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Kell Blood Group System
Introduction
The Kell blood group system is vast, with 38 blood group antigens.[1] The Kell system is notorious for its immunogenicity, which is third after ABO and Rhesus D.[2] This system is involved in severe forms of hemolytic disease of the fetus and newborn and hemolytic transfusion reactions. Further, this blood group system is associated with chronic granulomatous diseases and a multisystem syndrome involving neurological, cardiovascular, and hematologic symptoms called McLeod syndrome.[3] The symbol of the Kell blood group system as per "International Society of Blood Transfusion" (ISBT) is KEL; ISBT number: 006.
History: The Kell blood group system was described in 1946 and named after Mrs Kelleher, whose newborn child died of hemolytic disease of fetus and newborn (HDFN) due to an antibody against his red blood cells (RBCs). This antibody also reacted with her daughter's and husband's RBCs and was named anti-K. Later, its antithetical antigen k was discovered in 1949, and the null phenotype (K0) in 1957.[4]
Genetics: The KEL gene encodes the Kell antigens and is located at chromosome 7q34, comprising 20 exons spanning 21.25 kb of genomic DNA. This gene is also known as Kell metallo-endopeptidase, ECE3, or CD238. Single nucleotide polymorphisms are responsible for multiple Kell antigens. Another important XK gene required for the expression of Kell antigen is present on the short arm of chromosome X (Xp21.1) and is responsible for forming the Kx antigen.[5]
Structure of Kell glycoprotein: The KEL gene encodes the polymorphic Kell and para-Kell glycoproteins, structurally single-pass RBC membrane proteins, or type II glycoproteins. The N terminal is intracytoplasmic, and the C terminal is multi-folded, bound by disulfide bonds, and extracytoplasmic. They constitute around 732 amino acids; mutations in these lead to the formation of a multitude of Kell antigens.[6] The Kell glycoprotein is covalently linked to the Kx protein via a single disulfide bond. This Kx antigen protein traverses the RBC membrane 10 times. The absence of Kx protein leads to McLeod syndrome.[7] The Kell glycoproteins have been found to have a similar sequence as the neprilysin (M13) family of zinc endopeptidases and, hence, act like proteolytic enzymes. They share a pentameric sequence HEXXH, which is needed to add zinc and proteolytic activity. Kell preferentially cleaves big endothelin-3, converting it to the bioactive peptide endothelin-3. This potent vasoconstrictor peptide leads to vascular endothelial growth factor formation.[8][9]
Antigens: The Kell system is highly polymorphic, consisting of 38 different blood group antigens.[10][11] The Kell antigens are found on erythroid cells and progenitor myeloid cells and are also present in skeletal muscles and testes.[12][13]
- ISBT symbol: KEL1
- ISBT number: 006.001
- Low prevalence antigen
- Antithetical antigen: k (KEL 2)
- Cord RBCs: Expressed
The K antigen is detected on fetal RBCs as early as the tenth gestational week and is well-developed at birth. The KEL1 antigen is strongly immunogenic after the Rh blood group system. Study results have reported that every 1 out of 10 Kell antigen-negative individuals transfused with Kell antigen-positive donor red cells can develop anti-K antibodies after transfusion.
The K antigen is not denatured by the enzymes ficin and papain but is destroyed by combined trypsin and chymotrypsin. Additionally, dithiothreitol (DTT), 2-mercaptoethanol, 2-aminoethylisothiouronium bromide, and ZZAP (mixture of a sulfhydryl reagent [dithiothreitol] and a proteolytic enzyme [papain or ficin]) can also destroy the Kell antigen. DTT, a reducing agent, interferes with the disulfide bonds between amino acids essential for the structural integrity of specific proteins and maintaining the pentameric structure of immunoglobulin (Ig) M molecules. Treating RBCs with DTT can denature other blood group antigens, including Kell, Lutheran, Yt, John Milton Hagen (JMH), Landsteiner-Wiener (LW), Cromer, Indian, Dombrock, and Knops systems—potentially impacting the recognition of these antigens by their specific antibodies.
- ISBT symbol: KEL2
- Formerly termed as Cellano
- ISBT number: 006.002
- High prevalence antigen
- Antithetical antigen: K (KEL1)
- Cord RBCs: Expressed
- Detected as early as seven weeks of gestation.
- Resistance and sensitivity to enzymes and chemicals are the same as those of KEL1
- ISBT symbol: KEL3
- ISBT number: 006.003
- Low prevalence antigen
- Antithetical antigen: Kpb (KEL4) Kpc (KEL21)
- Cord RBCs: Expressed
- Resistant to enzymes (ficin, papain, chymotrypsin)
- ISBT symbol: KEL4
- ISBT number: 006.004
- High prevalence antigen
- Antithetical antigen: Kpa (KEL3) Kpc (KEL21)
- Cord RBC's: Expressed
- Resistant to enzymes (ficin, papain, chymotrypsin)
- ISBT symbol: KEL6
- ISBT number: 006.006
- Low prevalence antigen
- Antithetical antigen: Jsb (KEL7)
- Cord RBCs: Expressed
- Resistant to enzymes (ficin, papain, chymotrypsin)
- ISBT symbol: KEL7
- ISBT number: 006.007
- High prevalence antigen
- Antithetical antigen: Jsa (KEL6)
- Cord RBC: Expressed
- Resistant to enzymes (ficin, papain, chymotrypsin)
These are further divided as high and low-prevalence antigens:
High prevalence antigens: Ku (KEL5), KEL11, KEL12, KEL13, KEL14, KEL16, KEL18, KEL19, Km (KEL20), KEL22, TOU (KEL26), RAZ (KEL27), KALT (KEL29), KTIM (KEL30), KUCI (KEL32), KANT (KEL33), KASH (KEL34), KELP (KEL35), KETI (KEL36), KHUL(KEL37), KYOR(KEL38), KEL40
Low prevalence antigens: Ula (KEL10), Wka (KEL17), KEL21, KEL23, KEL24, VLAN (KEL25), VONG (KEL28), KYO (KEL31), KEAL (KEL39), KEL41
Anti-K antibodies, commonly IgG antibodies, do not bind complement and mostly react at 37 °C with the anti-human globulin (AHG) phase. Anti-K antibodies can also react at room temperature in the saline phase if they are IgM-type; they are usually formed in response to exposure following pregnancy or transfusion, but some examples of naturally occurring anti-K can also be seen. These IgM antibodies have been found in patients with Escherichia coli infections, which disappear after recovery.[14]
Anti-K antibodies may show depressed reactivity with some low–ionic-strength solution reagents, so an AHG phase is required to detect these antibodies.[15] Anti-K has been implicated in severe hemolytic transfusion reactions and HDFN. If a patient develops antibodies to high-prevalence Kell antigens like k, it is challenging to find compatible units due to the low percentage of antigen-negative donors; antibody formation is rare due to its high prevalence.
Identifying antibodies against low-prevalence antigens is difficult as their corresponding antigens are not included in antibody identification panels, which can rarely present as unexpected HDFN or transfusion reactions (see Table. Kell Blood Group Frequencies in Different Populations by Percentage). Anti-K will react well with K+k+ and K+k− red cells in antibody panels, showing no dosage phenomena. A rare case report of anti-Jsb was found in the Nigerian population, where this antibody was associated with decreased red cell survival.[16]
Table. Kell Blood Group Frequencies in Different Populations by Percentage
|
Phenotype |
Caucasian |
Black |
Arabic |
Indian |
Chinese |
Japanese |
Brazilian |
|
K+k- |
9% |
2% |
20% |
4% |
<0.1% |
<0.1% |
5% |
|
K-k+ |
99.8% |
99.9% |
99.1% |
>99.9% |
>99.9% |
>99.9% |
K0 phenotype and anti-Ku antibody: K0 or Kell null phenotype was identified by Chown et al in 1957, and it lacks all Kell antigens on the RBCs. The Kell null phenotype shows a prevalence of 0.001% except in populations of Finland and Japan.[21][22] These individuals show the inheritance of 2 recessive K0 genes in homozygotes (K0 K0). The absent antigens do not cause any functional abnormality in these RBCs.[5] The alloantibody in K0 individuals post-transfusion has been called anti-Ku (anti-KEL5), which is clinically significant.[23] These recipients should only be transfused with the K0 red cell type. One case report shows that anti-Ku specificity and anti-H were also identified in co-trimoxazole (trimethoprim and sulfamethoxazole) dependent antibodies.[24] If there is a diminished presence of Kell antigens in place of complete absence, the phenotype is called Kmod. This is due to multiple missense mutations in the glycoprotein. Both K0 and Kmod show increased Kx protein. Kmod individuals may also form anti-Ku-type antibodies, but neither are similar.[25]
McLeod phenotype: This rare phenotype occurs due to the absence of the Kx protein. Kell glycoprotein is covalently linked to Kx protein by a single disulfide bond, and hence, in its absence, it lacks a high prevalence Kell antigen and has depression of the rest. Individuals with this phenotype develop a neuromuscular syndrome, McLeod syndrome.[26] This condition is an X-linked recessive disorder where females are carriers and males are affected. At the molecular level, it can be due to a hemizygous XK pathogenic variant (90%) or a hemizygous deletion of Xp21.1 (10%).[27] The Kell blood group system antigens are expressed weakly in individuals with McLeod syndrome, except for the Km antigen (KEL20), which is absent. The XK gene encodes a protein that helps properly express antigens of the Kell blood group system on the RBC surface. When this gene is mutated, it leads to the functional ineffectiveness of the Kell antigens.[28]
Depressed Kell antigen (Cellano) in Gerbich-negative phenotypes: Both Muller and Debien reported reduced expression of 'k' antigens in RBCs of Gerbich group-negative phenotype (Ge:-2,-3) in individuals using monoclonal anti-k. This may be due to conformational changes in epitopes of the Kell blood group system, which shift the protein 4.1 complex to proteins like glycophorin C in the RBC membrane.[29][30]
Determining the Kell blood group involves various methodologies, each with advantages and limitations. These methods can be broadly categorized into serological and molecular techniques.[31] In serological methods, hemagglutination tests such as forward typing are commonly used to detect the presence of Kell antigens on RBCs by utilizing specific antibodies like anti-K. Agglutination indicates the presence of the K antigen, while a lack of agglutination suggests its absence. Although this method is rapid and straightforward, it may lack sensitivity for weakly expressed antigens, particularly in partial or weak Kell phenotypes.[32] Reverse typing involves testing the serum for anti-K antibodies to confirm the results of forward typing, which is crucial for ensuring accurate blood typing before transfusions. This step helps identify any unexpected antibodies that could lead to transfusion reactions.[33] Another technique, gel centrifugation, employs a gel medium to separate agglutinated from non-agglutinated cells, thereby improving sensitivity and specificity. This method is particularly beneficial in reducing false-negative results and is often used in blood banks for routine testing.[34]
In molecular methods, polymerase chain reaction (PCR)-based techniques are highly sensitive and detect specific genotypes associated with Kell antigens. This approach is particularly useful in cases where serological methods may fail, such as in patients with autoimmune hemolytic anemia or those who have been recently transfused, as these conditions can obscure antigen expression.[35] PCR with sequence-specific primers (PCR-SSP) enables the determination of specific alleles associated with Kell antigens; this is both cost-effective and reliable, making it suitable for routine testing in blood banks. This method can also identify rare phenotypes that may not be detected through serological means.[36] PCR with restriction fragment length polymorphism (PCR-RFLP) analyzes variations in DNA sequences corresponding to different Kell antigens, providing detailed genetic information about blood group polymorphisms. This level of detail can be crucial for understanding compatibility in transfusions and organ transplants.[37][38] Microarray technology, which can simultaneously analyze multiple blood group antigens, including Kell, is highly efficient for large-scale screenings and provides comprehensive data on various blood group systems. This method allows for rapid screening of donors and patients alike, facilitating better matching processes.[39]
Clinical Significance
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Clinical Significance
Functional Role of Kell Blood Group System:
- RBC adhesion: Kell antigens are involved in RBC adhesion with vascular endothelium and act by cleaving endothelin-3.[8]
- RBC cell signaling: Results from recent studies show that recipient type-1 interferon production regulates RBC alloimmunization with Kel1 antigen.[40]
- Red cell structural integrity: All Kell blood group antigens and the Cartwright (Yta) antigen are completely denatured on treatment with DTT in the same concentration range, showing possible relation related to the disulfide bond integrity of the RBC membrane.[41]
- Erythroid lineage suppression: The presence of Kell antigens on erythroid precursors has been proven by suppression with anti-Kell antibodies on RBC production. These antibodies inhibit the colony-forming units and cause severe fetal anemia in the case of HDFN.[42]
- Role in platelet inhibition: Besides the erythroid series, Kell antigens are also on the megakaryocytic precursors. In the case of anti-Kell antibody formation, these antibodies inhibit the precursor cells and lead to thrombocytopenia.[43][44]
- Association with gram-negative bacterial infection: IgM-type Kell antibodies have been identified in patients afflicted with E coli 0125:B15 enterocolitis.[14][45]
- Association with mycobacterium: IgM-type naturally occurring anti-Kell antibodies have been identified in a previously non-sensitized individual suffering from pulmonary tuberculosis.[14]
Kell Blood Group System and Disease Association
McLeod syndrome is an X-linked recessive disorder due to the absence of Kx protein, resulting in the loss of Kell antigen functions in red blood cells. Hematologically, it is characterized by irregular protrusions or acanthocytes on the red cell membrane, leading to decreased survival of RBCs and presenting with chronic, compensated hemolytic anemia. Patients with this condition also have several neuromuscular abnormalities termed McLeod neuro-acanthocytosis syndrome.
The neurological manifestation comprises movement disorders such as choreiform movements or facial tics and neuropsychiatric symptoms involving depression, anxiety, psychosis, obsessive-compulsive features, and cognitive dysfunction. These patients develop slow progressive muscular dystrophy, which starts in middle age and worsens with time. Cardiac symptoms include cardiomegaly, atrial fibrillation, and arrhythmia. Additionally, patients may also have seizures, dysarthria, dysphagia, and areflexia. There are increased creatinine kinase and carbonic anhydrase III levels in biochemical parameters.[46]
Chronic granulomatous disease and McLeod syndrome: Chronic granulomatous disease (CGD) is an X-linked disorder caused by mutations in CYBB, which encodes the nicotinamide adenine dinucleotide phosphate oxidase complex crucial for phagocytes to kill ingested pathogens. CGD is occasionally associated with McLeod syndrome due to contiguous gene deletion on the X chromosome.[47]
Hematological malignancies: In hematological malignancies, anti-Kell antibodies may be warm-type autoantibodies or naturally occurring alloantibodies against the Kell antigen.[48][49]
HDFN and neonatal jaundice: Antibodies to the Kell system can cause severe HDFN and fetal death. These IgG antibodies destroy mature fetal RBCs and the erythroid precursor cells by inhibiting erythropoiesis. In the Kell blood group-related HDFN, the degree of anemia and bilirubin levels are unrelated to the severity of the disease.[50][51] A noninvasive prenatal test involving cell-free fetal DNA can be used for fetal antigen genotyping to diagnose HDFN.[52]
Transfusion: The Kell antigens are the most immunogenic, third only after ABO and Rhesus blood group systems. Antibodies to the Kell system are predominantly IgG and clinically significant. They are known to cause acute and delayed hemolytic transfusion reactions, which can be severe as well.[53]
Enhancing Healthcare Team Outcomes
Understanding the Kell blood group system is crucial for improving patient outcomes and equally important for clinical and laboratory clinicians. Continued research into the KEL gene and its associated protein is necessary across different diseases and to examine transfusion outcomes and clinical consequences. The nursing team must verify the availability of a Kell antigen-negative blood unit and the other mandatory pretransfusion checks when planning transfusions for patients with Kell antibodies.
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Level 3 (low-level) evidence