To the Editor.—
During the past several years, the molecular basis for leukocyte trafficking into the skin of psoriasis lesions, as well as other inflammatory and neoplastic cutaneous disorders has begun to be defined.1 The main focus of this work has centered around the β-2 integrin LFA-1, which is expressed by infiltrating leukocytes, and intercellular adhesion molecule-1 (ICAM-1) expressed by the overlying epidermal keratinocytes. There is excellent spatial colocalization and temporal correlation between intraepidermal LFA-1-positive cells and ICAM-1-expressing keratinocytes.1 Much of this in vivo work was derived from our earlier in vitro discovery that normal cultured keratinocytes (which are ICAM-1 negative) do not bind lymphocyte/monocytes, but, after exposure to cytokines such as interferon-γ, there was dramatic increase in binding mediated by induction on the keratinocyte of ICAM-1 that facilitated LFA-1/ICAM-1 interaction. We have recently discovered a second adhesion pathway involving binding between cultured keratinocytes and lymphocytes that is
Nickoloff BJ. Anti—ß-4 Integrin Antibody Prominently Stains Nerves in Psoriatic Skin. Arch Dermatol. 1991;127(2):271–272. doi:10.1001/archderm.1991.01680020143029
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