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>Single Humanized Immune-Checkpoint Mice
B-hCD137(4-1BB) mice
This co-stimulatory signal can also multiply antigen presenting cells and result in cell factor secretion. Experiments show that CD137 co-stimulation regulates T cell and antigen presenting cell function for antitumor immunity, providing new targets for tumor immunological therapies.
B-hBTLA mice
BTLA binds to its ligand HVEM (a member of the tumor necrosis factor receptor superfamily) to transmit a co-inhibition signal. BTLA plays a negative regulatory role in the body's anti-tumor immune response, and is associated with the immune escape mechanism of the tumor. BTLA inhibitors enhance the TCR signaling pathway and restore T cell function, and become potential novel targets for tumor biotherapy.
B-hCD27 mice
Treating mice with a CD27 agonist antibody effectively enhanced the antitumor immune response for lymphoma and B16 melanoma, providing putative targets for tumor immunotherapy.
B-hCD28 mice
T cell stimulation through CD28 in addition to the T-cell receptor (TCR) can provide a potent signal for the production of various interleukins (IL-6 in particular). CD28 is the only B7 receptor constitutively expressed on naïve T cells. Association of the TCR of a naive T cell with MHC:antigen complex without CD28:B7 interaction results in a T cell that is anergic.The agonistic antibody of CD28 is now under phase II clinical trials.
B-hCD40 mice
Interaction with its trimeric ligand CD154 on activated T helper cells results in APC activation, which has been found to be essential in mediating a broad variety of immune and inflammatory responses including T cell-dependent immunoglobulin class switching, memory B cell development, and germinal center formation.
B-hCD47 (B/c) mice
CD47 is widely expressed on cell surface and interacts with the signal regulatory protein α (SIRPα), thrombospondin-1 (TSP1) and integrins to mediate a series of responses including apoptosis, proliferation and immunity. CD47 is an important “self” mark on the cell surface and inhibits macrophagocytosis by interaction with SIRPα on macrophage surface.​

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