RESUMO
Accurate typing of patients for platelet-specific (human platelet) antigens (HPA) is required in several different clinical situations, and blood services need to maintain panels of HPA-typed apheresis platelet donors and whole-blood donors to support HPA alloimmunized patients. Six clinically relevant HPA alloantigen systems have been described and, in addition, a significant number of HPA alloantigens with a highly skewed allele frequency or of very low immunogenicity have been reported. Certain well-characterized biallelic systems such as Gov have not as yet been included in the HPA nomenclature but are included in this review. Biochemical studies have identified the platelet membrane proteins on which the HPA antigens are localized. Cloning of the genes encoding these proteins and the realization that there is adequate mRNA in fresh platelets has led to identification of the molecular basis of HPA antigens over the last decade. All but one of the biallelic platelet-specific alloantigen systems are based on a single nucleotide polymorphism in the DNA sequence, corresponding to a single amino acid substitution in the encoded primary protein sequence. The discovery of the genetic basis of the alloantigens has allowed the development of polymerase chain reaction-based techniques for HPA genotyping using genomic DNA. The genetic basis of the HPA alloantigens, the most commonly used genome typing techniques and their pitfalls, and future developments, are discussed in this review.
Assuntos
Antígenos de Plaquetas Humanas/genética , Análise Mutacional de DNA/métodos , Polimorfismo de Nucleotídeo Único , Análise Mutacional de DNA/normas , Erros de Diagnóstico , Genótipo , HumanosRESUMO
Severe fetomaternal alloimmune thrombocytopenia requires urgent treatment with compatible platelet concentrates. As prompt treatment is sometimes delayed owing to the unavailability of compatible platelets, we established an accredited platelet donor panel to provide effective and timely transfusion support for fetal and neonatal therapy. After a mass screening programme of over 60,000 blood donations, 45 HPA-1a-negative donors with no antibodies to HPA, HLA, red cell antigens and granulocytes/lymphocytes, and with low titre anti-A and/or -B were accredited. All accredited donors were fully genotyped for HPA-1, -2, -3 and -5 by PCR-SSP. Ninety-one per cent of the accredited donors were also negative for HPA-5b.
Assuntos
Antígenos de Plaquetas Humanas , Doadores de Sangue , Transfusão de Plaquetas , Trombocitopenia/terapia , Feminino , Humanos , Recém-Nascido , Integrina beta3 , Plaquetoferese , Gravidez , Trombocitopenia/embriologiaRESUMO
Human peripheral blood lymphocytes were found to give an opsonic adherence reaction with IgM-coated erythrocytes. This reactivity could only be detected after incubating the lymphocytes at 37 degrees, was confined to the T-lymphocyte population and could be inhibited by IgM but not IgG. It is concluded that human T lymphocytes possess a receptor for IgM.
Assuntos
Imunoglobulina M , Linfócitos T/imunologia , Sítios de Ligação de Anticorpos , Membrana Celular/imunologia , Complemento C3 , Humanos , Imunoglobulina G , Técnicas Imunológicas , Técnicas In VitroRESUMO
Immunoglobulin (Ig) bearing, antigen-binding and antibody-secreting cells were investigated for the presence of membrane receptors for the Fc part of IgG and for C3b on their surface. Fc and C3b receptors were detected on the surface of most Ig-bearing and of most antigen-binding cells. Fc receptors were also detected on IgM antibody-secreting cells but not on IgG-secreting cells. C3b receptors were not detected on any antibody-secreting cells. These receptors are either lost from the B cell surface as they differentiate into antibody-secreting cells or are blocked in vivo by immune complexes or C3b.
