In leprosy, the causative bacteria, Mycobacterium leprae, will not threaten the lives of the hosts directly because they proliferate only slowly in the Schwann cells of the peripheral nerves. It is the “reactions” which give the patients irreversible morbidity through the inflammatory damages to the peripheral nerves. Physicians should be aware of the possibility of the state of the “reaction” when they examine leprosy patients. They also should be aware of the possibility of leprosy and the state of the “reaction” when they examine patients with cutaneous lesions and/or peripheral nerve disturbances, because it may be the first presenting symptom of the disease. In this review, recent advances on the issue about the reactions are discussed including pathogenesis, immunology, clinical features, pathology, treatment and prevention.

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The incidence of overt diabetes was completely prevented by a single intradermal inoculation of Mycobacterium leprae (M. leprae) into Non-obese diabetic (NOD) mice as young as 6-7 weeks. Partial prevention was also observed in cases when 65kD heat-shock protein (hsp65) with Freund's incomplete adjuvant (FIA) was injected, and no prevention was observed by 38kD with FIA immunization. Histological examination of pancreata demonstrated that control and M. leprae-immunized mice at 24 weeks of age developed the insulitis eventhough the number of lymphocytes infiltrated in the treated ones were less than the controls. However, later, at 47 weeks of age, even the immunized mice become to develop very severe insulitis. Thus, M. leprae-immunization did not prevent the incidences of insulitis. The spontaneous development of serum antibody against hsp65 and 38kD protein preceded the onset of diabetes in NOD mice.
Lymphocytes response, IFN-γ and IL-10 production of splenocytes cultures stimulated with hsp65 were examined to clue the reasons for the prevention of IDDM incidence by M. leprae immunization. The spontaneous development of anti-hsp65 T lymphocytes preceded the outbreak of overt IDDM in control NOD mice, but also appeared in M. leprae immunized cases in which the IDDM incidence was prevented, and both control and M. leprae immunized groups produced IFN-γ and IL-10 by stimulation with hsp65.

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We have established a congenic hypertensive nude rat strain, SHR/NCrj-rnu, carrying nude (rnu) and hypertension genes which was produced using females of the SHR/NCrj rat and males of the F344/NJcl nude rat by crossintercross system for 12 generations. We demonstrated the susceptibility to M. leprae infection of SHR/NCrj-rnu rats as compared with F344/NJcl-rnu rats. SHR/NCrj-rnu rats were highly susceptible to M. leprae, and the SHR/NCrj-rnu rats of both sexes showed massive swelling of legs due to multiplication of M. leprae. However, F344/NJcl-rnu rats of both sexes revealed very poor susceptibility to M. leprae. There was a wide difference in the susceptibility to M. leprae between the SHR/NCrj-rnu and the F344/NJcl-rnu rats. We also examined the cytokine production. The resident peritoneal macrophages of SHR/NCrj-rnu rats produced IL-1 α, IL-6, IL-10 and TNF α, whereas those of F344/NJcl-rnu rats produced only TNF α.

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[in Japanese]

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