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Jon M. Hanifin, MD

Arch Dermatol. 1996;132(10):1230-1232.

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

A CLASSIC PROBLEM with understanding the pathogenesis of most common chronic inflammatory diseases is finding the cell or mediator that directly confers damage. Erythema, edema, and pruritus are the primary clinical features of atopic dermatitis (AD), but we have minimal understanding of the effector mechanisms that cause this inflammation in AD. What cells constitute the inflammatory infiltrate and how do they get into the skin? Is the inflammation of AD unique or is there a similar final mechanistic pathway causing nummular eczema, allergic contact dermatitis, and other spongiotic dermatoses?

Since there is no confirmed experimental model for AD (though a recently described mouse model appears promising,¹ as does the aeroallergen patch test²), we are forced to focus on lesional skin of the patient with AD. Morphologically, the primary lesion of AD is complex and the confusion has been heightened by the frequent repetition of the catchy Jacquet description . . . [Full Text PDF of this Article]

Author Affiliations
Oregon Health Sciences University 3181 SW Sam Jackson Park Rd Portland, OR 97201-3098

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