The inhibition of T-cell activation involves the blockade of the interaction between T-lymphocytes and antigen presenting cells by binding to an adhesion molecule involved in this process, LFA-1 [5].
It is largely thought that the benefit derives from blockade of the interaction between VEGF and its receptor VEGFR2 on endothelial cells, which mediates key functions in angiogenesis and vascular function [2].
The reduction in hydrolysis ability may be caused by the blockade of the interaction between the enzyme and the substrate, resulting from the alkylation of the Cys residue at the subsite by a cystein protease inhibitor.
Our data suggest that ICOS plays an important role in the immunopathogenesis of SLE and support the possibility that blockade of the interaction between ICOS and B7RP-1 may have therapeutic value in treating this intractable autoimmune disorder.
The protective effects of anti-HMGB1 mAb might be explained by its blockade of the interaction between HMGB1 and RAGE, a key mechanism in the initiation of inflammatory and oxidative responses.
Selective blockade of the interaction between VCAM-1 and its ligand, integrin- α4, on leukocytes has been shown to abolish leukocyte recruitment and the associated neurological deficit in EAE models [ 37].
These findings suggest that ICOS is involved in abnormal T cell activation in SLE, and that blockade of the interaction between ICOS and its receptor may have therapeutic value in the treatment of this intractable disease.
16 Moreover, evidence has recently been accumulated from several clinical trials of immune checkpoint blockade with therapeutic mAbs, including the interaction between PD-L1 and PD1, with encouraging clinical effects such as prolonged overall survival and an improved response rate, 17– 20 suggesting that the immune checkpoint may play a pivotal role in anti-tumor immunity.
We hypothesized that increasing the tumor-specific T-cell frequency through vaccination would allow us to better observe the interaction between 4-1BB andivation and CTLA-4 blockade in the B16 melanoma system.
