title: Studies of human leprosy lesions in situ using suction-induced blisters. 2. Cell changes and soluble interleukin 2 receptor (Tac peptide) in reversal reactions.
abstract: To examine the pathogenesis of type 1 (reversal) reactions in leprosy, we studied cellular and soluble immunologic components of skin lesions in 10 patients with reactions, 24 active patients without reactions, and 33 control patients whose leprosy had been treated and cured. Cells and Tac-peptide levels were obtained from fluid aspirated from blisters induced by suction directly over representative skin lesions. During reversal reactions: a) the lesions contained an increased number and percentage of CD4+ (T-helper) cells; b) Tac-peptide levels were elevated in half of the lesions; c) the increases in Tac peptide and CD4+ cells were directly correlated; and d) systemic administration of corticosteroids appeared to cause a reduction in the intralesional CD4+ cell population. These findings were localized to the skin, and do not represent simple filtration of these components from the peripheral blood. We conclude that spontaneous lymphocyte activation in situ, primarily of CD4+ cells, is an important feature of reversal reactions, and may be an intermittent or cyclic phenomenon during the reaction. Findings in active patients without reactions are consistent with the hypothesis that differing states of immunologic equilibrium have been established in different portions of the leprosy spectrum. In reversal reactions we may, therefore, be examining immunologic processes set in motion when a pre-existing equilibrium has been upset by spontaneous, natural events. The mechanism of such spontaneous changes in immunity in leprosy is of considerable interest, not only to understand the reaction, but also to examine the underlying determinants of delayed-type hypersensitivity and cell-mediated immunity in leprosy and the potential for artificially manipulating these responses, as proposed with vaccines or immunotherapy.
authors.affiliation: Department of Pathology, University of Hawaii School of Medicine, Leahi Hospital, Honolulu 96816.
authors.forename: D M
authors.initials: DM
authors.lastname: Scollard
authors.forename: V
authors.initials: V
authors.lastname: Suriyanon
authors.forename: L
authors.initials: L
authors.lastname: Bhoopat
authors.forename: D K
authors.initials: DK
authors.lastname: Wagner
authors.forename: T C
authors.initials: TC
authors.lastname: Smith
authors.forename: K
authors.initials: K
authors.lastname: Thamprasert
authors.forename: D L
authors.initials: DL
authors.lastname: Nelson
authors.forename: C
authors.initials: C
authors.lastname: Theetranont
mesh_terms: D000328:Adult; D015496:CD4-Positive T-Lymphocytes; D002452:Cell Count; D005260:Female; D006801:Humans; D007918:Leprosy / Q000209:etiology / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000032:analysis*; D006377:T-Lymphocytes, Helper-Inducer
chemical_list: D015375:Receptors, Interleukin-2