The Lyme Disease Network
|Title:||Why is Chronic Lyme Borreliosis Chronic?|
|Authors:||Aberer E; Koszik; Silberer M|
|Conference:||9th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, Westin Copley Plaza Hotel, Boston, MA, April 19-20, 1996|
|Presenter:||Elizabeth Aberer, M.D.|
Department of Dermatology
University of Graz
In spite of marked cellular and humoral immune responses in acrodematitis chronica atrophicans (ACA) B. burgdorferi (Bb) can be isolated from long-standing skin lesions. Recently, it was shown that the most important cell for antigen presentation, the epidermal Langerhans cell (LC), is heavily damaged in erythema migrans (EM). To evaluate whether the immune response and the number or function of LC is altered we studied the immunophenotype of cutaneous leukocytes in ACA. Lesional skin biopsies from 19 patients with ACA and 9 patients with EM were investigated by immunoperoxidase single labeling or double-labeling procedures. In EM the total number of CD1a+ cells reduced in the epidermis of ACA skin semi-automatic image analysis revealed a density of 811(+336 SD) CD1a+ but only 13(+143 SD) HLA-DR+ dendritic cells while in normal skin most of the epidermal CD1a+ cells are HLA-DR+. The majority of cells in the dermis of ACA were composed of CD68+ macrophages and CD45+ memory T-cells with a predominance of helper/inducer cells. About 75% of the cells were further activated expressing HLA-DR and CD54 and its receptor CD18. In this study, the most prominent immunohistochemical changes were seen on the epidermal dendritic cell population. Our data suggest that MHC class II molecules are strongly down regulated on LC not only in the early but also in the late stage skin manifestation of LB. This phenomenon [of?] antigen presenting cells might be a protective mechanism against the presentation of cellular auto antigens and might be the cause for the impaired capacity of LC to eliminate Bb antigens.
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