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Frequency of the polymorphonuclear neutrophil Fc gamma receptor III
deficiency in the French population and its involvement in the development
of neonatal alloimmune neutropenia
P Fromont, A Bettaieb, H Skouri, C Floch, E Poulet, N Duedari and P Bierling
Centre de Transfusion, Hopital Henri Mondor, Creteil, France.
We report the case of a healthy woman (K.M.) who, after multiple
pregnancies, developed an antibody directed against a nonpolymorphic region
of the polymorphonuclear neutrophil (PMN) Fc gamma receptor III
(FcRIII-CD16), which caused transient neonatal alloimmune neutropenia
(NAIN). The antigenic target of the antibody was determined by an
immunoprecipitation procedure and by phenotyping the mother's PMN. These
latter did not react with monoclonal CD16 or polyclonal and monoclonal NA1
and NA2 antibodies, demonstrating the absence of PMN- FcRIII and,
consequently, the NA-null phenotype. We also determined the frequency of
the NA-null phenotype in a healthy, white population. Among 3,377 random
blood donors, only four (in addition to K.M.) were PMN-FcRIII-deficient.
These five individuals were healthy and only one (K.M.) presented an
allo-CD16 antibody. The gene frequency of the NA- null phenotype was
calculated as 0.0274 +/- 0.0059. We conclude that PMN-FcRIII deficiency is
a rare phenomenon that can lead to CD16 alloimmunization and thus cause
NAIN.
Volume 79,
Issue 8,
pp. 2131-2134,
04/15/1992
Copyright © 1992 by The American Society of Hematology
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