Inhibition of LFA-1/ICAM-1 Interaction: A Therapeutic Strategy for Surmounting Inflammation Gaba Monika1,*, Gaba Punam1, Singh Sarbjot2, Dhingra Neelima3,** 1Department of Pharmaceutical Sciences, ASBASJSM College of Pharmacy, Bela, Ropar, Punjab, India 2Drug Discovery Research, Panacea Biotech Pvt. Ltd., Mohali, Punjab, India 3University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India *Corresponding Author E-mail: monikagaba12@gmail.com
**neelimad08@gmail.com
Online published on 2 May, 2015. Abstract Leukocyte function associated antigen-1 (LFA-1, CD11a/CD18, αLβ2) is a cell surface adhesion protein expressed on leukocytes. Interaction of LFA-1 with its counter receptor intercellular adhesion molecule-1 (ICAM-1) promotes the migration of leukocytes to the site of inflammation and is responsible for a variety of cell adhesion events required for normal and pathological functions of the immune system. Thus, the LFA-1/ICAM-1 interaction is thought to play a role in the pathogenesis of inflammatory and auto-immune disease conditions such as psoriasis, multiple sclerosis, asthma, rheumatoid arthritis, inflammatory bowel disease and transplant rejection. LFA-1/ICAM-1 interaction inhibitors have been extensively studied as a therapeutic target for clinically important diseases; leading to the development of therapeutic antibodies, peptides, peptidomimetics, allosteric and competitive inhibitors. However, despite of promising preclinical results, the outcome of clinical trials with LFA-1/ICAM-1 interaction inhibitors has been inconsistent and met with limited clinical success. This article gives a brief account of rationale and efficacy of different LFA-1/ICAM-1 interaction inhibitors as promising therapeutic strategy for surmounting inflammatory disorders. Top Keywords Inflammation, LFA-1, ICAM-1, Leukocytes, Therapeutic strategy. Top |