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Brian J. Nickoloff, MD, PhD

Arch Dermatol. 1999;135:1104-1110.

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

INTRODUCTION

In 1991, a comprehensive review was published highlighting the importance of cytokines in the immunopathogenesis of psoriasis.¹ Since then, many advances have been made regarding the critical role for pathogenic T cells as causing this common and enigmatic skin disease. While epidermal keratinocytes are clearly involved as participants in establishment of the appropriate cytokine milieu as presented earlier, more recent data point to T lymphocytes as triggering the chain reaction of cellular and molecular networks that culminate in the formation of a psoriatic plaque. In this review, 3 major topics will be addressed.

A DYNAMIC IMMUNOLOGIC MODEL IN WHICH 3 DIFFERENT IMMUNOCYTES COOPERATE FOLLOWING SEQUENTIAL 2-CELL INTERACTIONS

In 1986, Valdimarsson et al² suggested that psoriasis was a skin disease in which keratinocyte proliferation was initiated by T-cell infiltration and activation. A decade later using severe combined immunodeficient mice engrafted with symptomless (PN) skin, direct in vivo evidence was provided that T lymphocytes could indeed induce conversion of PN skin . . . [Full Text of this Article]

ACTIVATED, IMMUNOCYTE-DERIVED CYTOKINES MEDIATE ALTERED-KERATINOCYTE PHENOTYPE

GENETIC CONTROL AND POTENTIAL RECEPTOR-LIGAND INTERACTIONS THAT REGULATE IMMUNE REACTIONS

From the Department of Pathology, Skin Cancer Research Laboratories, Loyola University Medical Center, Cardinal Bernardin Cancer Center, Maywood, Ill.

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