Abstract

The pathogenesis of leprosy is almost totally attributable to the immune response of the host towards Mycobacterium leprae, a virtually non-toxic intra-cellular parasite. At one end of the leprosy spectrum are tuberculoid leprosy patients, who develop immunity but also delayed-type hypersensitivity towards M. leprae; at the other end are lepromatous leprosy patients, who lack helper T cell activity and therefore do not develop immunity, but who can nevertheless produce antibodies that may cause immunopathology due to immune complexes. A range of immunopathology is seen between these poles.