Therapeutic targeting of molecules involved in leukocyte-endothelial cell interactions.
Inflammation is traditionally viewed as a physiological reaction to tissue injury. Leukocytes contribute to the inflammatory response by the secretion of cytotoxic and pro-inflammatory compounds, by phagocytotic activity and by targeted attack of foreign antigens. Leukocyte accumulation in tissues is important for the initial response to injury. However, the overzealous accumulation of leukocytes in tissues also contributes to a wide variety of diseases, such as atherosclerosis, chronic inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis, vasculitis, systemic inflammatory response syndrome, juvenile diabetes and psoriasis. Many therapeutic interventions target immune cells after they have already migrated to the site of inflammation. This review addresses different therapeutic strategies, used to reduce or prevent leukocyte-endothelial cell interactions and communication, in order to limit the progression of inflammatory diseases.
Kaneider
Nicole C
NC
Molecular Oncology Research Institute, Tufts-New England Medical Center, Boston, MA, USA.
Leger
Andrew J
AJ
Kuliopulos
Athan
A
D000818:Animals; D002450:Cell Communication / Q000187:drug effects*; D042783:Endothelial Cells / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000209:etiology; D016023:Integrins / Q000037:antagonists & inhibitors / Q000502:physiology; D007962:Leukocytes / Q000502:physiology*; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000502:physiology; D019087:Selectins / Q000187:drug effects / Q000502:physiology
D016023:Integrins; D043562:Receptors, G-Protein-Coupled; D019087:Selectins