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Evidence that the Mechanism of Immunological Tolerance (‘Central Failure’) Is Operative in the Lack of Host Resistance in Lepromatous Leprosy
59
Citations
32
References
1972
Year
Clinical ImmunologySusceptible HostLaboratory ImmunologyImmunodeficienciesImmunologyImmune RegulationImmunodominancePathologyAntigen ProcessingM. LepraeInnate ImmunityImmune SystemImmunotherapyHost ResponseDisease ResistanceLepromatous LeprosyInfection ControlImmunopathologyCellular Immune DefectLeprosyAutoimmune DiseaseImmune SurveillanceAutoimmunitySelf-toleranceHumoral ImmunityImmune FunctionImmunologic DiseaseInborn Error Of ImmunityImmune Cell DevelopmentPathogenesisImmunological ToleranceHost ResistanceMedicine
The cellular immune defect in lepromatous leprosy has been studied. The following observations have been made: 1) Three lepromatous patients who had been on anti‐leprosy treatment for more than 10 years still failed to respond to M. leprae by lymphocyte transformation (mean 0.2%) while they responded strongly to BCG (mean 34.2%) and PPD (mean 56.1%). 2) Lepromatous serum failed to inhibit M. leprae ‐induced lymphocyte transformation and M. leprae ‐induced leukocyte migration inhibition. 3) Lepromatous lymphocytes revealed a reduced capacity to attach M. leprae to their surface. The only experimental condition compatible with the observed characteristics would seem to be a state of immunological tolerance to an antigen (or antigens) of M. leprae. The lasting nature of this non‐responsive state suggests that it plays a primary role in the pathogenesis of lepromatous leprosy.
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