1. Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2017.107
Figure 3 Strategies for neutralizing or re‑programming autoreactive T cells
Figure 3 | Strategies for neutralizing or re‑programming autoreactive T cells. a | Autoreactive T cells can be detected with MHC–peptide tetramers coupled to a fluorescent dye and eliminated with MHC–peptide tetramers coupled to a toxin. Ethylene carbodiimide (ECDI)-fixed apoptotic cells coupled with antigen (antigen-coupled carrier cells) can be used to induce tolerance of autoreactive T cells either directly by presenting antigen to T cells to induce anergy, or indirectly by being taken up by host antigen presenting cells (APCs), which subsequently present antigens to T cells to induce regulatory T (Treg) cell differentiation and expansion. Peptide-coated nanoparticles containing rapamycin or encapsulated peptide-containing nanoparticles can also be taken up by host APCs to induce Treg cell differentiation. Finally, tetramerized MHC–peptide complexes and peptide-coated nanoparticles can directly induce Treg cell differentiation. b | T cells can be engineered to specifically target autoimmunity. Chimeric antigen receptors (CARs), consisting of an autoantibody-derived antigen-binding domain and a T cell signalling domain (that is, the CD137 and the CD3ξ signalling domain of the T cell receptor), can be introduced to T cells, in addition to the murine Foxp3 gene, to create autoantigen-specific Treg cells (CAR Treg cells). Introduction of the chimeric autoantibody receptor (CAAR), consisting of an autoantigen epitope recognized by autoreactive B cell receptors (BCRs) and CD137 + CD3ξ signalling domain of the T cell receptor, can enable a T cell to specifically kill autoantigen-specific B‑cells .
Pozsgay, J. et al. (2017) Antigen-specific immunotherapies in rheumatic diseases
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