Mark Steven Cragg

This paper introduces Duality vaccination, a method that delivers both activating and inhibitory stimuli to shape antibody responses, using nanoparticle-based immunogens.

The paper characterizes two anti-HPA-1a antibodies from a severe FNAIT case, showing functional differences in platelet activation through FcγRIIa engagement.

This study shows that Fc receptor engagement is necessary for the efficacy of SARS-CoV-2 therapeutics, including mAbs and BiKEs, and demonstrates the effectiveness of ACE2 decoy Fc-fusions and BiKEs against multiple variants.

This paper evaluates two TNFR2-targeting antibodies, showing ligand-blocking antibodies deplete T regs and reprogram myeloid cells, while agonists directly co-stimulate T and NK cells, both leading to anti-tumor effects.

This study shows that agalactosylated IgG N-glycans in RA reduce neutrophilic inflammation by decreasing FcγR binding and downstream signaling, suggesting they may act as a compensatory anti-inflammatory mechanism.

This study shows that bispecific antibody architecture and TNFRSF target selection influence CD8+ T cell differentiation and anti-tumour immunity, with 4-1BB being the most effective target.

The paper shows TRIM21 becomes an autoantigen by forming pro-inflammatory immune complexes after lytic cell death, which are taken up by macrophages and drive inflammation.

This paper introduces LAffAb, a method to co-optimize antibody affinity and stability through combinatorial mutation design, achieving significant affinity gains while maintaining developability.

This study shows that FcγRIIb promotes α-syn propagation and neurotoxicity in vivo, suggesting it as a therapeutic target for synucleinopathies.

This study shows genotoxic chemotherapy increases CD59 expression, reducing complement-dependent cytotoxicity and rituximab efficacy in DLBCL via Chk1-mediated regulation.

This study shows that Fc receptors trigger autophagy, which modulates monocyte functions like cytokine production and phagocytosis.

This study shows that excessive microglial proliferation in Alzheimer's disease leads to replicative senescence and disease-associated microglia, contributing to Aβ pathology.