1. Use of monoclonal antibodies that specifically target the CD89 receptor. The antibodies can bind to CD89 and block its interaction with IgA, effectively neutralizing its activity.
2. Small molecules and peptides that can disrupt the CD89-IgA interaction can be designed to fit into the binding site of the receptor or the antibody, preventing them from coming together.
3. Another strategy would be to involve the use of decoy proteins that mimic the natural ligands of CD89 without triggering an immune response. These decoys can compete with IgA for binding to CD89, thereby reducing the effective interaction between the receptor and its natural ligand.
As far as antibodies are concerned, there are commercially available antibodies.
1. Mouse anti-human CD89 antibody clone MIP8a, which is known to recognize an epitope within the EC1 domain of human CD89, bound to ‘human EC1-CD89’ and not to ‘human EC2-CD89.'
2. Mouse anti-human CD89 antibody clone A59, which recognizes an epitope within the EC2 domain of human CD89, bound to ‘human EC2-CD89’ and not to ‘human EC1-CD89’.
3. Mouse anti-human CD89 antibody clone A3, which recognizes an epitope depending on parts from both EC1 and EC2 domains of human CD89, bound to ‘human EC2-CD89’ but not to ‘human EC1-CD89’.
For more information, you may want to refer to the articles provided below.
Article Antagonizing FcαR1 (CD89) as treatment in IgA-mediated chron...
Article Pentraxins and IgA share a binding hot-spot on FcαRI
Article Immunoglobulin-binding Sites of Human Fc RI (CD89) and Bovin...
Additionally, an invention in the link below discloses an antibody that can bind an extra-cellular part of human CD89 (human FcaRI) on human CD89 expressing cells that prevents binding of human IgA to human CD89 when the antibody is bound to said cells and that induces less cell death in said human CD89 expressing cells when compared to the antibody MIP8a.