01760nas a2200277   4500000000100000008004100001260001300042653002100055653001100076653001800087653001200105653002400117653002500141653002500166653001600191653002900207653002500236653000900261653002500270100001700295245007400312300001000386490000700396520106500403022001401468       1991                            d  c1991 Apr10aErythema Nodosum10aHumans10aInterleukin-210aleprosy10aLeprosy, Borderline10aLeprosy, lepromatous10aLeprosy, Tuberculoid10aMacrophages10aReceptors, Interleukin-210aRecombinant Proteins10aSkin10aT-Lymphocyte Subsets1 aScollard D M00aInside the skin: the local immune and inflammatory milieu in leprosy.  a17-230 v443 a<p>Skin lesions of leprosy have become a rich source of new information about the mechanisms involved in the uniquely broad spectrum of human responsiveness to M. leprae. Recent technological advances in immunology and molecular biology have been applied to the study of skin lesions using 3 approaches: immunohistologic studies of skin biopsies from leprosy lesions, correlated assessment of cell subsets and soluble immunologic mediators, and studies of the effects of the inoculation of exogenous lymphokines into the lesions. Results from these studies suggest that an immunologic equilibrium may exist among long-established lesions across the spectrum so that, although T-helper and -suppressor cells are present in different proportions, immunologic activity is at a low, similar level in all types of lesions. Exogenous lymphokines can alter this equilibrium and temporarily change the histologic picture. Spontaneous immunologic changes occurring in acute leprosy reactions may also lead to changes in T cell subsets and quantities of lymphokines.</p>  a0002-9637