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Maternal genomic neutrophil FcRIII deficiency leading to neonatal isoimmune
neutropenia [see comments]
TW Huizinga, RW Kuijpers, M Kleijer, TW Schulpen, HT Cuypers, D Roos and AE von dem Borne
Central Laboratory of The Netherlands Red Cross Blood Transfusion Service,
Amsterdam.
The healthy mother of a child with transient immune neutropenia was found
to be "NA-null." The mother's neutrophils did not react with anti- NA1 and
anti-NA2 antibodies (polyclonal human alloantibodies and mouse monoclonal
antibodies). A healthy donor was discovered during routine neutrophil
antigen typing whose neutrophils were also "NA-null." This NA-phenotype was
due to the absence of FcRIII (CD16 antigen) on neutrophils as demonstrated
with anti-FcRIII monoclonal antibodies. The neutrophils of these two
individuals were not able to bind dimeric immunoglobulin G. However, their
cells had a normal expression of other phosphatidylinositol (PI)-linked
membrane glycoprotein (CD24, CD67, and CLB gran/5 antigens), ruling out the
existence of a PI-linkage defect, such as paroxysmal nocturnal
hemoglobinuria. The mother (propsitus) had isoantibodies in her blood
against neutrophil-FcRIII without allospecificity, apparently produced
during pregnancy and responsible for the neutropenia of her child. The
expression of FcRIII on natural killer lymphocytes of both individuals was
normal. FcRIII is encoded by two separate genes, one (FcRIII-1) for the
neutrophil-PI-linked receptor, another (FcRIII-2) for the natural killer
cell and macrophage- transmembrane receptor. By messenger RNA and DNA
analysis (with an FcRIII-cDNA probe and restriction endonucleases) the
neutrophil-FcRIII deficiency appeared to be due to deletion of the FcRIII-1
gene in both individuals, while the FcRIII-2 gene was normally present. The
parents of the propositus were found to be heterozygous for this defect.
Thus, FcRIII-1 gene deficiency of the mother may be a cause of (iso)immune
neutropenia of the newborn. Whether this deficiency may have other clinical
consequences has to be studied.
Volume 76,
Issue 10,
pp. 1927-1932,
11/15/1990
Copyright © 1990 by The American Society of Hematology
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