PURPOSE OF REVIEW: This review summarizes the current genetic, molecular and functional information on human neutrophil alloantigens (HNAs), which are implicated in autoimmune and alloimmune neutropenia and in transfusion-related acute lung injury. Identification and functional characterization of these antigens improve the understanding of HNA-antibody-induced diseases and may lead to the development of antibody detection assays and new therapeutic concepts. RECENT FINDINGS: HNA-3 is localized on choline transporter-like protein 2 (CTL2) and originates from an Arg154Gln amino acid (aa) substitution. The HNA-3a epitope is conformation sensitive. The additional single-nucleotide polymorphism (SNP) at aa 153 impairs genotyping and lowers the reactivity with some HNA-3a-antibodies. CD177 (HNA-2) interacts with PECAM-1, mediating neutrophil evasion. The percentage of the CD177-positive neutrophil subpopulation and the occurrence of two neutrophil subsets, differing in their CD177 expression, are associated with five SNPs. Glycosylphosphatidylinositol-linked CD177 anchors proteinase 3 on the cell membrane forming a potential signaling complex together with CD11b/CD18 (HNA-4a) in lipid rafts. SUMMARY: Characterization of the HNA-3 system allows identification of blood donors at risk to develop HNA-3-antibodies. FcγRIIIb (HNA-1) and CD177 (HNA-2) seem to be important in bacterial host defense. Activation of neutrophils by HNA-1 and HNA-2-antibodies potentially occurs via mPR3 and CD11b/CD18 (HNA-4a).
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Muschter et al. (2011) studied this question.
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