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  Vol. 144 No. 11, November 2008 TABLE OF CONTENTS
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Cytokine Milieu in Psoriasis and Cardiovascular Disease May Explain the Epidemiological Findings Relating These 2 Diseases

Srdjan Prodanovich, MD; Michael L. Shelling, MD; Daniel G. Federman, MD; Robert S. Kirsner, MD, PhD

Arch Dermatol. 2008;144(11):1518-1519.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Interleukin-12, Interleukin-23, and Psoriasis: Current Prospects
Torti DC, Feldman SR
J Am Acad Dermatol. 2007;57(6):1059-1068

The clinical phenotype of psoriasis results from infiltration of T cells in the skin and elaboration of inflammatory cytokines. Interleukin (IL)-12 and, more recently, IL-23 have been implicated in the pathogenesis of psoriatic lesions. New therapies, including a monoclonal antibody against a subunit shared by IL-12 and IL-23, have been developed to treat psoriasis. Our purpose was to review the literature on IL-12 and IL-23 as a basis for understanding the use of anti-IL-12/IL-23 therapy for psoriasis. A review of English-language articles was performed using PubMed to identify articles pertaining to IL-12, IL-23, and psoriasis. IL-12 and IL-23 share a common subunit (p40) and have a distinct subunit (p35 and p19, respectively). Transgenic mice that overexpress IL-12 p40 . . . [Full Text of this Article]

COMMENT

AUTHOR INFORMATION

Departments of Dermatology and Cutaneous Surgery (Drs Prodanovich, Shelling, and Kirsner) and Epidemiology and Public Healing (Dr Kirsner), University of Miami Miller School of Medicine, Miami, Florida; and Department of Medicine, Veterans Administration Medical Center (Dr Federman), and Department of Internal Medicine, Yale University School of Medicine (Dr Federman), West Haven, Connecticut







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