IgG Conformer's Binding to Amyloidogenic Aggregates

PLoS One. 2015 Sep 14;10(9):e0137344. doi: 10.1371/journal.pone.0137344. eCollection 2015.

Abstract

Amyloid-reactive IgGs isolated from pooled blood of normal individuals (pAbs) have demonstrated clinical utility for amyloid diseases by in vivo targeting and clearing amyloidogenic proteins and peptides. We now report the following three novel findings on pAb conformer's binding to amyloidogenic aggregates: 1) pAb aggregates have greater activity than monomers (HMW species > dimers > monomers), 2) pAbs interactions with amyloidogenic aggregates at least partially involves unconventional (non-CDR) interactions of F(ab) regions, and 3) pAb's activity can be easily modulated by trace aggregates generated during sample processing. Specifically, we show that HMW aggregates and dimeric pAbs present in commercial preparations of pAbs, intravenous immunoglobulin (IVIg), had up to ~200- and ~7-fold stronger binding to aggregates of Aβ and transthyretin (TTR) than the monomeric antibody. Notably, HMW aggregates were primarily responsible for the enhanced anti-amyloid activities of Aβ- and Cibacron blue-isolated IVIg IgGs. Human pAb conformer's binding to amyloidogenic aggregates was retained in normal human sera, and mimicked by murine pAbs isolated from normal pooled plasmas. An unconventional (non-CDR) component to pAb's activity was indicated from control human mAbs, generated against non-amyloid targets, binding to aggregated Aβ and TTR. Similar to pAbs, HMW and dimeric mAb conformers bound stronger than their monomeric forms to amyloidogenic aggregates. However, mAbs had lower maximum binding signals, indicating that pAbs were required to saturate a diverse collection of binding sites. Taken together, our findings strongly support further investigations on the physiological function and clinical utility of the inherent anti-amyloid activities of monomeric but not aggregated IgGs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid / immunology
  • Amyloid / metabolism*
  • Animals
  • Antibodies, Monoclonal / metabolism*
  • Humans
  • Immunoglobulin G / metabolism*
  • Mice
  • Protein Aggregation, Pathological / metabolism*
  • Protein Binding

Substances

  • Amyloid
  • Antibodies, Monoclonal
  • Immunoglobulin G

Grants and funding

These studies were funded by an investigator initiated research grant (IIRG) from Baxter BioScience (Baxter International Inc., Deerfield, IL) (BO), and by a research grant from the SENS Research Foundation (BO). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.