anti-JMH

OBJECTIVE: To investigate the effectiveness and safety of low concentration dithiothreitol (DTT) in removing the interference of monoclonal anti-CD38 on transfusion compatibility testing, and develop a reasonable clinical transfusion strategy. METHODS: The blood type, direct antiglobulin testing (DAT) and antibody screening were tested according to standard methods. Antibody screening cells and donor's red blood cells were treated by DTT 0.2, 0.1, 0.05, 0.02, 0...

The clinical significance of the specific anti-John Milton Hagen (JMH) alloantibody in inherited JMH-negative patients remains unclear. During clinical blood transfusion, it is often classified as an anti-JMH autoantibody in acquired JMH-negative patients, which might further lead to the occurrence of haemolysis events. In this study, we found that the proportion of inherited JMH-negative people in the Guangzhou population was 0.41%, based on the study of 243 blood samples by flow cytometry. Gene sequencing analysis revealed two novel variants located in exon 11 (c...

BACKGROUND: Plasma of patients taking anti-CD38 monoclonal antibodies (MoAbs) leads to panagglutination in the indirect antiglobulin test (IAT), that can mask clinically significant alloantibodies. of test RBCs is the more widespread method for avoiding this interference. Current DTT 0.2 mol/L method is time consuming and damages several red blood groups antigens. This study aims to evaluate low concentration DTT treatment of RBCs adapted for gel testing. MATERIALS AND METHODS: Four DTT concentrations (0...

The JMH blood group system consists of six high-prevalence antigens. These antigens are located on the Sema7A protein. The molecular basis of the JMH1- phenotype is not known; however, single nucleotide changes in the SEMA7A gene on chromosome 15 account for the other JMH antigens. JMH1, commonly known as JMH, is most notable because transient depression of the antigen occurs and anti-JMH may develop. These antibodies are most commonly observed and are not significant in transfusion. Antibodies developed in the rare JMH variant types may cause reduced red cell survival...

We encountered a broadly reactive red cell alloantibody in 1991, reacting unlike any other known antibody, and named it anti-KANNO after the first patient. A total of 28 cases of anti-KANNO in the Japanese literature were reviewed. To distinguish KANNO from other antibodies against high-frequency antigens, including anti-JMH, anti-Ch/Rg, and anti-Jr(a), we conducted serologic studies with proteolytic enzyme and chemical treatments, complement sensitization against red cells, and serum neutralization techniques...

BACKGROUND: At present, identification of antibodies against the high-prevalence JMH antigen is difficult and limited to reference laboratories having panels of rare red blood cell (RBC) specimens in stock. Here, a novel method is described for detection of anti-JMH with particles coated with recombinant semaphorin 7A (Sema7A, CD108), the protein that carries the JMH blood group antigens. STUDY DESIGN AND METHODS: Recombinant Sema7A protein was generated and coupled onto superparamagnetic particles coated with streptavidin...

The authors studied an example of red cell anti-JMH (John Milton Hagen) that exhibited several characteristics of a possible clinically significant antibody able to cause red cell destruction in vivo. Strong serological reactivity, a positive monocyte monolayer assay, and immunoglobulin subclass determination as IgG3 all indicate possible ability to destroy red cells. A51Cr-labeled red cell survival study was not done as the patient did not require red cell transfusions but may be recommended for this patient if transfusions become necessary...

BACKGROUND AND OBJECTIVES: In the present article, we report on two patients with acute haemolytic transfusion reactions (AHTRs), and whom we were unable to transfuse, owing to alloantibodies that in vitro did not seem to be clinically significant. MATERIALS AND METHODS: The patients were a 67-year-old male and a 64-year-old female, both of whom developed antibodies to red blood cells (RBCs) after repeat blood transfusions. Serological analyses were carried out using standard techniques...

BACKGROUND: CDw108 is a cluster-of-differentiation antigen that resides on a glycosylphosphatidylinositol (GPI)-linked protein; it has not previously been shown to be expressed on red cells. JMH is a high-frequency red cell blood group antigen that resides on a GPI-linked protein of molecular weight similar to that bearing CDw108. The purpose of this study was to investigate whether CDw108 is expressed on red cells and whether it resides on the same membrane protein as does JMH. STUDY DESIGN AND METHODS: Murine monoclonal antibodies to CDw108, MEM-121 and MEM-150, as well as a murine monoclonal antibody and human antibodies to JMH were used in radioimmunoassay, inhibition assay, Western blotting, and monoclonal antibody-specific immobilization of erythrocyte antigen assay...

The monoclonal antibody H8, previously described as anti-JMH, has the same specificity as a JMH-related antibody, R.M. H8 blocks the reaction of human anti-JMH and related antibodies with JMH+ cells, suggesting that the JMH-related antigens are very closely situated to each other on the red cell membrane.

Anti-JMH was identified in the serum of an 80-year-old JMH-negative man. Before transfusion, his direct antiglobulin test was weakly positive with polyspecific reagents, anti-C3 and anti-IgG. An eluate prepared from his red cells contained anti-JMH. Chromium-51-labeled JMH-positive cells which were weakly incompatible in vitro appeared to survive normally. Following transfusion with three JMH-positive units, the patient's hematocrit increased from 20.7 percent to 32.1 percent.

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The long-term survival of serologically incompatible red cell units was measured in five patients with antibodies to high-frequency antigens. Initially, the survival of 1 ml of 51Cr-labeled incompatible red cells was measured over 1 hour. After demonstrating that the 1-hour survival times were successful (greater than 70%), each patient then received 5 ml of the same 51Cr-labeled red cells followed by the transfusion of the remainder of the red cell unit. The long-term T 1/2Cr survival for each case was patient 1 (anti-McCa), 15 days; patient 2 (anti-JMH), 12 days; patient 3 (anti-Kna), 31 days; patient 4 (anti-McCa), 12 days; and patient 5 (anti-Hya), 14 days...