1. Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2017.107
Figure 2 Strategies for detecting or eliminating autoreactive B cells and/or autoantibodies
Figure 2 | Strategies for detecting or eliminating autoreactive B cells and/or autoantibodies. a | Autoreactive B cells can be detected using biotinylated autoepitope peptides that are tetramerized with fluorescently-labelled avidin; in this manner, autoreactive B cells can be purified and enriched from peripheral blood. These cells can also be selectively depleted using nanoparticles coated with an autoepitope peptide and a complement-activating peptide. The complement-activating peptide initiates the complement cascade to lyse the autoreactive B cell (complement-mediated cytoxicity). Autoreactive B cells can be silenced with autoepitope peptides coupled to anti-Fcγ receptor IIb (FcγRIIb) antibodies. In this scenario, the peptide–antibody complex crosslinks the B cell receptor (BCR) and FcγRIIb, silencing the B cell. b | Autoreactive plasma cells can be detected using affinity matrix technology in which both the secreted autoantibodies and the plasma cell bind to a matrix made up of F(ab)2 fragments of antibodies reactive towards the plasma cell marker CD138 coupled with autoepitope peptides. The marked cell is subsequently killed by the complement system. Autoantibodies can be cleared using an antigen-based heteropolymer system. In this system, an anti-complement receptor 1 (CR1) antibody is linked to a double stranded DNA (dsDNA) motif. Anti-dsDNA autoantibodies are cleared from the peripheral blood by binding to CR1‑expressing red blood cells. Abetimus sodium, a tetramerized double-stranded oligodeoxyribonucleotide attached to a carrier platform, can also clear anti-dsDNA autoantibodies.
Pozsgay, J. et al. (2017) Antigen-specific immunotherapies in rheumatic diseases
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