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 peripher...
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Veröffentlicht in: | Clinical immunology and immunopathology 1984, Vol.30 (1), p.134-141 |
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Zusammenfassung: | 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 lymhocytes 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 < 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. |
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ISSN: | 0090-1229 1090-2341 |
DOI: | 10.1016/0090-1229(84)90014-X |