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It is an established fact, that human leprosy is characterized by its variation in the ability to mount and maintain cell-mediated immune (CMI) response against Mycobacterium leprae and thereby to control the infection. Tuberculoid leprosy patients exhibit strong CMI against M. leprae(1-3), they have few lesions in which few or no bacilli ace found. On the other hand, patients with lepromatous leprosy are devoid of CMI against M. leprae(1-3), these patients harbour many lesions which contain vast number of bacilli. Between the two polar types there is a continuous spectrum of intermediate forms classified as borderline leprosy (4,5). However, CMI is believed to play a major role, the basis for the variation in the host resistance against leprosy is at present poorly understood. Various attempts have been made to establish an experimental model closely reproducing the spectrum of human leprosy. Footpad inoculation of M. leprae in mice leads to a limited multiplication of the bacilli terminated by an immune reaction after several months(6,7). The histological features of the lesion arising at the inoculation site resemble human borderline leprosy(8). In the thymectomized irradiated mouse model(9), disseminated growth of M. leprae occcurs after foot-pad inoculation