Acne: 1991-2001.

Proliferation of follicular keratinocytes Knaggs H, Holland K, Morris C, Wood E, Cunliffe W. Quantification of cellular proliferation in acne using the monoclonal antibody Ki67. J Invest Dermatol 1994;102:89-92. Keratinocyte proliferation was assessed in normal follicles and acne follicles by using the antibody Ki-67. Cellular proliferation was greater in normal follicles from acne-affected areas compared with areas not affected by acne. Proliferation was also greater in comedones compared with normal follicles. The authors conclude that normal follicles from skin affected with acne may be “acne-prone” compared with normal follicles from areas of skin not affected by acne. Role of cytokines: Interleukin 1 Guy R, Green M, Kealey T. Modeling of acne in vitro. J Invest Dermatol 1996;106:176-82. Using a model of human infrainfundibular segments to study the process of follicular hyperkeratinization, these authors found that the addition of interleukin 1 (IL-1) to the infrainfundibular segments caused hyperkeratinization similar to that seen in comedones. This effect could be blocked by addition of IL-1 receptor antagonist. These authors suggest that changes in sebum secretion or composition could lead to the release of IL-1 by follicular keratinocytes, which in turn may stimulate comedogenesis.