Analysis Biomolecular Interactions of mAb757 with I-Ag7/p8G and I-Ag7/p8E Complexes by BLI (CAT#: STEM-MB-0201-CJ)

Introduction

mAb757 is the new antibody , which showed broader specificity and higher affinity, particularly to the ligands of “type B” cells. And mAb757 was significantly more effective in protecting young mice from developing T1D than mAb287. Importantly, mAb757 was effective at late pre-diabetic stages. The NOD mouse can only expresses a single MHC class II glycoprotein (I-Ag7). Like HLA-DQ8, the molecule conferring the greatest genetic risk for T1D in humans, I-Ag7 lacks an Asp at position 57 of the beta chain. This residue normally forms a salt bridge with a conserved Arg at position 76 of the α chain to “close” the P9 peptide-binding pocket. Substitution of Aspβ5,7 with Ser (I-Ag) or Ala (DQ8) “loosens” the pocket and creates a preference for peptides with acidic residues at P9. A large number of CD4+ T cell clones and hybridomas reactive with B:9–23/I-Ag7 have been generated from insulitic lesions from NOD mice, and many will cause disease when adoptively transferred to immunodeficient animals.