@article{10.37349/ei.2023.00125,
abstract = {Adaptor proteins are involved in various immune responses via the modulation of many signaling pathways. Signal-transducing adaptor protein-2 (STAP-2) is an adaptor protein that contains typical domains such as the pleckstrin homology (PH) domain, Src homology domain, and a proline-rich region from the N-terminal region. In T cells, STAP-2 positively regulates T cell receptor (TCR)-mediated signaling by associating with CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (LCK). Therefore, a peptide that inhibits the interaction between STAP-2 and CD3ζ ITAMs is likely to suppress TCR-mediated T cell activation, as well as T cell-mediated diseases. As expected, the peptide successfully inhibited the STAP-2/CD3ζ ITAM interaction and suppressed TCR-mediated signaling, cell proliferation, and interleukin (IL)-2 production in human/murine T cells. Furthermore, this inhibitor suppressed the pathogenesis of experimental autoimmune encephalomyelitis (EAE), which is widely recognized as a mouse model of multiple sclerosis, via the downregulation of T cell activation and infiltration of T helper (Th) 1/Th17 cells. These results suggest a new strategy for the treatment of multiple sclerosis and other immune diseases.},
author = {Sasaki, Yuto and Kawahara, Shoya and Sekine, Yuichi and Kashiwakura, Jun-ichi and Oritani, Kenji and Matsuda, Tadashi},
doi = {10.37349/ei.2023.00125},
journal = {Exploration of Immunology},
pages = {604--612},
title = {{Potential therapeutic applications of targeting signal-transducing adaptor protein-2 in autoimmune diseases}},
url = {https://www.explorationpub.com/Journals/ei/Article/1003125},
volume = {3},
year = {2023},
number = {6}
}