Abstract
Immunofluorescent staining was performed on cryostat sections of 3 skin eruptions of ENL and 3 skin lepromas of lepromatous leprosy without ENL. In the indirect incubation method, the antibody labelled with fluorescenn isothiocyanate to the pooled serum immunoglo-bulins of the lepromatous leprosy with ENL was prepared in rabbits. The final fluorescein-protein ratio of the conjugate was to 1.3. The sera of 10 lepromatous leprosy with ENL, 15 lepromatous leprosy without ENL and of 4 tuberculoid leprosy were examined. Sections were treated with the patient's own serum, at a 1: 30 dilution, and subsequently with fluorescent antibody at a 1:100 dilution. In the sera of ENL, the prominent fluorescence indicated that immunoglobins were presented within the cytoplasma of the plasma cells, small lymphocytes and of histiocytes at the site of eruptions of ENL. The cell nuclei of the round or oval histio-cytes were also often fluorescent. These reactions were not observed, however, in the sera of lepromatous leprosy without ENL and of tuberculoid leprosy.
The results of the previous reports suggest that there are immunological tissue damage at the stage of ENL. It is probable that tissue cell degeneration in case of persistent lepromatous inflammatory changes is responsible for the production of antibodies. In advanced lepromatous leprosy, especially in those of the systemic or diffuse forms in which the episode of ENL are frequently observed, the presence of delayed hypersensitivity due to degenerated leprosy bacilli or altered self cell components may rather be important in causing the production of many humoral self factors (antibodies). One of the interesting facts is that phospholipids may be the intrinsic factors for the occurrence of ENL at the later stage of lepromatous leprosy. M. leprae has phospholipid antigen similar to that of human heart, blood vessels, nerve tissues and joints. Needless to say, antigens of the bacillary components presumably become cross antigens to those tissues, and M. leprae causes autoantibody formations against heart, vessels, nerve and/or joints. It is conceivable that the autoantibodies found in the sera of ENL may arise through this mechanism.
