S. H. M. Rooijakkers

This paper detects MGUS using LC-MS and determines M-protein sequences from serum, providing molecular detail for monoclonal gammopathies.

This study identifies and characterizes two high-affinity anti-C5 nanobodies that inhibit C5 cleavage and recognize distinct epitopes, including a variant not targeted by Eculizumab.

This study shows that colistin resistance mutations in K. pneumoniae increase sensitivity to IgM-mediated complement killing via PhoQ activation.

The paper shows that activated neutrophils release soluble SIRL-1 via proteinase 3 cleavage, and that sSIRL-1 is present in vivo in RSV and COVID-19 patients.

The paper investigates how soluble MAC (sMAC) is formed during bacterial infections, finding that MAC-resistant bacteria convert C5 into C5b more efficiently and release sMAC, which can lyse bystander erythrocytes.

This study shows that C9 polymerization enhances MAC pore-mediated bacterial killing and is impaired in complement-resistant strains.

This study shows that C1r2s2 proteases stabilize C1q binding to surface-bound IgG, with subclass-specific effects and improved phagocytosis with hexamer-enhanced IgGs.

This study shows Staphylococcal protein A inhibits IgG hexamer formation, blocking complement activation, but IgG3 can still induce complement activation despite SpA.

This study shows how MAC pores in Gram-negative bacteria's outer membrane make them more susceptible to immune system components like lysozyme and phospholipases, enhancing bacterial clearance.