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aAllelic polymorphisms that show differences in IgG binding; NA1/NA2 variants have multiple amino acid differences (Ory et al., 1989); SH+ individuals (Bux et al., 1997) carry three copies of FcyRIIIb (Koene et al., 1998); the FcyRIIc null phenotype is due to a nonsense mutation (Metes et al., 1998). bMultiple mRNA transcripts from FcyRIb, IIa, and IIb are the result of alternative splicing of primary transcripts. cSoluble forms of FcyRIIa and IIb (sIIa, sIIb) are devoid of the hydrophobic transmembrane exon; GPI, glycosyl-phosphatidylinositol.

dITAM, immunoreceptor tyrosine-based activation motif; ITIM, immunoreceptor tyrosine-based inhibition motif. eNumbers represent the relative order of IgG subclass binding to variants of FcyRIIa (Warmerdam et al., 1990), FcyRIIIa (Koene et al., 1997; Wu et al., 1997), and FcyRIIIb (Salmon et al., 1990; Bredius et al., 1994a). Abbreviation: NK, natural killer.

aAllelic polymorphisms that show differences in IgG binding; NA1/NA2 variants have multiple amino acid differences (Ory et al., 1989); SH+ individuals (Bux et al., 1997) carry three copies of FcyRIIIb (Koene et al., 1998); the FcyRIIc null phenotype is due to a nonsense mutation (Metes et al., 1998). bMultiple mRNA transcripts from FcyRIb, IIa, and IIb are the result of alternative splicing of primary transcripts. cSoluble forms of FcyRIIa and IIb (sIIa, sIIb) are devoid of the hydrophobic transmembrane exon; GPI, glycosyl-phosphatidylinositol.

dITAM, immunoreceptor tyrosine-based activation motif; ITIM, immunoreceptor tyrosine-based inhibition motif. eNumbers represent the relative order of IgG subclass binding to variants of FcyRIIa (Warmerdam et al., 1990), FcyRIIIa (Koene et al., 1997; Wu et al., 1997), and FcyRIIIb (Salmon et al., 1990; Bredius et al., 1994a). Abbreviation: NK, natural killer.

FcyRIIa has low affinity for IgG (<107 M-1) and interacts mainly with antigen-antibody complexes (Warmerdam et al., 1991; Parren et al., 1992). The copy number of FcyRIIa expressed on resting platelets varies among healthy individuals but is stable (Rosenfeld et al., 1987). There is roughly a 3-fold variation among individuals, with the copy number ranging from 600 to 1500 molecules per platelet when assayed using an intact murine monoclonal antibody IV.3 (McCrae et al., 1990) and 1500 to more than 4500 when tested with a Fab preparation (Tomiyama et al., 1992; Brandt et al., 1995). There are no major differences in FcyRIIa copy number between sexes, among platelets from persons of different ages, or for the three genotypic classes of FcyRIIa-Arg/His131 (Brandt et al., 1995).

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