular studies showed he had the sidered to belong to the Kell blood group system; how- Kpa/Kpa genotype and that his XK gene had a single base ever, the inheritance of the McLeod phenotype is change within the donor splice consensus sequence of X-linked.
Load more

Recommended publications
  • Blood, Lymph, and Immunity Joann Colville
    Blood, Lymph, and Immunity Joann Colville CHAPTER OUTLINE .»: BLOOD Function Introduction Lymphatic Structures Plasma THE IMMUNE SYSTEM Cellular Components of Blood Function Red Blood Cells Immune Reactions Platelets Immunization: Protection Against Disease White Blood Cells THE LYMPHATICSYSTEM Lymph Formation Characteristics LEARNING OBJECTIVES • List and describe the functions of blood • List the functions of the lymphatic system • Describe the composition of blood plasma • Describe the structure and functions of the lymph nodes, • Describe the characteristics of mature erythrocytes spleen, thymus, tonsils, and GALT Describe the structure of the hemoglobin molecule and • List the functions of the immune system explain the fate of hemoglobin following intravascular and • Differentiate between specific and nonspecific immune extravascular hemolysis reactions • Give the origin of thrombocytes and describe their • Differentiate between cell-mediated and humoral immunity characteristics and functions • List the components involved in cell-mediated immunity • Listthe types of leukocytes and describe the functions of each and explain the role of each • Describe the formation of lymph fluid and its circulation List and describe the classes of immunoglobulins through the lymphatic system • Differentiate between active and passive immunity BLOOD vessels of the cardiovascular system. It has three main func- tions: transportation, regulation, and defense. INTRODUCTION Blood. Say the word, and some people cringe, others faint, Function and if you believe authors Bram Stoker, Stephen King, and 1. Blood is a transport system. Christopher Moore (all authors of vampire books), others • It carries oxygen, nutrients, and other essential com- drool. But no matter what you think about blood, animals pounds to every living cell in the body.
    [Show full text]
  • The Diagnosis of Paroxysmal Nocturnal Hemoglobinuria: Role of Flow Cytometry
    THE DIAGNOSIS OF PAROXYSMAL NOCTURNAL HEMOGLOBINURIA: ROLE OF FLOW CYTOMETRY Alberto Orfao Department of Medicine, Cancer Research Centre (IBMCC-CSIC/USAL), University of Salamanca, Salamanca, Spain Paroxysmal nocturnal hemoglobinuria (PNH) on one or multiple populations of peripheral blood is an acquired clonal disorder typically affecting red cells and/or leucocytes of PNH patients, this young adults, which involves the phosphatidylino- translating into a new diagnostic test. Because sitol glycan anchor biosynthesis class A gene of this flow cytometry became an essential tool (PIGA) coded in chromosome X, in virtually every in the diagnosis of PNH. In turn, it could be also case. The altered gene encodes for a defective pro- demonstrated that investigation of the presence of tein product, the pig-a enzyme which is involved GPI-deficient cells among circulating mature neu- in the early steps of the synthesis of glycosylphos- trophils and monocytes, increases the sensitivity phatidylinositol (GPI). This later molecule (GPI) of red blood cell screening because of the shorter acts as an anchor of a wide range of proteins to lifetime of both populations of leucocytes. Despite the cell surface. At present a large number of GPI- all the above, routine assessment of CD55 and anchor associated proteins have been described CD59 is also associated with several limitations which are expressed by one or multiple distinct due to distinct patterns of expression among dif- compartments of hematopoietic cells. The altered ferent cell populations, dim and heterogeneous PIGA gene leads to an altered GPI anchor which expression among normal individuals and the lack leads to defective expression of GPI-AP on the of experience in many labs as regards the normal cytoplasmic membrane, on the cell surface.
    [Show full text]
  • Chapter 06 Lecture Outline
    Chapter 06 Lecture Outline See separate PowerPoint slides for all figures and tables pre- inserted into PowerPoint without notes. Copyright © 2016 McGraw-Hill Education. Permission required for reproduction or display. 1 Cardiovascular System: Blood © SPL/Science Source, (inset) © Andrew Syred/Science Source 2 Points to ponder • What type of tissue is blood and what are its components? • What is found in plasma? • Name the three formed elements in blood and their functions. • How does the structure of red blood cells relate to their function? • Describe the structure and function of each white blood cell. • What are disorders of red blood cells, white blood cells, and platelets? • What do you need to know before donating blood? • What are antigens and antibodies? • How are ABO blood types determined? • What blood types are compatible for blood transfusions? • What is the Rh factor and how is this important to pregnancy? • How does the cardiovascular system interact with other systems to maintain homeostasis? 3 6.1 Blood: An Overview What are the functions of blood? • Transportation: oxygen, nutrients, wastes, carbon dioxide, and hormones • Defense: against invasion by pathogens • Regulatory functions: body temperature, water- salt balance, and body pH 4 6.1 Blood: An Overview What is the composition of blood? • Remember: blood is a fluid connective tissue. • Formed elements are produced in red bone marrow. – Red blood cells/erythrocytes (RBCs) – White blood cells/leukocytes (WBCs) – Platelets/thrombocytes 5 6.1 Blood: An Overview What is the composition of blood? • Plasma – It consists of 91% water and 9% salts (ions) and organic molecules. – Plasma proteins are the most abundant organic molecules.
    [Show full text]
  • Hematology Unit Lab 1 Review Material
    Hematology Unit Lab 1 Review Material Objectives Laboratory instructors: 1. Facilitate lab discussion and answer questions Students: 1. Review the introductory material below 2. Study and review the assigned cases and questions in small groups before the Lab. This includes the pathological material using Virtual Microscopy 3. Be prepared to present your cases, questions and answers to the rest of your Lab class during the Lab Erythropoiesis: The process of red blood cell (RBC) production • Characterized by: − Increasing hemoglobin synthesis Erythroid maturation stages (Below): − Decreasing cell size - Average of 4 cell divisions during maturation − Decreasing cytoplasmic basophilia [One pronormoblast gives rise to 16 red cells] (increasing pink color) - pronormoblast → reticulocyte = 7 days − Progressive chromatin condensation of the - reticulocytes → mature RBC =1-2 days nuclei − Extrusion of nucleus (orthochromatic stage) − Extruded nuclei are subsequently phagocytized − Loss of mitotic capability after the early stage of polychromatophilic normoblast • Picture below: Erythroid progenitors (normoblasts) cluster around macrophages (arrows) in the bone marrow and spleen • Macrophages store iron • Iron is transferred from macrophages to erythroid precursor cells • Iron is used by normoblasts for hemoglobin synthesis aka nucleated rbc aka reticulocyte 1 Mature Red Blood Cell 7-8 microns; round / ovoid biconcave disc with orange-red cytoplasm, no RNA, no nucleus; survives ~120 days in circulation Classification of Anemia by Morphology 1.
    [Show full text]
  • CD59: a Long-Known Complement Inhibitor Has Advanced to a Blood Group System
    B LOOD G ROUP R EVIEW CD59: A long-known complement inhibitor has advanced to a blood group system C. Weinstock, M. Anliker, and I. von Zabern The blood group system number 35 is based on CD59, a 20-kDa by Zalman et al.1 from the group of H.J. Muller-Eberhard in La membrane glycoprotein present on a large number of different Jolla, California, and in 1988 by Schönermark et al. from the cells, including erythrocytes. The major function of CD59 is to group of G.M. Hänsch in Heidelberg (Germany).2 This inhibitor protect cells from complement attack. CD59 binds to complement components C8 and C9 and prevents the polymerization of C9, was published under the designations “HRF (homologous which is required for the formation of the membrane attack restriction factor)” and “C8bp (C8 binding protein),” complex (MAC). Other functions of CD59 in cellular immunity respectively, to describe its properties.1,2 “C8bp” indicates the are less well defined. CD59 is inserted into the membrane by a glycosylphosphatidylinositol (GPI) anchor. A defect of this anchor binding capacity for C8. The name “HRF” points to a species causes lack of this protein from the cell membrane, which leads to incompatibility of this “factor” that provides protection from an enhanced sensitivity towards complement attack. Patients with complement attack more effectively in a homologous (e.g., paroxysmal nocturnal hemoglobinuria (PNH) harbor a varying human erythrocytes as a target of human complement) than in percentage of red blood cell clones with a defect in GPI-anchored proteins, including CD59. The most characteristic symptoms of a heterologous system (e.g., human erythrocytes as a target of this disease are episodes of hemolysis and thromboses.
    [Show full text]
  • SEED Haematology Sysmex Educational Enhancement and Development October 2012
    SEED Haematology Sysmex Educational Enhancement and Development October 2012 The red blood cell indices The full blood count has been used in conjunction with the traditional red The complete blood count (CBC) is central to clinical deci- cell indices in order to narrow down the possible causes sion making. This makes it one of the commonest laboratory of anaemia in an individual patient. investigations performed worldwide. Whilst the definition of what constitutes an CBC is influenced by the number Impedance technology and type of parameters measured by different haematology The RBC, HCT and MCV are all closely interrelated as they analysers, the traditional red cell indices that are widely are derived from information obtained from the passage used to classify anaemias are common to all. of cells through the aperture of the impedance channel of an automated haematology analyser. The impedance The laboratory approach to anaemia technology is based on the principle that an electrical field, Anaemia is an extremely common global healthcare prob- created between two electrodes of opposite charge, can lem. However, anaemia is merely a symptom which can be used to count and determine the size of cells. Blood result from a multitude of causes. Effective treatment is cells are poor conductors of electricity. The diluent in which only possible if the underlying cause is correctly identified. they are suspended as they pass through the aperture To this end, several classification systems have been devis- during counting is an isotonic solution which is a good ed. The most useful and widely used classification system conductor of electricity.
    [Show full text]
  • Apheresis Red Cell Exchange/Transfusions
    APHERESIS RED CELL EXCHANGE/TRANSFUSIONS In a patient treated in Manchester, parasitemia was virtually eliminated over eight hours by a 3.5 liter exchange blood transfusion (Plasmodium Falciparum Hyperparasitemia: Use of Exchange Transfusion in Seven Patients and a Review of the Literature). Several cases of severe babesiosis refractory to appropriate antibiotic therapy have been reported to respond promptly and dramatically to red blood cell (RBC) exchange transfusion. Asplenic patients, however, generally have a more severe course of illness, with hemolytic anemia, acute renal failure, disseminated intravascular coagulation, and pulmonary edema. Primary therapy is with antibiotics including clindamycin and quinine, with RBC exchange transfusion reported to be effective in severe cases. The RBC exchange transfusions succeeded in reducing significantly the level of parasitemia, dramatically improving the condition of an extremely ill patient. Our report adds to the small but growing literature on severe Babesia infection in humans, and provides further evidence to support the use of RBC exchange transfusion to treat severe babesiosis. Its single great advantage over antibiotic therapy is its rapid therapeutic effectiveness (Treatment of Babesiosis by Red Blood Cell Exchange in an HIV-Positive Splenectomized Patient). There was rapid clinical improvement after the whole-blood exchange transfusion. In cases of severe babesiosis, prompt institution of whole-blood exchange transfusion, in combination with appropriate antimicrobial therapy, can be life-saving. In patients with progressive babesiosis, early intervention with exchange transfusion, along with appropriate antimicrobial therapy, should be considered to speed clinical recovery. (Fulminant babesiosis treated with clindamycin, quinine, and whole-blood exchange transfusion. However, asplenic patients may have a much more serious clinical course.
    [Show full text]
  • Indicators of the Iron Status of Populations: Red Blood Cell Parameters Sean Lynch
    AnneX 1 Indicators of the iron status of populations: red blood cell parameters SEAN LYNch 19 Indicators OF the iron statUS OF popUlations: red blood cell parameters Contents 1. Introduction 22 2. Relationship between anaemia and iron deficiency 23 2.1 Physiological control of haemoglobin levels 23 2.2 Relationship between iron deficiency and anaemia 24 3. Red blood cell parameters 26 3.1 Haemoglobin 26 3.2 Hematocrit or packed cell volume 26 3.3 Mean cell volume and mean cell haemoglobin 27 3.4 Red cell distribution width 27 3.5 Reticulocyte haemoglobin concentration and percentage of hypochromic red cells 27 4. Role of haemoglobin as a screening indicator for iron deficiency 27 5. Conclusions 28 6. References 29 21 Assessing the iron statUS OF popUlations 1. Introduction Iron is an essential nutrient that plays a central role in many metabolic processes. Aerobic metabolism is critically dependent on maintaining normal concentrations of several iron-containing proteins that mediate oxygen transport, storage and utili- zation, particularly when the tissue demand for oxygen is increased by physical ac- tivity. Pioneering research over the last 50 years, much of it stemming from concepts developed and validated experimentally by Dr Clement Finch and his coworkers, led to the recognition that a negative iron balance resulting from an iron intake insuf- ficient to match losses from the body despite compensatory changes in the rate of absorption and, to a more limited extent, excretion could be divided into three stages based on the severity of the potential effect on physiological functions. The evalua- tion of functional impairment was related entirely to erythropoiesis for two reasons: the effects of changes in iron status on blood elements are readily evaluated, while the effect on the enzymes in other tissues necessitates obtaining biopsy samples.
    [Show full text]
  • Jka, Jkb, Jk – Co-Dominant Inheritance – Jk Is a Silent Allele
    Kidd Blood Group System Qun Lu, MD Assistant Professor Division of Transfusion Medicine Department of Pathology and Laboratory Medicine UCLA, School of Medicine Los Angeles, California 02-05-2009 History of Kidd Blood Group System . Jka was discovered in 1951 by Allen: Mrs. Kidd had hemolytic disease of newborn (HDN) in her son. A new RBC alloantibody was detected in her serum, reacted with her husband’s RBCs. Jkb was found in 1953 by Plaut . The antigens were independent of other known blood groups. They named after Mrs. Kidd. Jk null phenotyp was found in 1959 by Pinkerton. Since the specificities were inseparable, the antibody was renamed anti-Jk3 which recognizes an antigen found whenever Jka or Jkb is present. ISBT Human Blood Group Systems ISBT Number Name Abbreviation 001 ABO ABO 002 MNS MNS 003 P P 004 Rh RH 005 Lutheran LU 006 Kell KEL 007 Lewis LE 008 Duffy FY 009 Kidd JK 010 Diego DI 011 Cartwright YT 012 XG XG 013 Scianna SC 014 Dombrock DO 015 Colton CO 016 Landsteiner-Wiener LW 017 Chido/Rodgers CH/RG 018 Hh H 019 Kx XK 020 Gerbich GE 021 Cromer CROM 022 Knops KN 023 Indian IN 024 Ok OK 025 Raph RAPH Kidd Antigens . Genotype: – Genes located on chromosome 18 – Three alleles Jka, Jkb, Jk – Co-dominant Inheritance – Jk is a silent allele . Common antigen ---- JK3 Ag: – Present with Jka and/or Jkb antigens – Whenever you have Jka or Jkb antigens on the RBC you also have Jk3 antigen. – Anti- Jk3 is against Jka,Jkb, Jk3 antigens, transfuse with Jk(a-b-) blood, very difficult to find Homozygous Heterozygous for Jka or Jkb for JKa and Jkb.
    [Show full text]
  • Recommendations for Collecting Red Blood Cells by Automated Apheresis Methods
    Guidance for Industry Recommendations for Collecting Red Blood Cells by Automated Apheresis Methods Additional copies of this guidance document are available from: Office of Communication, Training and Manufacturers Assistance (HFM-40) 1401 Rockville Pike, Rockville, MD 20852-1448 (Tel) 1-800-835-4709 or 301-827-1800 (Internet) http://www.fda.gov/cber/guidelines.htm U.S. Department of Health and Human Services Food and Drug Administration Center for Biologics Evaluation and Research (CBER) January 2001 Technical Correction February 2001 TABLE OF CONTENTS Note: Page numbering may vary for documents distributed electronically. I. INTRODUCTION ............................................................................................................. 1 II. BACKGROUND................................................................................................................ 1 III. CHANGES FROM THE DRAFT GUIDANCE .............................................................. 2 IV. RECOMMENDED DONOR SELECTION CRITERIA FOR THE AUTOMATED RED BLOOD CELL COLLECTION PROTOCOLS ..................................................... 3 V. RECOMMENDED RED BLOOD CELL PRODUCT QUALITY CONTROL............ 5 VI. REGISTRATION AND LICENSING PROCEDURES FOR THE MANUFACTURE OF RED BLOOD CELLS COLLECTED BY AUTOMATED METHODS.................. 7 VII. ADDITIONAL REQUIREMENTS.................................................................................. 9 i GUIDANCE FOR INDUSTRY Recommendations for Collecting Red Blood Cells by Automated Apheresis Methods This
    [Show full text]
  • Blood Groups – Kell Group
    Blood Groups – Kell Group Qun Lu, MD Assistant Professor Division of Transfusion Medicine Department of Pathology and Laboratory Medicine UCLA, School of Medicine Los Angeles, California 2008-12-17 1 History . Discovered in 1946: an antibody was identified in Mrs. Kellacher, the antibody reacted with her newborn infant, her older daughter, her husband, and about 9% of the white population. Antigen is named after her, called Kell . In 1949, k antigen was discovered by Levine, called Cellano antigen . Kpa, Kpb antigens were discovered in 1957, 1958 . Jsa, Jsb antigens were discovered in 1957, 1963 . Inheritance patterns and statistics confirmed these antigens are related to the Kell system 2 History . K0 (null phenotype) was discovered in 1957. It helped to figure out the relationship between K, k, Kpa, Kpb, Jsa, Jsb antigens, because anti- K0 reacted with these antigen positive cells . McLeod phenotype was discovered by Allen and coworkers in 1961: weaken expression of Kell antigens 3 Xk Gene KEL gene codes for the entire Kell system KEL Gene glycoprotein, some 720 amino acids. It also codes for the Km antigen. RBC Kell system glycoprotein: Kx Km Kell Ag’s reside here. Kx is NOT a Kell system antigen -but there is interaction between the Kell protein and the Kx antigen. The Xk gene is located on the X chromosome 4 Kell Antigens . Routinely tested Kell antigens: K, k, Kpa, Kpb, Jsa, Jsb . Other Kell antigens: Ku, Ula, Wka, Kx, Km, Kpc,(only exist on Kpa-, Kpb- cells), Cent, Callais… . Ku – an universal Kell antigen present on all cells except K0 cells (K null phenotype)\ .
    [Show full text]
  • Package Insert
    [US] 1 / 2 • Caution: Do not pipette by mouth. The absence of all viruses has not been determined. Blood Grouping Reagent • Caution: This Product Contains Natural Rubber Latex Which May Cause Allergic Reactions. Anti-K (KEL1) • Warning: Contains sodium azide (NaN3), which may react with lead or ® Seraclone Human Monoclonal copper plumbing to form explosive azides. If discarded in the sink, flush with (MS56) large amounts of water to prevent the build-up of explosive metal azides. • The bovine albumin used for the production of this reagent is sourced from FOR IN VITRO DIAGNOSTIC USE donor animals of U.S. origin that have been inspected and certified by U.S. For Tube Testing Veterinary Service inspectors to be disease free. MEETS FDA POTENCY REQUIREMENTS • Consult downloads.bio-rad.com to download the valid version of this instruction for use. U.S. License Number: 1845 Rx only SPECIMEN COLLECTION Fresh samples of clotted, EDTA or citrate anticoagulated whole blood collected PACKAGE SIZE following general blood sampling guidelines are acceptable. The specimen ® [REF] 808090100 [VOL] 5 mL Seraclone Anti-K (KEL1) should be tested as soon as possible after collection. If testing is delayed, specimens should be stored at 2 to 8°C, citrated specimens (donor segments) INTENDED USE may be stored at temperatures as low as 1°C. For the determination of the Kell (KEL1) antigen of red blood cells using the tube Note: Blood specimens exhibiting gross hemolysis or contamination should not test. be used. Clotted samples or those collected in EDTA may be tested within ten days from SUMMARY collection.
    [Show full text]