01825nas a2200373 4500000000100000008004100001260001300042653002400055653004400079653002400123653002200147653001400169653004100183653001100224653003000235653001800265653001200283653001400295653001800309100001300327700001500340700001100355700001700366700001100383700001500394700001400409700001300423700001300436245007600449300001200525490000700537520089300544022001401437 1986 d c1986 May10aAntigens, Bacterial10aAntigens, Differentiation, T-Lymphocyte10aAntigens, Protozoan10aAntigens, Surface10aEpidermis10aHistocompatibility Antigens Class II10aHumans10aHypersensitivity, Delayed10aLeishmaniasis10aleprosy10aMonocytes10aT-Lymphocytes1 aKaplan G1 aWitmer M D1 aNath I1 aSteinman R M1 aLaal S1 aPrasad H K1 aSarno E N1 aElvers U1 aCohn Z A00aInfluence of delayed immune reactions on human epidermal keratinocytes. a3469-730 v833 a
The epidermal changes that occur in human cutaneous immune responses have been investigated in the tuberculin reaction and in the lesions of tuberculoid and lepromatous leprosy and cutaneous leishmaniasis. In each situation, there was a dermal accumulation of monocytes and T cells, and the epidermis exhibited thickening. In the tuberculin response, the thickness of the epidermis sometimes doubled in 48-72 hr, and this was attributed to increases in both size and number of keratinocytes. In addition, the phenotype of the keratinocytes changed from Ia- to Ia+. Similar changes in keratinocyte Ia-antigen expression occurred in the epidermis overlying untreated tuberculoid leprosy and cutaneous leishmaniasis lesions, but not in lepromatous leprosy. We suggest that one or more epidermal growth factors may be generated in the course of a delayed immune reaction in the dermis.
a0027-8424