Figures & data
Figure 1 Adhesion molecules (integrins) mediate the selective binding between the leukocytes and the endothelial cells to migrate from the vessels to the inflamed intestinal muocsa, through four phases: attachment, rolling, arrest, and transmigration. The toxic metabolites, cytokines, and chemioactractans, produced by the inflammation source, induce and drive the trafficking of immune cells to final destination.
![Figure 1 Adhesion molecules (integrins) mediate the selective binding between the leukocytes and the endothelial cells to migrate from the vessels to the inflamed intestinal muocsa, through four phases: attachment, rolling, arrest, and transmigration. The toxic metabolites, cytokines, and chemioactractans, produced by the inflammation source, induce and drive the trafficking of immune cells to final destination.](/cms/asset/257de4fa-295c-4844-818d-8731d21fe35b/dbtt_a_12160309_f0001_b.jpg)
Figure 2 Pharmacological targets of natalizumab. Several adhesion molecules are espressed on the surface of endothelial and immune system cells. In particluar, natalizumab inhibits the interaction between α4β1and α4β7 integrins expressed on the surface of T lymphocyte cells, and VCAM-1 and MAdCAM-1 expressed on the surface of endothelial cells.
![Figure 2 Pharmacological targets of natalizumab. Several adhesion molecules are espressed on the surface of endothelial and immune system cells. In particluar, natalizumab inhibits the interaction between α4β1and α4β7 integrins expressed on the surface of T lymphocyte cells, and VCAM-1 and MAdCAM-1 expressed on the surface of endothelial cells.](/cms/asset/be97ec68-acc1-482d-affd-fe1a34bd1d38/dbtt_a_12160309_f0002_b.jpg)