Abstract
The host immune response to Mycobacterium leprae is critical for control of the infection but also responsible for the immunopathological damage to skin and nerves. The complex and varied immune responses to the organism are the basis for the clinical spectrum of disease ranging from tuberculoid to lepromatous leprosy. The cellular interactions underlying this spectrum are discussed and the antigenic components of the bacillus briefly reviewed. M. leprae has evolved a variety of mechanisms to avoid macrophage bactericidal mechanisms. These result in the persistence of bacilli and the release of cytokines leading to chronic granulomatous inflammation. The immune response to M. leprae is dynamic and spontaneous variations in cellular reactivity occur with time leading to type I and II leprosy reactions. The factors which preset the host immune response to a tuberculoid or lepromatous pattern and which precipitate reactional episodes remain to be elucidated.
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