Immunohematology
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Other Blood Group Systems—Diego,Yt, Xg, Scianna, Dombrock
Review: other blood group systems—Diego, Yt, Xg, Scianna, Dombrock, Colton, Landsteiner- Wiener, and Indian K.M. B YRNE AND P.C. B YRNE Introduction Diego Blood Group System This review was prepared to provide a basic The Diego blood group system (ISBT: DI/010) has overview of “Other Blood Groups.” Some of the more expanded from its humble beginnings to now include major blood group systems, i.e., ABO, Rh, Kell, Duffy, up to 21 discrete antigens (Table 1). 3 Band 3, an anion and Kidd, are also reviewed in this issue and are not exchange, multi-pass membrane glycoprotein, is the covered here. The sheer mass of data on the MNS basic structure that carries the Diego system antigenic blood group system is so extensive and complicated determinants. 4 The gene that encodes the Band 3 that it justifies a review all of its own, and it is therefore protein is named SLC4A1 and its chromosomal location not discussed in this article. However, various aspects is 17q12–q21. 4 of MNS were described in recent papers in Di a and Di b are antithetical, resulting from a single Immunohematology. 1,2 nucleotide substitution (2561T>C) that gives rise to The blood group systems that are covered are those amino acid changes in the Band 3 protein (Leu854Pro). that most workers believe to have some degree of To date, the Di(a–b–) phenotype has not been clinical importance or interesting features: Diego (DI), described. The Di a and Di b antigens are resistant to Yt (YT), Xg (XG), Scianna (SC), Dombrock (DO), Colton treatment with the following enzymes/chemicals: (CO), Landsteiner-Wiener (LW), and Indian (IN). -
Requirements for Blood and Blood Components Intended for Transfusion Or for Further Manufacturing Use
Requirements for Blood and Blood Components Intended for Transfusion or for Further Manufacturing Use Office of Blood Research and Review CBER, FDA Ask the FDA Session – AABB Annual Meeting October 26, 2015 1 Outline • Overview – Historical Background – Intent of the Rule – Organization of the Rule • Selected Provisions – Relevant Transfusion-Transmitted Infection – Control of Bacterial Contamination of Platelets – Medical Supervision – Donor Acknowledgement – Alternative Procedures – Donor Eligibility • Implementation 2 GAO Oversight and FDA Concerns • Publish in the form of regulations the guidelines that FDA deems essential to ensure the safety of the blood supply • Concern about the delay in requiring testing for emerging infectious agents, e.g. HTLV • Concern about blood safety and the regulations being out-of-date • Concerns about donor safety 3 Intent of the Final Rule • To better assure the safety of the blood supply and to help protect donor health • To make donor eligibility and testing requirements more consistent with current practices and to provide flexibility with regard to emerging infectious diseases • To accommodate technological advances • To establish requirements for donor education, donor history, and donor testing 4 Organization of the Final Rule - 1 • A. General • B. Definitions (§§ 606.3, 610.39, 630.3, 640.125) • C. Standard Operating Procedures (§ 606.100) • D. Control of Bacterial Contamination of Platelets (§ 606.145) • E. Records (§ 606.160) • F. Test Requirements (§§ 610.40, 640.5, 640.71(a)) • G. Donor Deferral (§ 610.41) 5 Organization of the Final Rule - 2 • H. Purpose and Scope (§ 630.1) • I. Medical Supervision (§ 630.5) • J. General Donor Eligibility Requirements(§ 630.10) • K. Donor Eligibility Requirements Specific to Whole Blood, Red Blood Cells and Plasma Collected by Apheresis (§ 630.15) • L. -
27. Clinical Indications for Cryoprecipitate And
27. CLINICAL INDICATIONS FOR CRYOPRECIPITATE AND FIBRINOGEN CONCENTRATE Cryoprecipitate is indicated in the treatment of fibrinogen deficiency or dysfibrinogenaemia.1 Fibrinogen concentrate is licenced for the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenaemia and hypofibrinogenaemia,2 and is currently funded under the National Blood Agreement. Key messages y Fibrinogen is an essential component of the coagulation system, due to its role in initial platelet aggregation and formation of a stable fibrin clot.3 y The decision to transfuse cryoprecipitate or fibrinogen concentrate to an individual patient should take into account the relative risks and benefits.3 y The routine use of cryoprecipitate or fibrinogen concentrate is not advised in medical or critically ill patients.2,4 y Cryoprecipitate or fibrinogen concentrate may be indicated in critical bleeding if fibrinogen levels are not maintained using FFP. In the setting of major obstetric haemorrhage, early administration of cryoprecipitate or fibrinogen concentrate may be necessary.3 Clinical implications y The routine use of cryoprecipitate or fibrinogen concentrate in medical or critically ill patients with coagulopathy is not advised. The underlying causes of coagulopathy should be identified; where transfusion is considered necessary, the risks and benefits should be considered for each patient. Specialist opinion is advised for the management of disseminated intravascular coagulopathy (MED-PP18, CC-PP7).2,4 y Cryoprecipitate or fibrinogen concentrate may be indicated in critical bleeding if fibrinogen levels are not maintained using FFP. In patients with critical bleeding requiring massive transfusion, suggested doses of blood components is 3-4g (CBMT-PP10)3 in adults or as per the local Massive Transfusion Protocol. -
Duffy, and Mnss Group Systems
Blood Groups – Duffy, and MNSs Group Systems Qun Lu, MD Assistant Professor Division of Transfusion Medicine Department of Pathology and Laboratory Medicine UCLA, School of Medicine Los Angeles, California 2009-03-12 Duffy Blood Group System History . 1950: Mrs. Duffy, a multiply transfused hemophiliac woman, developed an antibody not reacting with the known RBC antigens. Corresponding antigen was named after Mrs. Duffy . 1951: Fyb antibody was described in a woman with 3 pregnancies. 1955: Majority of blacks tested Fy(a-b-) . 1975: Fy(a-b-) RBCs were shown to resist infection by malaria organism Plasmodium vivax. Later: more Duffy antigens (Fy3, Fy4, Fy5, Fy6) were discovered . ISBT: 008 for the Duffy Blood Group Duffy Antigens . Most common: Fya and Fyb. Present at 6 weeks of gestation, well developed at birth – anti- Fy can cause hemolytic disease of newborn . Duffy antigens can be destroyed by enzymes such as ficin, papain, bromelain, chymotrypsin, ZZAP . When compared to Rh or Kell antigens, Duffy antigens are not very immunogenic. So, anti-Fya or anti-Fyb is not common. Fy (a-b-) is not Fy null, but homozygous for Fyb gene, they express Fyb antigen in other tissues, but not on RBCs → only will produce anti-Fya, not anti-Fyb. Fy (a-b-) is negative for Fy6 antigen which is the receptor for P. vivax (Fy6 is + when Fya + or Fyb+) Duffy Antigens . Phenotype Frequencies Chinese Phenotype Whites % Blacks % % Fy (a+b-) 17 9 90.8 Fy (a+b+) 49 1 8.9 Fy (a-b+) 34 22 0.3 Fy (a-b-) rare 68 0 White donor population: Fya: 66% Caucasians, 10% Blacks, 99% Asians Fya – units: 35% Fyb: 83% Caucasians, 23% Blacks, 18.5% Asians Fyb – units: 15% Fy3: 100% Caucasians, 32% Blacks, 99.9% Asians Duffy Antigens . -
Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only. -
Role of C5ar1 and C5L2 Receptors in Ischemia-Reperfusion Injury
Journal of Clinical Medicine Article Role of C5aR1 and C5L2 Receptors in Ischemia-Reperfusion Injury Carlos Arias-Cabrales 1,* , Eva Rodriguez-Garcia 1, Javier Gimeno 2, David Benito 3, María José Pérez-Sáez 1, Dolores Redondo-Pachón 1, Anna Buxeda 1, Carla Burballa 1, Marta Crespo 1, Marta Riera 3,* and Julio Pascual 1,* 1 Department of Nephrology, Parc de Salut Mar, 08003 Barcelona, Spain; [email protected] (E.R.-G.); [email protected] (M.J.P.-S.); [email protected] (D.R.-P.); [email protected] (A.B.); [email protected] (C.B.); [email protected] (M.C.) 2 Department of Pathology, Parc de Salut Mar, 08003 Barcelona, Spain; [email protected] 3 Kidney Research Group, Hospital del Mar Medical Research Institute, IMIM, 08003 Barcelona, Spain; [email protected] * Correspondence: [email protected] (C.A.-C.); [email protected] (M.R.); [email protected] (J.P.) Abstract: The role of C5a receptors (C5aR1 and C5L2) in renal ischemia-reperfusion injury (IRI) is uncertain. We generated an in vitro model of hypoxia/reoxygenation with human proximal tubule epithelial cells to mimic some IRI events. C5aR1, membrane attack complex (MAC) and factor H (FH) deposits were evaluated with immunofluorescence. Quantitative polymerase chain reaction evaluated the expression of C5aR1, C5L2 genes as well as genes related to tubular injury, inflammation, and profibrotic pathways. Additionally, C5aR1 and C5L2 deposits were evaluated in kidney graft biopsies (KB) from transplant patients with delayed graft function (DGF, n = 12) and compared with Citation: Arias-Cabrales, C.; a control group (n = 8). We observed higher immunofluorescence expression of C5aR1, MAC and FH Rodriguez-Garcia, E.; Gimeno, J.; as higher expression of genes related to tubular injury, inflammatory and profibrotic pathways and Benito, D.; Pérez-Sáez, M.J.; of C5aR1 in the hypoxic cells; whereas, C5L2 gene expression was unaffected by the hypoxic stimulus. -
Viewed Under 23 (B) Or 203 (C) fi M M Male Cko Mice, and Largely Unaffected Magni Cation; Scale Bars, 500 M (B) and 50 M (C)
BRIEF COMMUNICATION www.jasn.org Renal Fanconi Syndrome and Hypophosphatemic Rickets in the Absence of Xenotropic and Polytropic Retroviral Receptor in the Nephron Camille Ansermet,* Matthias B. Moor,* Gabriel Centeno,* Muriel Auberson,* † † ‡ Dorothy Zhang Hu, Roland Baron, Svetlana Nikolaeva,* Barbara Haenzi,* | Natalya Katanaeva,* Ivan Gautschi,* Vladimir Katanaev,*§ Samuel Rotman, Robert Koesters,¶ †† Laurent Schild,* Sylvain Pradervand,** Olivier Bonny,* and Dmitri Firsov* BRIEF COMMUNICATION *Department of Pharmacology and Toxicology and **Genomic Technologies Facility, University of Lausanne, Lausanne, Switzerland; †Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts; ‡Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia; §School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia; |Services of Pathology and ††Nephrology, Department of Medicine, University Hospital of Lausanne, Lausanne, Switzerland; and ¶Université Pierre et Marie Curie, Paris, France ABSTRACT Tight control of extracellular and intracellular inorganic phosphate (Pi) levels is crit- leaves.4 Most recently, Legati et al. have ical to most biochemical and physiologic processes. Urinary Pi is freely filtered at the shown an association between genetic kidney glomerulus and is reabsorbed in the renal tubule by the action of the apical polymorphisms in Xpr1 and primary fa- sodium-dependent phosphate transporters, NaPi-IIa/NaPi-IIc/Pit2. However, the milial brain calcification disorder.5 How- molecular identity of the protein(s) participating in the basolateral Pi efflux remains ever, the role of XPR1 in the maintenance unknown. Evidence has suggested that xenotropic and polytropic retroviral recep- of Pi homeostasis remains unknown. Here, tor 1 (XPR1) might be involved in this process. Here, we show that conditional in- we addressed this issue in mice deficient for activation of Xpr1 in the renal tubule in mice resulted in impaired renal Pi Xpr1 in the nephron. -
The Membrane Complement Regulatory Protein CD59 and Its Association with Rheumatoid Arthritis and Systemic Lupus Erythematosus
Current Medicine Research and Practice 9 (2019) 182e188 Contents lists available at ScienceDirect Current Medicine Research and Practice journal homepage: www.elsevier.com/locate/cmrp Review Article The membrane complement regulatory protein CD59 and its association with rheumatoid arthritis and systemic lupus erythematosus * Nibhriti Das a, Devyani Anand a, Bintili Biswas b, Deepa Kumari c, Monika Gandhi c, a Department of Biochemistry, All India Institute of Medical Sciences, New Delhi 110029, India b Department of Zoology, Ramjas College, University of Delhi, India c University School of Biotechnology, Guru Gobind Singh Indraprastha University, India article info abstract Article history: The complement cascade consisting of about 50 soluble and cell surface proteins is activated in auto- Received 8 May 2019 immune inflammatory disorders. This contributes to the pathological manifestations in these diseases. In Accepted 30 July 2019 normal health, the soluble and membrane complement regulatory proteins protect the host against Available online 5 August 2019 complement-mediated self-tissue injury by controlling the extent of complement activation within the desired limits for the host's benefit. CD59 is a membrane complement regulatory protein that inhibits the Keywords: formation of the terminal complement complex or membrane attack complex (C5b6789n) which is CD59 generated on complement activation by any of the three pathways, namely, the classical, alternative, and RA SLE the mannose-binding lectin pathway. Animal experiments and human studies have suggested impor- Pathophysiology tance of membrane complement proteins including CD59 in the pathophysiology of rheumatoid arthritis Disease marker (RA) and systemic lupus erythematosus (SLE). Here is a brief review on CD59 and its distribution, structure, functions, and association with RA and SLE starting with a brief introduction on the com- plement system, its activation, the biological functions, and relations of membrane complement regu- latory proteins, especially CD59, with RA and SLE. -
Mcleod Neuroacanthocytosis Syndrome
NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993- 2017. McLeod Neuroacanthocytosis Syndrome Hans H Jung, MD Department of Neurology University Hospital Zurich Zurich, Switzerland [email protected] Adrian Danek, MD Neurologische Klinik Ludwig-Maximilians-Universität München, Germany ed.uml@kenad Ruth H Walker, MD, MBBS, PhD Department of Neurology Veterans Affairs Medical Center Bronx, New York [email protected] Beat M Frey, MD Blood Transfusion Service Swiss Red Cross Schlieren/Zürich, Switzerland [email protected] Christoph Gassner, PhD Blood Transfusion Service Swiss Red Cross Schlieren/Zürich, Switzerland [email protected] Initial Posting: December 3, 2004; Last Update: May 17, 2012. Summary Clinical characteristics. McLeod neuroacanthocytosis syndrome (designated as MLS throughout this review) is a multisystem disorder with central nervous system (CNS), neuromuscular, and hematologic manifestations in males. CNS manifestations are a neurodegenerative basal ganglia disease including (1) movement disorders, (2) cognitive alterations, and (3) psychiatric symptoms. Neuromuscular manifestations include a (mostly subclinical) sensorimotor axonopathy and muscle weakness or atrophy of different degrees. Hematologically, MLS is defined as a specific blood group phenotype (named after the first proband, Hugh McLeod) that results from absent expression of the Kx erythrocyte antigen and weakened expression of Kell blood group antigens. The hematologic manifestations are red blood cell acanthocytosis and compensated hemolysis. Allo-antibodies in the Kell and Kx blood group system can cause strong reactions to transfusions of incompatible blood and severe anemia in newborns of Kell-negative mothers. -
Policy and Procedure
Policy and Procedure Title: Exchange Transfusion for Sickle Cell Division: Medical Management Disease Department: Utilization Management Approval Date: 2/9/18 LOB: Medicaid, Medicare, HIV SNP, CHP, MetroPlus Gold, Goldcare I&II, Market Plus, Essential, HARP Effective Date: 2/9/18 Policy Number: UM-MP224 Review Date: 1/18/19 Cross Reference Number: Retired Date: Page 1 of 7 1. POLICY: Exchange Transfusion for Sickle Cell Disease 2. RESPONSIBLE PARTIES: Medical Management Administration, Utilization Management, Integrated Care Management, Claims Department, Provider Contracting 3. DEFINITIONS • Sickle cell disease – Sickle cell disease (SCD) refers to a group of inherited disorders characterized by sickled red blood cells (RBCs), caused either by homozygosity for the sickle hemoglobin mutation (HbSS; sickle cell anemia) or by compound heterozygosity for the sickle mutation and a second beta globin gene mutation (e.g., sickle-beta thalassemia, HbSC disease). In either HbSS or compound heterozygotes, the majority of Hgb is sickle Hgb (HgbS; i.e., >50 percent). • Transfusion – Simple transfusion refers to transfusion of RBCs without removal of the patient's blood. • Exchange Transfusion – Exchange transfusion involves transfusion of RBCs together with removal of the patient's blood. Exchange transfusion can be performed manually or via apheresis (also called cytapheresis or hemapheresis) using an extracorporeal continuous flow device. 4. PROCEDURE: A. Exchange transfusion for sickle cell disease will be covered as an ambulatory surgery procedure when all the following criteria are met: i) The member has documented SCD. ii) The exchange transfusion is a pre-scheduled procedure. iii) The purpose of the exchange transfusion is to prevent stroke, acute chest syndrome, or recurrent painful episodes. -
Sickle Cell Disease: Chronic Blood Transfusions
Sickle Cell Disease: Chronic Blood Transfusions There may be times when sickle cell patients require a blood transfusion. Such situations include preparing for surgery, during pregnancy, or during a severe complication such as an aplastic crisis, splenic sequestration or acute chest syndrome. In these cases, transfusion is a one-time intervention used to reduce the severity of the complication you are experiencing. However, if you have had a stroke, or an MRI or TCD shows that you are at high risk for having a stroke, your hematologist may recommend you begin chronic blood transfusions. What Does a Blood Transfusion Do? What are The Risks? Chronic (monthly) blood transfusions have been proven to Blood transfusions are not without risks. One risk is drastically reduce a sickle cell patient’s risk of stroke. They alloimmunization, a process in which the patient receiving have also been shown to reduce the frequency, severity blood transfusions creates antibodies to certain types of and duration of other sickle cell complications. Sickle cell blood. As a result he/she may have a reaction to the blood patients usually have a hemoglobin S level of about 80- that was transfused. Alloimmunization makes it more 90%. This means 80-90% of the circulating red blood cells difficult to find blood that is a good match for the patient. are cells that can sickle and cause complications. The goal In order to prevent alloimmunization, some centers of chronic blood transfusion therapy is to bring that routinely perform RBC phenotyping (special testing for percentage down below 30%. This will mean fewer sickle antibodies) on sickle cell disease patients so that they may cells circulating in the body, and a lower risk of give blood that is a better match for the patient. -
4-6 Weeks Old Female C57BL/6 Mice Obtained from Jackson Labs Were Used for Cell Isolation
Methods Mice: 4-6 weeks old female C57BL/6 mice obtained from Jackson labs were used for cell isolation. Female Foxp3-IRES-GFP reporter mice (1), backcrossed to B6/C57 background for 10 generations, were used for the isolation of naïve CD4 and naïve CD8 cells for the RNAseq experiments. The mice were housed in pathogen-free animal facility in the La Jolla Institute for Allergy and Immunology and were used according to protocols approved by the Institutional Animal Care and use Committee. Preparation of cells: Subsets of thymocytes were isolated by cell sorting as previously described (2), after cell surface staining using CD4 (GK1.5), CD8 (53-6.7), CD3ε (145- 2C11), CD24 (M1/69) (all from Biolegend). DP cells: CD4+CD8 int/hi; CD4 SP cells: CD4CD3 hi, CD24 int/lo; CD8 SP cells: CD8 int/hi CD4 CD3 hi, CD24 int/lo (Fig S2). Peripheral subsets were isolated after pooling spleen and lymph nodes. T cells were enriched by negative isolation using Dynabeads (Dynabeads untouched mouse T cells, 11413D, Invitrogen). After surface staining for CD4 (GK1.5), CD8 (53-6.7), CD62L (MEL-14), CD25 (PC61) and CD44 (IM7), naïve CD4+CD62L hiCD25-CD44lo and naïve CD8+CD62L hiCD25-CD44lo were obtained by sorting (BD FACS Aria). Additionally, for the RNAseq experiments, CD4 and CD8 naïve cells were isolated by sorting T cells from the Foxp3- IRES-GFP mice: CD4+CD62LhiCD25–CD44lo GFP(FOXP3)– and CD8+CD62LhiCD25– CD44lo GFP(FOXP3)– (antibodies were from Biolegend). In some cases, naïve CD4 cells were cultured in vitro under Th1 or Th2 polarizing conditions (3, 4).