Marion Kleijer

TL;DR: Differences in IgG binding among the three Fc gammaRIIIa-48L/R/H isoforms are a consequence of the linked, biallelic Fc Gamma receptor IIIa-158V/F polymorphism at amino-acid position 158.

TL;DR: It is found that patients with paroxysmal nocturnal haemoglobinuria (PNH) have only about 10% of the normal levels of FcRIII on their neutrophils, whereas the expression of F cRII is unaffected, and lipid linkage of the receptor on neutrophil suggests that its release may be important for its function.

TL;DR: In this article, a mutation in IgG3 was shown to reduce binding to the neonatal Fc receptor, which can be competitively blocked by IgG1 and IgG2.

TL;DR: Genotyping showed a normal Fc gamma RIIa phenotype distribution among the F c gamma RIIIb-negative individuals, thus excluding the possibility that the presence of the favorable IgG2-binding low-responder isoform of Fc Gamma RIIA (131-H) contributed to the overall absence of recurrent bacterial infections.

TL;DR: Patients with an acquired clonal disorder of their hematopoietic cells, paroxysmal nocturnal hemoglobinuria (PNH) and PNH patients appeared to have a strongly reduced expression of FcRIII on their neutrophils, suggesting that plasma F cRIII originates from neutrophil release in vivo.