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Post-transfusion alloimmunisation is the main complication of all those observed after one or more transfusion episodes. Alloimmunisation is observed after the transfusion of red blood cell concentrates but also of platelet concentrates. Besides alloimmunisation due to antigens carried almost exclusively by red blood cells such as those of the Rhesus-Kell system, alloimmunisation often raises against HLA antigens; the main responsibility for that, apart from platelet transfusions, lies with residual leukocytes in the products transfused, hence the central importance of effective leukoreduction right from the blood product preparation stage. Alloimmunization is not restricted to transfusion, but it is also observed during pregnancies, carrying out microtransfusions of blood from the fetus immunizing the mother through the placenta (in a retrograde way). Preexisting maternal-fetal immunization can complicate a transfusion program and intensify the creation of alloantibodies in several blood and tissue group systems. The occurrence of autoantibodies, created by several pathogenic reasons, can also interfere with the propensity of certain recipients of blood components to produce alloantibodies. The genetic condition of individuals is in fact strongly linked to the ability or not to recognize antigenic variants foreign to their own biological program and mount an alloimmune response. Some hemoglobin diseases, in carriers of which transfusions can be iterative and lifelong, are complicated by frequent alloimmunizations and amplification of the complications of these alloimmunizations, imposing even stricter transfusion rules. This review details the mechanisms favoring the occurrence of alloimmunization and the immunological principles for the production of molecular and cellular tools for alloimmunization. It concludes with the main preventive measures available to limit the occurrence of these frequent complications of varying severity but sometimes severe.

The importance of identifying variant alleles among blood donors is significant to the safety of transfusion for recipients. Molecular methods have become more prominent in the routine process of antigen typing donor units. Some variant antigens cannot be detected using only serologic methods. Molecular testing allows the determination of nucleotide sequences that are used to predict a phenotype. Antigens of the Kell blood group system are known for being highly immunogenic and causing adverse reactions upon antibody formation. A female white blood donor who typed Kp(b-) using serologic methods on multiple donations since 2005 was the subject of a typing discrepancy investigation. Routine genotyping using a commercial genotyping kit (HemoID DQS Panel; Agena Bioscience, San Diego, CA) predicted the donor to type Kp(a+b+). Investigation of the discrepancy between these two results identified a rare single nucleotide variant in the

Background: The frequency of ABO, Rh and Kell blood group antigens differs among populations of different ethnic ancestry. There are low-frequency antigens (90%). A rare blood group is defined as the absence of a high-frequency antigen in the general population, as well as absence of multiple frequent antigens within a single or multiple blood group systems. Aim: To perform red blood cell typing and to calculate the antigen and phenotype frequencies, in order to identify rare blood group donors within the clinically most important АВО, Rh and Kell systems. Material and Methods: АВО, Rh (D, C, E, c, e) and Kell (K) antigen typing was performed using specific monoclonal sera and microplate technique, while Cellano (k) typing was performed with a monoclonal anti-k, antihuman globulin and column agglutination technique. Weak ABO subgroups were determined using the absorption elution method or molecular genotyping (PCR-SSP). Results: ABO antigen frequency is: A (40.89%), O (34.22%), B (16.97%), AB (7.92%) and weak ABO subgroups (0, 009 %). The established genotypes were AxO1 (0, 0026%) and AxB (0, 001%). Rh antigen frequency is: D (85.79%), C (71.7%), c (76.0%), E (26.0%) and е (97.95%). The most common Rh pheno-type is the DCcee (32.7%) while the rarest phenotype is the DCCEE phenotype (0. 003%). The prevalence of K and k antigen is 7.5% and 99.94%, respectively. The frequency of the rare phenotype K+k- is 0.06%. Conclusion: Large scale phenotyping of blood group antigens enables the identification of blood donors with rare blood groups for patients with rare phenotypes or with antibodies to high-frequency antigens and to frequent antigens within one or more blood group systems.

Rh and Kell blood group systems are amongst the most important blood group systems; being highly immunogenic after ABO system. The aim of this study was to evaluate the frequencies of Rh antigens, haplotypes and K antigen among blood donors belonging to various ethnicities in Samtah, Jazan, Saudi Arabia.This study was conducted during January 2019 and August 2020 at Samtah General Hospital, Samtah. Records of all blood donors recruited during this period were included for data acquisition. A total of 4977 blood donors' records were reviewed and data were analysed. A total of 3863 donors' results were considered in the final analysis.In comparison to Saudi blood donors, C antigen was less frequent in Sudanese donors (69.7% and 34.0%), the c antigen was less frequent in Indian (79.2% and 59.3%) and Philippine (79.2% and 40.0%) donors and more frequent in Sudanese (79.2% and 97.9%) donors, the E antigen was less frequent in Yemini (27.0% and 19.5%) and the e antigen was more frequent in Yemini (96.7% and 99.2%) donors. The DcE haplotype was less frequent (3.1% and 0.7%) and the ce haplotype was more frequent (4.3% and 7.6%) in Yemini donors. The K antigen was less frequent in Pakistani (11.9% and 4.1%; p = .041) and Indian (11.9% and 1.9%; p = .023) donors.Rh and K antigens showed marked variations in their frequencies among blood donors of different ethnicities. Utilization of blood from various ethnicities warrant extended phenotyping of Rh and K antigens to avoid the risk of alloimmunization in multiply transfused patients.

Polyclonal anti-D (Rh immune globulin [RhIg]) therapy has mitigated hemolytic disease of the newborn over the past half century, although breakthrough anti-D alloimmunization still occurs in some treated females. We hypothesized that antiviral responses may impact the efficacy of immunoprophylaxis therapy in a type 1 interferon (IFN)-dependent manner and tested this hypothesis in a murine model of KEL alloimmunization. Polyclonal anti-KEL immunoprophylaxis (KELIg) was administered to wild-type or knockout mice in the presence or absence of polyinosinic-polycytidilic acid (poly[I:C]), followed by the transfusion of murine red blood cells (RBCs) expressing the human KEL glycoprotein. Anti-KEL alloimmunization, serum cytokines, and consumption of the transfused RBCs were evaluated longitudinally. In some experiments, recipients were treated with type 1 IFN (IFN-α/β). Recipient treatment with poly(I:C) led to breakthrough anti-KEL alloimmunization despite KELIg administration. Recipient CD4+ T cells were not required for immunoprophylaxis efficacy at baseline, and modulation of the KEL glycoprotein antigen occurred to the same extent in the presence or absence of recipient inflammation. Under conditions where breakthrough anti-KEL alloimmunization occurred, KEL RBC consumption by inflammatory monocytes and serum monocyte chemoattractant protein-1 and interleukin-6 were significantly increased. Poly(I:C) or type I IFN administration was sufficient to cause breakthrough alloimmunization, with poly(I:C) inducing alloimmunization even in the absence of recipient type I IFN receptors. A better understanding of how recipient antiviral responses lead to breakthrough alloimmunization despite immunoprophylaxis may have translational relevance to instances of RhIg failure that occur in humans.

High-titer antibodies are a cause of false-negative reactions in red blood cell antigen phenotyping, an event referred to as blocked antigen phenomenon (BAP). In hemolytic disease of the fetus and newborn, BAP complicates laboratory workups as fetal phenotype is helpful in confirming the responsible antibody. Acid elution techniques, techniques using ethylenediaminetetraacetic glycine acid, as well as those using chloroquine diphosphate have been used to resolve BAP; however, ethylenediaminetetraacetic glycine acid destroys K-antigen expression and chloroquine diphosphate is not always effective. We report a case of severe hemolytic disease of the fetus and newborn from anti-K where a modified gentle heat elution resolved BAP. Although infrequently considered with isolated reports in the literature, heat elution is simple, is effective, and involves readily available materials in most blood banks.

Allo-antibodies produced by K-negative pregnant women against a fetal K antigen from the Kell blood group system may cause hemolytic disease of the fetus and newborn (HDFN). Predicting the fetal K antigen using noninvasive prenatal testing (NIPT) is important for decisions concerning management of pregnancies. Digital and droplet digital PCR techniques permit the detection of fetal single nucleotide variant with a higher specificity and sensitivity than real-time polymerase chain reaction (PCR).The aim was to evaluate and compare protocols for fetal KEL*01.01 genotyping using different assays and digital PCR platforms.DNA isolated from 59 pregnant women (9-39 weeks of gestation, 49 with anti-K) was tested using home-made and custom-ordered KEL*01.01/KEL*02 assays with Droplet Digital™ and QuantStudio™3D. The results were compared with fetal/neonatal genotypes/phenotypes.Fetal KEL*01.01 results using all tested protocols were concordant with fetal/neonatal KEL*01.01 genotypes/phenotypes. None of the tested combinations of assays or digital PCR platforms gave false KEL*01.01-negative results, but inconclusive KEL*01.01 reads were observed in all tested protocols. For 36 cases compared using two digital PCR platforms and assays, there were not statistically significant differences in a level of fetal KEL*01.01 fraction (p .72).Independent of the applied dPCR and ddPCR platforms and KEL*01.01 assays, prediction of the fetal KEL*01.01 is highly reliable. Before implementation in routine practice further validation of the KEL*01.01 protocol with a larger group of pregnant women should be performed.

McLeod syndrome (MLS) is a rare X-linked neurohematologic disorder caused by loss-of-function mutations in the XK gene. However, variations in the XK gene remain to be elucidated. Here, we report the clinical phenotype and genetic features of a patient with MLS caused by a novel frameshift mutation in the XK gene.A 44-year-old man presented with chorea, cognitive impairment, mental disorders, and seizures accompanied by peripheral neuropathy, hyperCKemia, and acanthocytosis. The proband's mother had a mild chorea. One older brother who died 10 years ago without a confirmed diagnosis showed symptoms of both chorea and mental disorders, while the other brother also developed mild chorea.The patient was diagnosed with MLS based on the family history, clinical manifestations, and accessory examinations. Whole-exome sequencing studies revealed a novel frameshift mutation resulting from a nucleotide variation in exon 2 (452delA) that leads to an amino acid residue conversion from Gln to Arg and early termination of the XK protein (Gln151ArgfsTer2). The patient and one of his older brothers were hemizygotes, and his mother was heterozygous.The patient was treated with haloperidol to control chorea and levetiracetam to control seizures.Six months after treatment, the proband was seizure-free, but showed little improvement in chorea and cognitive dysfunction.We describe a family with MLS caused by a novel frameshift mutation in the XK gene. The causes of the mild clinical presentation in the proband's mother require further investigation.

Maternal alloantibodies directed against fetal red blood cell (RBC) antigens may cause potentially life-threatening haemolytic disease of the fetus and newborn (HDFN). Dutch transfusion guidelines therefore prescribe preventive cEK matching for all (pre-)fertile females. To quantify the impact of cEK matching, we compared overall and antigen-specific cumulative RBC alloimmunisation incidences in females and males aged

Naturally occurring anti-Kp

BACKGROUND: Only a fraction of red blood cell (RBC) transfusion recipients form alloantibodies, and variables determining responsiveness or non-responsiveness are poorly understood. We and others have previously shown in animal models that pre-treatment with toll-like receptor (TLR) agonists that mimic different types of infections impacts the magnitude or frequency of RBC alloantibody responses. We hypothesized that influenza infection, co-existent with transfusion, would impact responses to transfused RBCs in a manner dependent on type 1(α/β) interferon (IFN) signaling, and tested this in a murine model. STUDY DESIGN AND METHODS: Wild-type mice or mice lacking the ability to respond to type 1 IFN were infected with influenza prior to the transfusion of transgenic murine RBCs (K1) expressing the human KEL glycoprotein or the triple fusion HOD protein. Alloantibody responses were measured longitudinally post-transfusion by flow cytometric crossmatch, and post-transfusion RBC recovery and survival was evaluated. RESULTS: Influenza-infected mice transfused with K1 RBCs developed robust anti-KEL alloantibodies, whereas animals transfused in the absence of infection remained non-responders; influenza-associated RBC alloimmunization was also observed after transfusion of HOD RBCs. Recipient type 1 interferon production was critical to the mechanism of action of influenza-induced RBC alloimmunization, with alloimmunization being significantly decreased in mice unable to sense type 1 IFN (through antibody blockade or genetic approaches). CONCLUSION: These and other data suggest that type 1 IFN responses to TLR agonists or infections regulate RBC alloantibody responses. Studies investigating whether such a correlation exists in humans may be informative.

Blood banks in developing countries have limited capability to typify common blood groups creating disparities in the access to blood units for patients with rare blood genotypes. We report the case of a Peruvian woman with metastatic breast cancer with KELnull phenotype (K0), a rare blood group characterized by the lack of expression of all Kell antigens on the red blood cells (RBCs). The molecular studies identified that the patient's RBCs were homozygous for the nonsense c.1546C > T mutation predicted to encode p.Arg516Ter (KEL*02 N.17 allele), which confirmed the K0 phenotype. We conducted a local and international search of compatible blood units. Finally, the Japanese Red Cross donated the blood units for the patient. We present here the first report for a K0 phenotype in Peru and the challenging genetic disparities that many patients have to face to access to blood units in our country.

Alloantibodies developing after exposure to red blood cell (RBC) alloantigens can complicate pregnancy and transfusion therapy. The only method currently available to actively inhibit RBC alloantibody formation is administration of antigen-specific antibodies, a phenomenon termed antibody-mediated immune suppression (AMIS). A well-known example of AMIS is RhD immune globulin prophylaxis to prevent anti-D formation in RhD− individuals. However, whether AMIS is specific or impacts alloimmunization to other antigens on the same RBC remains unclear. To evaluate the specificity of AMIS, we passively immunized antigen-negative recipients with anti-KEL or anti-hen egg lysozyme (HEL) antibodies, followed by transfusion of murine RBC expressing both the HEL-ovalbumin-Duffy (HOD) and human KEL antigens (HOD × KEL RBC). Significant immunoglobulin G deposition on transfused HOD × KEL RBC occurred in all passively immunized recipients. Complement deposition and antigen modulation of the KEL antigen occurred on transfused RBC only in anti-KEL–treated recipients, whereas HEL antigen levels decreased only in the presence of anti-HEL antibodies. Western blot analysis confirmed the specificity of antigen loss, which was not attributable to RBC endocytosis and appears distinct for the 2 antigens. Specifically, removal of KEL was attenuated by clodronate treatment, whereas loss of HEL was unaffected by clodronate in vivo but sensitive to protease treatment in vitro. Antigen-specific modulation correlated with antigen-specific AMIS, with anti-KEL treated recipients forming antibodies to the HOD antigen and anti-HEL–treated recipients developing antibodies to the KEL antigen. Together, these results demonstrate that passively administered antibodies can selectively inhibit the immune response to a specific antigen.

Background: During pregnancy, maternal red blood cell (RBC) antibodies can lead to life-threatening fetal hemolysis and anemia. Women can become immunized by a pregnancy or an unmatched transfusion. Our aim was to quantify the effect of a nationwide K-matched transfusion policy for women of childbearing age potential to prevent K-immunization in pregnancy.Study Design and Methods: In this nation-wide policy change evaluation study we determined the occurrence of RBC antibodies before and after introduction of a K-matched transfusion policy and evaluated the cause K alloimmunization 10 years after introduction of this measure. K-matched transfusion for females under 45 years of age is advised in the Dutch transfusion guideline since 2004. We used laboratory data from pregnancies with RBC antibodies identified in the period 1999-2018 obtained as part of a population-based screening program in the Netherlands.Results: Tests of 36 286 pregnancies produced a positive antibody screening result which concerned anti-K in 1550 pregnancies. The occurrence of anti-K decreased from 67.9 to 20.2 per 100 000 pregnancies. The relative risk reduction was 0.70 which largely exceeded the relative risk reduction of 0.27 for antibodies against RBC antigens for which no preventive matching is required. The number of pregnancies at risk for anti-K-mediated disease decreased from 9.7 to 4.2 per 100 000 pregnancies.Conclusions: A K-matched transfusion policy is associated with a major decrease in a number of pregnant women with anti-K and pregnancies at risk for anti-K-mediated disease. A relatively simple measure is now shown to impact prevention of hemolytic disease in the fetus and newborn.

Background The Kell blood group system has different types of antigens, which have immunogenic properties; therefore, it is considered as the third clinically significant blood group in blood transfusion. Patients that lack Kell antigen may produce antibodies that may cause transfusion reaction. This study is the first report on Kell antigen system distribution in blood donors in Makkah city which is important to improve transfusion services. Therefore, the aim of the current study is to determine the distribution of Kell antigens and phenotypes among blood donors in Makkah city, Saudi Arabia. Methods This is a retrospective study to determine the prevalence of Kell antigens among blood donors, who come to donate blood in Al Noor specialist hospital, Makkah city. The sample size was 150 donors with a minimum age of 18 years. Results The most common Kell antigens were k antigen (96%) and Kpb (98%), while the less common were K antigen (18.7%) and Kpa (3.3%). The two most common Kell phenotypes are Kp(a-b+) (95%) and K-k+ (79.3%), while the two least common Kell phenotypes are Kp(a-b-) (1.3%) and Kp(a+b-) (0.6%). Conclusions This is the first study that set out to determine the prevalence of Kell antigens and phenotypes among blood donors in Makkah city. This study showed that there is a variation in Kell antigen and phenotype distribution. The Kell blood group system has an important impact on transfusion medicine.

The development of hemolytic erythrocyte alloantibodies and autoantibodies complicates transfusion therapy in thalassemia patients. These antibodies ultimately increase the need for blood and intensify transfusion complications. There is a scanty data on the frequency of RBC alloimmunization and autoimmunization in Egyptian β thalassemia patients as pretransfusion antibody screening is not routinely performed. We studied the frequency of alloimmunization and autoimmunization among 200 multiply transfused β thalassemia patients and investigated the factors that possibly affect antibody formation. Of the 200 patients in our study, 94 were males and 106 females, with the age range of 2–37 years. Alloantibodies were detected in 36 (18%) of the patients, while autoantibodies were detected in 33 (16.5%). The dominant alloantibodies were directed against Kell (33%) and Rh (24.4%) groups. Alloimmunization had a significant relationship with treatment duration and the frequency of transfusion (P = 0.007, 0.001, respectively). The presence of autoantibodies was significantly related to age (P = 0.001), total number of transfused units (P = 0.000) and splenectomy (P = 0.000). The high prevalence of alloimmunization in the study population disclosed the need for providing phenotypically matched cells for selective antigens especially for Kell and Rh subgroups to reduce risk of alloimmunization and increase the efficiency of blood transfusion.

Maternal alloantibody-mediated hemolytic disease of the fetus and newborn (HDFN) ranges from no or mild symptoms to severe hydrops and intrauterine fetal demise. Hemolytic anti-D-mediated HDFN proceeds via a long-known mechanism, to which three other pathways to fetal/neonatal anemia may be added: (0) Fetal erythrocyte destruction can proceed by extravascular phagocytosis. (1) An apoptotic pathway has been described for anti-Kell, and anti-Ge3. (2) Erythropoietic suppression may arise from altered or deformed erythroblast architecture in anti-M-mediated disease. (3) Clonal escape from erythropoietic suppression is hypothesized to arise from maternal anti-Jra immune pressure, albeit this requires further elucidation. Alloantibody-mediated anemic disease of the fetus and newborn (ADFN) is a designation we favor for cases when hemolysis or hyperbilirubinemia are not the dominant features, such as those provoked by anti-Kell, anti-Ge3, anti-M, and anti-Jra.

Background Genetic variants in the SLC14A1, ACKR1, and KEL genes, which encode Kidd, Duffy, and Kell red blood cell antigens, respectively, may result in weakened expression of antigens or a null phenotype. These variants are of particular interest to individuals with sickle cell disease (SCD), who frequently undergo chronic transfusion therapy with antigen-matched units. The goal was to describe the diversity and the frequency of variants in SLC14A1, ACKR1, and KEL genes among individuals with SCD using whole genome sequencing (WGS) data. Study design and methods Two large SCD cohorts were studied: the Recipient Epidemiology and Donor Evaluation Study III (REDS-III) (n = 2634) and the Outcome Modifying Gene in SCD (OMG) (n = 640). Most of the studied individuals were of mixed origin. WGS was performed as part of the National Heart, Lung, and Blood Institute's Trans-Omics for Precision Medicine (TOPMed) program. Results In SLC14A1, variants included four encoding a weak Jka phenotype and five null alleles (JKnull ). JKA*01N.09 was the most common JKnull . One possible JKnull mutation was novel: c.812G>T. In ACKR1, identified variants included two that predicted Fyx (FY*X) and one corresponding to the c.-67T>C GATA mutation. The c.-67T>C mutation was associated with FY*A (FY*01N.01) in four participants. FY*X was identified in 49 individuals. In KEL, identified variants included three null alleles (KEL*02N.17, KEL*02N.26, and KEL*02N.04) and one allele predicting Kmod phenotype, all in heterozygosity. Conclusions We described the diversity and distribution of SLC14A1, ACKR1, and KEL variants in two large SCD cohorts, comprising mostly individuals of mixed ancestry. This information may be useful for planning the transfusion support of patients with SCD.

Individuals with the K0 phenotype are extremely rare. They may develop anti-Ku antibodies, which react with all antigens of the Kell blood group system, thereby leading to haemolytic transfusion reactions and haemolytic disease of the fetus and newborn.A primigravida who was transfused with one unit of red blood cells due to iron deficiency anaemia developed anti-Ku antibodies. The pregnancy was closely monitored by ultrasound and antibody titres. Maternal autologous blood collection was performed twice during the last trimester as back-up in case of maternal peripartum bleeding, and a few frozen K0 red blood cell units were provided in case of severe fetal anaemia. At gestational week 36+6, labour was induced due to increasing antibody titres and high blood velocities in the fetal middle cerebral artery during systole. The woman was delivered vaginally without need for transfusion. The infant was diagnosed with haemolytic disease of the fetus and newborn and treated with phototherapy, repeated infusions of intravenous immunoglobulin and iron supplements until normalisation of haemoglobin at three months of age.Iron deficiency anaemia should be treated primarily with iron supplementation before considering blood transfusions, which pose the risk of developing alloantibodies that can cause transfusion complications and haemolytic disease of the fetus and newborn.

BACKGROUND The reagent red blood cells used to screen and identify antibodies have to include K+ cells in all batch productions. The data of K/k phenotypes among differing Thai blood donor populations remains unknown; hence, mass screening for uncommon K+ donors by serological test has some limitations. Implementing K/k genotyping may be useful to predict uncommon K+ donors to overcome this challenge. This study aimed to establish an in-house K/k genotyping technique and to report KEL*01 and KEL*02 allele frequencies among three Thai blood donor populations to increase the selection of K+ donors in rare blood group databases. METHODS A total of 2,239 DNA samples obtained from 1,512 central, 427 southern, and 300 northern Thai blood donors were included. The KEL*01 and KEL*02 genotyping using PCR with sequence-specific primers (PCR-SSP) was developed and validated. All samples were genotyped using developed PCR-SSP. Moreover, the possibility of finding group O and predicted K+ phenotypes among Thai blood donor populations was calculated. RESULTS The DNA controls were validated using two sets of primer combinations and the results of KEL*01 and KEL*02 genotyping were in agreement. The KEL*01 allele frequencies were 0.0007, 0.0047, and 0.0000, and KEL*02 allele frequencies were 0.9993, 0.9953, and 1.0000 among central, southern, and northern Thai donors, respectively. In addition, mass screening among 3,795 and 566 donors in central and southern Thai populations was required to find at least one group O and predicted K+ phenotypes. CONCLUSIONS The in-house PCR-SSP for KEL*01 and KEL*02 genotyping provided reproducible and accurate results with cost effectiveness. Our results confirmed the low KEL*01 allele frequencies among Thais. PCR-SSP could be used as an alternative technique to simply increase the number of uncommon predicted K+ phenotypes for reagent red blood cell recruitments.

Background This study aims at alloantibody screening, determination of the types of these antibodies in multiple-transfused patients with chronic hematologic diseases. Patients and Methods This descriptive study was performed on 240 patients with chronic hematological diseases referred to public hospitals in Iran. Single blood sample was taken and tested for the presence of antibodies. In case of a positive antibody screening, antibody identification was performed using granulocyte agglutination test (GAT), granulocyte indirect immunofluorescence test (GIIFT), platelet indirect immunofluorescence test (PIIFT), monoclonal antibody-specific immobilization of platelet antigen (MAIPA) and panel cells. Results Out of 240 patients, 105 patients (43.75 %) had been alloimmunized. The incidence of alloantibodies against red blood cells (RBCs) in positive alloantibodies patients were 84.76% (89/105). The most common alloantibody was against antigens of the kell (anti-K) and Rh (anti-E) and (anti D) systems (46.66%, 18.09% and 11.43% respectively). The overall incidence of anti- human leukocyte antigen (HLA) antibodies were 65.7% (69/105). Polymorphonuclear (PMN)-specific antibodies were found in 6.66% (7/105). Also from 105 patients, 14 patients had alloantibodies against platelet. Discussion In general, it is recommend that to decrease the rate of alloantibody synthesis, the packed cells should be cross matched for minor blood groups especially for Rh (E) and kell. In addition, the use of leukodepleted blood products can decrease the frequency of alloimmunization against platelet (PLT), PMN and HLA antigens.