BB IMMUNOHEMATOLOGY HENRYS

A G802>A mutation, leading to Gly268Arg in the translated protein.

Immunohematology studies the serologic, genetic, biochemical, and molecular aspects of blood antigens and the immunologic properties and reactions of blood components.

It has contributed to understanding human genetics, immunology, membrane physiology, epidemiology, anthropology, and forensic science.

Single-nucleotide polymorphisms (SNPs), nonsense, frameshift, and translation-initiator mutations.

Codominance means that genetic heterozygotes at a particular locus will express both gene products.

IgG antibodies via the reticuloendothelial (RE) system.

Both A and B antigens.

Exposure to ABH-like substances found in nature, particularly on bacterial polysaccharides.

By 5 to 10 years of age.

IgM isotype.

Blood group antigens are involved in maintaining erythrocyte cytoskeleton integrity, membrane transport, cell signaling, immune complement regulation, and act as receptors/modulators of disease.

ABO typing discrepancies due to an absence of anti-A and/or anti-B.

A2, which results from a single-nucleotide deletion (nucleotide 1060) and frameshift.

An immunogen is an antigen that can elicit an antibody-mediated immunologic response in a responsive host.

Haptens are small chemical groupings that are not immunogenic by themselves but can induce an antibody response when attached to a carrier protein.

All reagent cells in the antibody screen are group O.

Hemolysis and a delay in erythroid and megakaryocyte engraftment.

Group O individuals.

FUT1 and FUT2 fucosyltransferases.

Antibody production and complement activation, resulting in hemolysis.

Mutations at the ABO gene locus, primarily within exon 7.

Immunoglobulin G (IgG) or IgM, although occasionally an IgA antibody is encountered.

They tend to be destroyed more slowly in the spleen, displaying a linear pattern of removal with a minimum half-life of 20 minutes.

A1, A2, and other weak A and B subtypes.

Patients.

Agreement between the forward and reverse types.

The molecular basis of group O and weak ABO subtypes.

As a result of immunization to foreign erythrocyte antigens through transfusion of blood components or through pregnancy.

The A, B, and RhD antigens are the most immunogenic.

They are sequestered initially but can escape destruction and are released back into circulation, where they survive normally.

The most potent immunogens are usually complex macromolecular glycoproteins and lipoproteins.

A phenotype where A and B antigens are synthesized by the same enzyme and are inherited as a single autosomal-dominant allele.

FUT1 (H gene) catalyzes the formation of type 2 chain H antigen, while FUT2 (Secretor gene) catalyzes the transfer of fucose to type 1 chain precursors.

They are integral to virtually all red cell antibody detection and identification techniques.

As alloantibodies, which react with a foreign antigen not present on the patient’s own erythrocytes, or autoantibodies, which react with an antigen on the patient’s own cells.

Intravascular hemolysis is the lysis of RBCs within blood vessels, usually caused by antibodies directed against ABO antigens.

Approximately 50% to 75% of D-negative individuals would produce anti-D antibodies if transfused with one unit of D-positive blood.

Antigen density contributes to the efficiency of antibody binding and the extent of complement activation, affecting the likelihood of RBC hemolysis.

Increasing use of probiotic nutritional supplements containing live bacteria.

Identifying weak A and B subgroups.

Studies like enzyme treatment, adsorption, and elution may be required to identify compatible blood for transfusion.

Alloantibodies where the antigenic stimulus is unknown, often appearing in the serum of persons who lack the corresponding antigen.

The immunogenicity of an antigen is determined by its degree of foreignness, molecular size and configuration, and antigenic complexity.

They lack a functional ABO gene and express the H antigen.

They are the consequence of hybrid alleles with characteristics of both A1 and B gene consensus alleles.

Hemolytic transfusion reactions (HTRs), hemolytic disease of the fetus and newborn (HDFN), and acute rejection in solid-organ transplantation.

On chromosome 9q34.

M/N and S/s antigens.

Group O.

To prevent transfusion reactions and hemolytic disease of the fetus and newborn.

Blood group refers not only to genetically encoded erythrocyte antigens but also to the immunologic diversity expressed by leukocytes, platelets, and plasma.

Epitopes are discrete, immunologically active regions of an antigen that can interact with specific lymphocyte membrane receptors or secreted complementary antibody.

By phagocytic cells via Fcγ receptors.

Anti-H is a naturally occurring antibody in the sera of A1 and A1B nonsecretors.

An autosomal-recessive phenotype due to homozygosity for amorph ABO alleles (ABO*O).

An antigen is a membrane-associated structure on blood cells capable of reacting with a complementary antibody or cell receptor.

A, B, AB, and O.

Enzymatic deacetylation of group A antigen in vivo, often in the setting of bacterial infection or cancer.

ABO titers have progressively decreased over the past two decades.

U–, Mk, and En(a–).

Due to the presence of anti-A and anti-B antibodies.

A nucleotide deletion and frameshift (G251D, fs88stop), accounting for 95% of all ABO*O alleles.

Complement is involved in the sensitization and destruction of transfused RBCs by alloantibody or autologous RBCs by autoantibody.

They stop the activation process at the C3/C4 level, preventing extensive RBC destruction.

Group O.

They are the most important antibodies in transfusion medicine.

They differ by four key amino acids at residues 176, 235, 266, and 268, which determine their enzyme activity.

Following immune stimulation by transfusion or pregnancy.

The ABO histo-blood group antigens.

Weak residual enzyme activity, although this has not been confirmed.

Traditional nomenclature, ISBT nomenclature, ISGN nomenclature, gene symbol, chromosome, and gene product name.

By antibody binding to RBC antigens or via a carrier–hapten antibody complex such as penicillin-coated RBCs and antipenicillin antibodies.

It is the biosynthetic precursor of both A and B antigens.

They are carbohydrate antigens, representing a post-translational modification of glycoproteins and glycolipids.

Anti-A1 is a naturally occurring antibody found in the sera of some A2, A2B, and other weak A subtypes.

The U– phenotype.

H antigen.

Most blood group genes are located on autosomal chromosomes and are inherited following Mendelian rules of inheritance.

A and B.

Techniques include radioimmunoassay, ELISA, electron microscopy using ferritin-labeled anti-immunoglobulin, and flow cytometry.

The MNS blood group system.

They tend to show accelerated removal by the liver.

An absence of all ABH antigens on RBCs.

Heart transplantation in children younger than 6 to 8 months of age and transplantation of A2 organs.

Hemolysis.

To prevent acute rejection caused by ABO antibodies.

At 3 to 6 months of age.

At room temperature with optimal reactivity at 4°C.

The M/N antigens reside on GYPA (CD235A), a major RBC membrane glycoprotein, which is a dimer usually associated with Band 3.