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Christopher E. M. Griffiths, MD, MRCP

Arch Dermatol. 1994;130(4):494-499.

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

THE LAST 15 YEARS have witnessed an immunologic revolution in dermatology, and it is accepted that immunologic mechanisms pervade a majority of cutaneous disorders. At first glance, some conditions are inherently immunologic, for instance, allergic contact dermatitis, whereas in others the role of the immune system is less obvious. Initially, it was believed that psoriasis fell into the latter, nonimmunologic group, and that the inflammatory infiltrate seen in this disease was secondary to the marked and characteristic epidermal hyperproliferation. The roles of T lymphocytes, antigen-presenting cells, cytokines, and adhesion molecules are nowadays recognized as paramount in the pathogenesis of psoriasis and have been investigated extensively. Ground-breaking work in Europe served notice that T lymphocytes are integral to the production and maintenance of psoriatic plaques and not innocent bystanders. Bjerke et al¹ observed that CD4⁺ (helper) T lymphocytes are present in psoriatic plaques, and then Baker et al² and . . . [Full Text PDF of this Article]

Author Affiliations
Department of Dermatology University of Michigan Medical Center 1910 Taubman Center 1500 E Medical Center Dr Ann Arbor, MI 48109-0314

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