Research further into the alpha beta integrin interaction with VCAM1 for Tysabri and Tecfidera activation of the Nrf-2 dependent pathway Investigate if any alterations can be made to these current...

Research further into the alpha beta integrin interaction with VCAM1 for Tysabri and
Tecfidera activation of the Nrf-2 dependent pathway.
Investigate if any alterations can be made to these current treatments.
T-cells migrate from blood to the infection site through a proper channeling network. T-cells
in blood and other lymphoid organs produce several glycoproteins alpha-beta integrins such as
α4β1, α4β7, etc., on their surface in response to the chemokines and other cytokines.
Other than T-cells, the endothelial and mucosal epithelial cells represent adhesion molecules
on their surface in response to the chemokines circulating in the body. These adhesion
molecules interact with the T-cell integrins that facilitate the T-cells to migrate and reach the
infection site (Yuan et al., 2021). This process is called as diapedesis.
Vascular Cell Adhesion Molecule-1 (VCAM-1) is an adhesion molecule expressed on
endothelial cells after the induction of chemokines and cytokines. They selectively interact
with α4β1 of the T-cells, which helps them cross the blood vessels (Mayer et al., 2006). For
instance, in multiple sclerosis, the interaction helps the T-cells to cross the blood-brain barrier,
thereby inflicting damage to the neurons (Kekre et al., 2021).
Tysabri and Tecfidera, otherwise scientifically called Natalizumab and Dimethyl fumarate
respectively, interact with cytokine-induced α integrins on the surface of the T-cells and block
their activity. Blockade of alpha integrins reduces T-cell activation and migration to the
infection site. It consequently reduces inflammation (Kekre et al., 2021) caused by the
cytotoxic effects of T-cells.
Nuclear factor erythroid 2-related factor (Nrf2) is a transcription factor that promotes the
expression of several genes responsible for wound healing and the anti-inflammation pathway.
When...