<i>FCGR3</i> variants and expression of human neutrophil antigen‐1a, ‐1b, and ‐1c in the populations of northern Germany and Uganda

Flesch, Brigitte K.; Doose, Sandra; Siebert, Reiner; Ntambi, Elisabeth; Neppert, J.

doi:10.1046/j.1525-1438.2002.00087.x

Cited by 44 publications

(57 citation statements)

References 21 publications

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“…FCGR3B deficiency has been found, with frequencies of ϳ0.1% in Germany (26) and France (27), 1% in Spain (28), and 2% in Uganda (24). When we included 1 affected offspring from each family, 3.1% of the patients carried SH, which was similar to the previously reported frequency in healthy Caucasians.…”

Section: Concise Communications 671supporting

confidence: 82%

See 1 more Smart Citation

Mice with osteopontin deletion remain predisposed to collagen‐induced arthritis

Ishii¹,

Ohshima²,

Ishida³

et al. 2004

Arthritis & Rheumatism

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Section: Concise Communications 671supporting

confidence: 82%

“…The frequency of the FCGR3B-SH allele has been shown to vary considerably among populations, e.g., 5% in northern Germany (24), 35% in Uganda (24), and 0% in Japan (25). FCGR3B deficiency has been found, with frequencies of ϳ0.1% in Germany (26) and France (27), 1% in Spain (28), and 2% in Uganda (24).…”

Section: Concise Communications 671mentioning

confidence: 99%

Mice with osteopontin deletion remain predisposed to collagen‐induced arthritis

Ishii¹,

Ohshima²,

Ishida³

et al. 2004

Arthritis & Rheumatism

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“…In contrast, FCGR3B*03 , the basis of HNA-1c distinguishes from FCGR3B*02 only in an additional Ala78Asp substitution [22]. Interestingly, many FCGR3B*03- positive individuals exhibit three HNA-1 antigens with a combination of the HNA-1a and HNA-1c encoding alleles on one chromosome, and, as expected, these individuals present with FcγRIIIb hyperexpression [3,21,31,32]. About 5% of German individuals carry the HNA-1c antigen, whereas it is much more frequent in African populations with 22-38% and missing in Chinese.…”

Section: Hna-1mentioning

confidence: 98%

“…This means that individuals may exhibit between zero and four FCGR3B alleles [21,22,23,24,25] which can be explained by gene duplication combined with recombination and/or unequal crossing-over during meiosis. This event may result in either two FCGR3B genes in close vicinity on the same chromosome or, conversely, in a FCGR3B gene deficiency [1,21,25,26] (fig. 1).…”

Section: Hna-1mentioning

confidence: 99%

Molecular Genetics of the Human Neutrophil Antigens

Flesch

Reil²

2018

Transfus Med Hemother

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Background and Objective: Antibodies to human neutrophil antigens (HNAs) have been implicated in transfusion-related acute lung injury and allo- and autoimmune neutropenia. To date, five HNA systems are assigned, and during the last decades enormous efforts have been undertaken to identify the underlying genes and to characterize the antigens. This review of the literature will provide the current genetic, molecular and functional information on HNAs. Recent Findings: New information on alleles and antigens has been added to nearly each of the five HNA systems. HNA-1d has been added as the antithetical epitope to HNA-1c that is located on the glycoprotein encoded by FCGR3B*02 but not by FCGR3B. FCGR3B*04 and *05 now are included as new alleles. A CD177*787A>T substitution was demonstrated as the main reason for the HNA-2-negative phenotype on neutrophils. The target glycoprotein of HNA-3 antibodies could be identified as choline transporter-like protein 2 (CTL2) encoded by SLC44A2. The conformation sensitive epitope discriminates between arginine and glutamine at position 152 resulting in HNA-3a and HNA-3b. An additional Leu151Phe substitution can impair HNA-3a antibody binding. Recently an alloantibody against HNA-4b which discriminates from HNA-4a by an Arg61His exchange of the glycoprotein encoded by the ITGAM gene was reported in neonatal alloimmune neutropenia. An update of the current HNA nomenclature based on the new findings was provided in 2016 by the ISBT Granulocyte Immunobiology Working Party nomenclature subcommittee. Conclusions: The molecular basis of each of the five HNA antigen systems has been decoded during the past decades. This enables reliable molecular typing strategies, antibody detection and specification as well as development of new assays based on recombinant antigens. However, research on HNA alleles, antigens, and antibodies is not finally terminated and also in the future will add new findings.

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“…These individuals can be immunized and produce anti-FcγRIIIb isoantibodies [27]. Furthermore, individuals can, as a result of gene duplication, have a higher expression of FcγRIIIb and subsequently be positive for more than two HNA-1 alleles [28,29,30,31]. Individuals who are HNA-2-positive mostly also have a CD177(HNA-2)-negative neutrophil subpopulation, due to lack of gene transcription in a subset of the cells [5,32,33].…”

Section: Pathologymentioning

confidence: 99%

Neonatal Alloimmune Neutropenia

Porcelijn

Haas

2018

Transfus Med Hemother

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Neonatal alloimmune neutropenia (NAIN, NAIN or NIN) is a neutrophil blood group antagonism, analogous to hemolytic disease of the fetus and newborn (HDFN) and fetal/neonatal alloimmune thrombocytopenia (FNAIT). A limited number of prospective screening studies showed that granulocyte-specific antibodies were detectable in 0.35-1.1% of random postnatal maternal samples and that the incidence of NAIN was below 0.1%. Symptoms vary from none to mild skin infections, omphalitis or more severe infections like pneumonia, sepsis, and meningitis. Treatment of neonatal infection with antibiotics and granulocyte-colony stimulating factor is advised.

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FCGR3 variants and expression of human neutrophil antigen‐1a, ‐1b, and ‐1c in the populations of northern Germany and Uganda

Cited by 44 publications

References 21 publications

Mice with osteopontin deletion remain predisposed to collagen‐induced arthritis

Mice with osteopontin deletion remain predisposed to collagen‐induced arthritis

Molecular Genetics of the Human Neutrophil Antigens

Neonatal Alloimmune Neutropenia

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