Christoph Q. Schmidt

TL;DR: The prevalence of factor H autoantibodies in the Newcastle cohort of aHUS patients is examined, whether such patients have additional susceptibility factors and/or mutations in the genes encoding complement regulator/activators are examined, and whether the presence of such autoantIBodies is always associated with deficiency offactor H-related proteins 1 and 3.

TL;DR: NMR and X-ray crystallography are used to study the C3d–FH19–20 complex in atomic detail and identify glycosaminoglycan-binding residues in factor H module 20 of the C 3d-FH19-20 complex and are consistent with a bent-back factor H molecule that binds through its termini to two sites on one C3b molecule and simultaneously to adjacent polyanionic host-surface markers.

TL;DR: In this article, the locations of binding sites for polyanions and C3b are reexamined rigorously by overexpressing factor H segments, structural validation, and binding assays.

TL;DR: It is demonstrated that CR1 is an erythrocyte receptor used by the parasite ligand PfRh4 for P. falciparum invasion, and that Parasite invasion via sialic acid–independent pathways is reduced in low-CR1 ERYthrocytes due to limited availability of this receptor on the surface.

TL;DR: Three‐dimensional structures of over half the 20 complement control protein (CCP) modules in CFH have been solved in the context of single‐, double‐ and triple‐module segments, including many of the residue positions at which sequence variations have been linked to three complement‐mediated disorders.