Targeting cells in motion: Migrating toward improved therapies

Authors

  • Jason W. Griffith,

    1. Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
    2. Pulmonary and Critical Care Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
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  • Andrew D. Luster

    Corresponding author
    1. Division of Rheumatology, Allergy & Immunology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
    • Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
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Full correspondence: Prof. Andrew D. Luster, Massachusetts General Hospital, Building 149, 13th Street, Charlestown, MA 02129, USA

Fax: +1-617-726-5615

e-mail: aluster@mgh.harvard.edu

Abstract

The development of clinical therapeutics that interfere with the migration of leukocytes has revolutionized the treatment of multiple sclerosis and holds great promise for the treatment of a wide range of inflammatory diseases. As the molecules essential for the multi-step adhesion cascade that mediates cellular migration have been elucidated, the number of potential targets available to modulate leukocyte trafficking has increased exponentially. In this Viewpoint, we briefly review our current understanding of these mole-cular targets and how these targets vary by tissue and leukocyte subset with emphasis on T cells. We then describe the two currently approved therapeutics that target cell migration, natalizumab and fingolimod, and discuss how an improved understanding of their function could pave the way for the development of safer and more efficacious therapies for inflammatory and autoimmune diseases.

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