Analysis Biomolecular Interactions of mAb287 with p8G/p8E Peptide by BLI (CAT#: STEM-MB-0244-CJ)

Introduction

MAb287 can Inhibit the Development of Insulitis by Suppressing T-Cell and B-Cell Infiltration. In vitro experiments demonstrated that mAb287 worked by blocking CD4 T-cell TCR interaction with IAg7-presented insulin.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.