Immunocompetent and accessory cells in dermatitis herpetiformis.

Monoclonal antibodies were used in conjunction with the biotin-avidin immunolectin method and the indirect immunofluorescence method to detect lymphocyte subsets in patients with dermatitis herpetiformis (DH) in 50% potassium iodide (KI)-induced skin lesions and in density-gradient-isolated peripheral blood. The proportions of T3-, T4-, and T8-positive lymphocytes in peripheral blood in patients with DH were 76 +/- 6, 48 +/- 7, and 28 +/- 4% and did not differ significantly from those in healthy controls. Among the inflammatory cells in situ in the reticular dermis, 82 +/- 5% were T3-positive lymphocytes, indicating a T-lymphocyte dominance in mature KI-induced DH lesions. The difference in the proportion of T4-positive lymphocytes in mature DH skin lesions and in patient blood was significant (63 +/- 9 and 48 +/- 7%, respectively (P less than 0.001), indicating that the composition of the dermal infiltrate does not reflect nonselective entrapment of blood mononuclear cells in situ. Studies of the kinetics of the local inflammatory response disclosed that at the preblister stage endogenous peroxidase-positive cells and granular, extracellular peroxidase were observed in the dermal papillae only 6 hr after induction, suggesting locally released proteinases as possible complement-degrading factors. Second, at the same time 63 +/- 15% of the inflammatory round cells in the dermis were Ia-positive, endogenous peroxidase-negative, T3- and T6-negative cells, indicating a pathomorphogenetic role for an early event no longer observable in the mature DH skin lesion.

Cellular infiltrate in situ and response kinetics of human intradermal and epicutaneous tuberculin reactions.

Monoclonal antibodies used in the avidin-biotin-peroxidase complex (ABC) method and a histochemical azo-dye method for acid alpha-naphthyl acetate esterase (ANAE) were used to identify T lymphocytes and their functional subpopulations, B cells, and mononuclear phagocytes in tuberculin-test reactions. At 6 and 24 hr up to 52% of all dermal inflammatory cells in situ were T6+, whereas at 72 hr no T6+ cells were observed in the dermis. This suggests that in the initial phases of tuberculin reactions the epidermal Langerhans cells are mobilized to the perivascular spaces in the dermis. At 6, 24, and 48 hr T3+ T lymphocytes usually formed the main inflammatory cell type in situ. The high proportion of Ia+ T lymphocytes and the variations in the local proportion and numbers of T4+ and T8+ cells suggest that T cells play an active role in the generation of a positive tuberculin reaction. At 72 hr T-pattern ANAE+ lymphocytes accounted for 64 +/- 9 and 35 +/- 10% of all cells in situ in epicutaneous and intradermal tuberculin reactions, respectively (P less than 0.05). The corresponding values for M-pattern ANAE+ macrophages were 27 +/- 9 and 53 +/- 10% (P less than 0.10). This indicates that the recruitment of mononuclear phagocytes is delayed if tuberculin is applied epicutaneously rather than injected intradermally.

Inflammatory cells in sarcoid granulomas detected by monoclonal antibodies and an esterase technique.

Inflammatory cells in situ in Kveim reaction papules were identified in 15 patients with avidin-biotin-peroxidase complex and biotin-avidin-peroxidase methods for surface epitopes and with a simultaneously capturing azo dye method for cytoplasmic acid alpha-naphthyl acetate esterase (ANAE). The spatial relationship of cells in granulomas indicates a concentric arrangement. Endogenous peroxidase-negative, ANAE+, but OKIa-negative immunoincompetent epithelioid cells were in the center. T3+, ANAE+ T lymphocytes formed 60-80% of all cells in the lymphocyte mantle surrounding the epithelioid core. T4/T8 was 2:1. Equal proportions (5-15%) of Ia+ lymphocytes and M pattern ANAE+, endogenous peroxidase-positive mononuclear phagocytes on the one hand and T3+ and T pattern ANAE+ cells on the other in individual patients indicate that the proportion of activated T blasts in situ was less than 15%. The close contacts between different immunocompetent cells in the periphery indicates this as the site for cellular interactions.