Journal
EMBO MOLECULAR MEDICINE
Volume 13, Issue 5, Pages -Publisher
WILEY
DOI: 10.15252/emmm.202013404
Keywords
autoimmune disease; B7 family; T cells; TAPBPL; tumor immunity
Categories
Funding
- NIH [1R01AI123131]
- Connecticut Regenerative Medicine Research Fund [16-RMB-UCONN-02]
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TAPBPL is a novel T cell co-inhibitory molecule that inhibits the proliferation, activation, and cytokine production of T cells, and has the potential to be used for the treatment of cancer, infections, autoimmune diseases, and transplant rejection.
T cell stimulatory and inhibitory molecules are critical for the regulation of immune responses. In this study, we identify a novel T cell co-inhibitory molecule TAPBPL, whose amino acid sequence shares homology with known B7 family members. TAPBPL protein is expressed on resting and activated T cells, B cells, monocytes, and dendritic cells (DCs), as well as on some tumor tissues. The putative TAPBPL receptor is expressed on activated CD4 and CD8 T cells. A soluble recombinant human TAPBPL-IgG Fc (hTAPBPL-Ig) fusion protein inhibits the proliferation, activation, and cytokine production of both mouse and human T cells in vitro. In vivo administration of hTAPBPL-Ig protein attenuates experimental autoimmune encephalomyelitis (EAE) in mice. Furthermore, an anti-TAPBPL monoclonal antibody neutralizes the inhibitory activity of hTAPBPL-Ig on T cells, enhances antitumor immunity, and inhibits tumor growth in animal models. Our results suggest that therapeutic intervention of the TAPBPL inhibitory pathway may represent a new strategy to modulate T cell-mediated immunity for the treatment of cancer, infections, autoimmune diseases, and transplant rejection.
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