To determine whether inhalant allergens could induce eczematous lesions we studied 17 patients with atopic eczema (with or without allergic rhinitis), 13 patients with allergic rhinitis without atopic eczema and 10 healthy control subjects. The allergens, birch pollen (Betula verrucosa) and house dust mite (Dermatophagoides pteronyssinus), were applied in aluminium chambers for 48 h on clinically normal skin. In 17 patients with atopic eczema, six epicutaneous test reactions of the delayed type to birch pollen and three to house dust mite were seen at 48 or 72 h. In 13 patients with allergic rhinitis without eczema there was one delayed reaction to birch pollen and none to house dust mite. No delayed type test reactions to either allergen were seen in the controls. Biopsies of the positive test sites revealed an eczematous reaction with epidermal spongiosis and microvesiculation. Immunostaining of cryostat sections showed dermal cell infiltrates consisting of mainly T lymphocytes (ratio of T4:T8, 2-6:I) and to a lesser degree Langerhans and indeterminate T6+ cells. 50-90% of the cells were Ia+. The numbers of basophils and mast cells did not exceed 10-15%.

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Optimal tissue processing conditions were defined for the immunohistochemical detection of inflammatory cell surface epitopes identified by OKT3, OKT4, OKT6, OKT8, OKIa1, OKM1, Leu7 and pan B cell antibodies. Snap-freezing in isopentan was superior to liquid nitrogen in preservation of morphology. Embedding of the tissues in Tissue-Tek II O.C.T. Compound diminished the intensity of immunostaining with all antibodies studied; however, the embedded tissues tolerated longer storage without drying. Optimal fixation with satisfactory preservation of morphology and immunogenicity was achieved with fixation of the frozen sections in acetone at 4 degrees C for 5 min. Blocking of the endogenous peroxidase with methanol-H2O2 treatment destroyed all epitopes studied except those identified with OKIa1, OKT6 and Leu7.

The phenotypes of the infiltrating cells in 13 patients with delayed hypersensitivity to topical glucocorticosteroids (GCS) were studied from sequential biopsies of positive epicutaneous test reactions by using the avidin-biotin-complex (ABC) technique. Monoclonal antibodies were used to identify the cells with the following phenotypes: T3, T4/T4a, T6, T8, T9, T11, M1, Ia1 (HLA-DR), interleukin-2 receptor/T26a, and dendritic reticular cell. The cellular kinetics of GCS hypersensitivity reactions were compared with delayed hypersensitivity reactions caused by allergens not related to GCS. In both GCS and non-GCS reactions the epidermal dendritic T6+ cells were more numerous than dendritic Ia1+ cells. There was a decrease in the number of both cell types during these reactions; in GCS reactions the decrease in the number of T6+ cells was seen later than in non-GCS reactions. Ia1+ keratinocytes were seen at sites near dermal infiltrates. Compared with the non-GCS delayed hypersensitivity reaction, there were fewer pan T (T11+/T3+) in the GCS reaction. The relative numbers of M1+ monocytes and the T4/T8 ratio were substantially lower in the latter; these findings can be explained as a GCS effect which modulates the delayed type hypersensitivity reaction.