Clin Immunol 2004 Oct;113(1):38-46
Genentech, Inc., South San Francisco, CA, USA.
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J Invest Dermatol 2008 May 15;128(5):1173-81. Epub 2007 Nov 15.
Department of Dermatology, Oregon Health & Science University, Portland, Oregon 97239, USA.
Efalizumab is an mAb directed against CD11a, a molecule involved in T-cell activation and extravasation from blood into tissue. Ten patients with severe atopic dermatitis were treated with efalizumab for 84 days, and peripheral blood mononuclear cells were analyzed for expression of activation and adhesion markers. Efalizumab treatment led to decreases in CD11a mean fluorescence intensity (MFI) on naive, central memory, and effector memory CD4+ and CD8+ T cell subsets. Read More
J Invest Dermatol 2008 May 31;128(5):1182-91. Epub 2008 Jan 31.
Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York 10065, USA.
Efalizumab (anti-CD11a) interferes with LFA-1/ICAM-1 binding and inhibits several key steps in psoriasis pathogenesis. This study characterizes the effects of efalizumab on T-cell activation responses and expression of surface markers on human circulating psoriatic T cells during a therapeutic trial. Our data suggest that efalizumab may induce a unique type of T-cell hyporesponsiveness, directly induced by LFA-1 binding, which is distinct from conventional anergy described in animal models. Read More
Arch Dermatol 2002 May;138(5):591-600
University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Clinical Research Center, New Brunswick, NJ 08903-0019, USA.
Background: Leukocyte function-associated antigen 1 (LFA-1), consisting of CD11a and CD18 subunits, plays an important role in T-cell activation and leukocyte extravasation.
Objective: To test whether blocking CD11a decreases immunobiologic and clinical activity in psoriatic plaques.
Design: Open-label, multicenter, dose escalation study. Read More
Skin Pharmacol Physiol 2007 13;20(2):96-111. Epub 2006 Dec 13.
Clinic for Dermatology and Venereology, Otto-von-Guericke-University, Magdeburg, Germany.
Efalizumab (Raptiva) is an immunomodulating recombinant humanized IgG1 monoclonal antibody that binds to CD11a, the alpha-subunit of leukocyte function antigen-1 (LFA-1). By blocking the binding of LFA-1 to ICAM-1, efalizumab inhibits the adhesion of leukocytes to other cell types and interferes with the migration of T lymphocytes to sites of inflammation (including psoriatic skin plaques). Analysis of the response in patients treated with efalizumab to date shows that distinct groups of responders and nonresponders to the drug exist. Read More