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A Naturally Occurring Mutation in FC RIIA: A Q to
K127 Change Confers Unique IgG Binding Properties to the
R131 Allelic Form of the Receptor
Cynthia F. Norris,
Luminita Pricop,
Sean S. Millard,
Scott
M. Taylor,
Saul Surrey,
Elias Schwartz,
Jane E. Salmon, and
Steven
E. McKenzie
From the Department of Pediatrics, Children's Hospital of
Philadelphia, Philadelphia, PA; the Department of Medicine, The
Hospital for Special Surgery and Graduate Program in Immunology,
Cornell University Medical College, New York, NY; the Departments of
Pediatrics and Research, duPont Hospital for Children, Wilmington, DE;
and the Department of Pediatrics, Jefferson Medical College,
Philadelphia, PA.
Fc RIIa is widely expressed on hematopoietic cells. There are two
known allelic polymorphic forms of FcRIIa,
FcRIIa-R131 and FcRIIa-H131, which differ
in the amino acid at position 131 in the second Ig-like domain. In
contrast to FcRIIa-R131, FcRIIa-H131
binds hIgG2 but not mIgG1, and this
differential binding has clinical implications for host defense,
autoimmune disease, immunohematologic disease, and response to
therapeutic monoclonal antibodies. We identified a novel FcRIIA
genotype in a healthy individual homozygous for FcRIIA
R/R131 in whom a C to A substitution at codon 127 changes
glutamine (Q) to lysine (K) in one of the two FcRIIA genes. This
individual's homozygosity for FcRIIA-R/R131 leads to
the prediction that the receptors on her cells would not bind
hIgG2. Monocyte and neutrophil phagocytosis of
hIgG2-opsonized erythrocytes was significantly higher
(P < .05) for cells from this K/Q127,
R/R131 individual than for Q/Q127, R/R
131 donors. Platelet aggregation stimulated by an
mIgG1 anti-CD9 antibody in this individual was
significantly different (P < .05) from Q/Q127,
H/R131 and Q/Q127, H/H131 donors
and similar to Q/Q127, R/R131. Our data show
that the K127/R131 receptors have a unique
phenotype, binding both hIgG2 and mIgG1. Further functionally significant mutations in human Fc receptors and
possible novel mechanisms for inherited differences in disease susceptibility should be sought with unbiased screening methods.
Blood, Vol. 91 No. 2 (January 15), 1998:
pp. 656-662
© 1998 by The American Society of Hematology.
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