01619nas a2200229 4500000000100000008004100001260001300042653001100055653003000066653002700096653001300123653001200136100001200148700001500160700001200175245006200187856004100249300001000290490000700300520106800307022001401375 1985 d c1985 Sep10aHumans10aHypersensitivity, Delayed10aImmunologic Techniques10aLepromin10aleprosy1 aDugan E1 aModlin R L1 aRea T H00aAn in situ immunohistological study of Mitsuda reactions. uhttp://ila.ilsl.br/pdfs/v53n3a06.pdf a404-90 v533 a
In an attempt to further define their immunopathogenesis, the cellular infiltrates of Mitsuda reactions were studied in situ using immunoperoxidase techniques and monoclonal antibodies. Lepromin A-elicited Mitsuda reactions from six patients with borderline tuberculoid leprosy (TT/BT or BT) and three healthy kindred and contacts of lepromatous patients were examined. In the dermis, cells bearing the Leu4 phenotype comprised a mean of 61% of the infiltrate; the Leu3a, 47%; the Leu2a, 17%; anti-IL-2, 0.2%; anti-Tac, 1.5%; and cells bearing the Ia phenotype were virtually universal; OKT6 positive cells were present. The Leu2 phenotype was sequestered to the periphery of epithelioid tubercules. In the epidermis, there were mild, focal lymphocytic infiltrates, hyperplasia of epidermal Langerhans' cells, and well-developed expression of Ia upon nucleated keratinocytes. These findings, when compared with those of a better-defined reaction, tuberculin, are further evidence that the Mitsuda response may be a delayed-type hypersensitivity phenomenon.
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