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  • 1995-1999  (2)
  • 1
    Electronic Resource
    Electronic Resource
    The NA"null" phenotype of a young man is caused by an FcγRIIIB gene deficiency while the products of the neighboring FcγRIIA and FcγRIIIA genes are present (1998)
    Springer
    Annals of hematology 76 (1998), S. 215-220 
    Details
    ISSN: 1432-0584
    Keywords: Key words FcγRIIIb deficiency ; NA1/NA2 polymorphism ; NA"null" ; SH antigen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A 27-year-old man with an allergy to house dust mites was found to lack the FcγRIIIb on his neutrophils. Cell surface marker and PCR techniques were used to investigate possible reasons for this deficiency. Agglutination and immunofluorescence assays using the man's neutrophils together with NA1- and NA2-specific antibodies were negative, and there was no reaction with the FcγRIII-specific mAb 3G8. Indirect immunofluorescence demonstrated the presence of the CD24 molecule, which, like the FcγRIIIb, is anchored to the cell membrane by glycosylphosphatidylinositol. Thus a lack of the FcγRIIIb cell membrane anchor was excluded. PCR analysis confirmed the absence of the NA1 and NA2 alleles. The individual was therefore typed as NA"null". The products of those genes located together with the FcγRIIIB gene within a complex on chromosome 1 (q23–24) were examined. FcγRII was demonstrated on monocytes and B cells with the use of FcγRII-specific monoclonal antibodies. About 5% of the individual's peripheral blood monocytes were positive with the 3G8 antibody, indicating the presence of FcγRIIIa. From these data we concluded that the FcγRIIIb deficiency on the neutrophil cell surface of this individual is due to a lack of the FcγRIIIB gene while excluding a lack of the FcγRIIA and the FcγRIIIA genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050392
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Inhibition of monocyte and polymorphonuclear granulocyte immune phagocytosis by monoclonal antibodies specific for FcγRI, II and III (1997)
    Springer
    Annals of hematology 74 (1997), S. 15-22 
    Details
    ISSN: 1432-0584
    Keywords: Key words mAb ; CD64 ; CD32 ; CD16 ; FcγRIIa HR ; FcγRIIa LR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We tested two Fcγ receptor I (FcγRI); six FcγRII; and six FcγRIII-specific monoclonal antibodies (mAb) for their capacitiy to inhibit monocyte and polymorphonuclear granulocyte (PMN) immune phagocytosis which is mediated by FcγR. We used human red blood cells (rbc) coated with hIgG1 or mIgG1 as FcγRI- and FcγRII-specific target cells, respectively. The FcγRI-specific mAbs 22.2 and 32.2 did not inhibit FcγRI- or FcγRII-specific monocyte immune phagocytosis. The FcγRII-specific mAbs IV.3, CIKM5, FLI8.2, FLI 8.26, 2E1, and 41H16 inhibited FcγRII-specific monocyte immune phagocytosis in all FcγRIIa high-responder (HR) individuals but did not inhibit FcγRI-specific phagocytosis. Using PMN, FLI8.2 and 2E1 only partially inhibited phagocytosis in HR individuals, but the FcγRIII-specific mAbs 3G8, DJ130c, MFM-154, B88-9 and MG38 completely inhibited FcγRII-specific phagocytosis if the corresponding antigen was available on the cell surface. In these cases phagocytosis inhibition may be explained by cross-linking of FcγRII and FcγRIII via one antibody molecule, with the Fab portion binding to FcγRIII and the Fc portion binding to FcγRII.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050249
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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