Nature: In addition to anti-PD-1, immunosuppressors can also be suppressed by phosphatase collection

Antibodies that antagonists interact with extracellular- and henant interactions can inhibit signaling of cell surface-borne bodies and are widely used in the treatment of a variety of diseases, including tumors.
, for example, co-subjects (such as PD-1 and CTLA-4) regulate T-cell signaling has been key to tumor immunotherapy.
the phosphatation of the phosphatization of the phosphatization is regulated by several processes, including the reverse regulation of phosphatases such as CD45.
anti-PD-1 antibodies effectively block the signaling of the mating body activation, but they do not inhibit the continuous intracellular PD-1 signaling, which continuously inhibits T-cell function.
, October 21, 2020, Nature published the journal K. Christopher Garcia's team, called Immune Receptors, has found that inhibiting receptors by phosphatase can enhance T-cell activity and significant progression of small cell lung and colon adenocarcinoma.
, the researchers used anti-CD3 to reseal Jurkat T cells and observed that CD69 and CD25 increased by about 50 percent in the absence of PD-1.
, the PD-1 over-expression inhibits the CD69 increase.
, PD-1 phosphatization can be detected in PD-1-conducted resting Jurkat T cells.
non-ligand-dependent PD1 signal reduction T cell activated CD45 is a formative active cell surface tyrosine phosphatase with a large extracellular domain (ECD), which can be selectively combined with dual-specific molecules using anti-CD45 antibodies to the ECD of PD-1.
the researchers designed a heterogeneic dual-specific double-priced antibody that binds to CD45 and PD-1 ECD, allowing PD-1 and CD45 to bind to the surface of T cells (RIPR-PD1).
results show that RIPR-PD1 enhances T-cell activity.
CD45 and PD-1 crosslinking enhances T-cell activity In addition, in mouse models of small cell lung cancer and colon cancer, mice RIBR-PD1 alone or in combination with chemotherapy drugs can increase the proportion of effect memory T cells in the near end of the tumor and the far end of the tumor lymph nodes, and inhibit tumor progression.
mouse models of small cell lung cancer and colon cancer, MICER-PD1 reduced tumor progression in general, and the study proposed an alternative method of weakening cell surface sensor signals, called inhibition of the subject through phosphatase collection (RIPR).
addition, the researchers designed RIPR-PD1, which induces crosslinking between PD-1 and CD45, inhibits signaling of complement and match activation, and has significant anti-tumor effects in mouse tumor models.
different types of cells express different cell surface phosphatases, the RIPR method is expected to serve as a tool for the suppression of a variety of kinase-specific ligands, opening up new directions for the treatment of many diseases.