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
Griffiths CEM. Cutaneous Leukocyte Trafficking and Psoriasis. Arch Dermatol. 1994;130(4):494–499. doi:10.1001/archderm.1994.01690040098016
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