Figure 1. Mechanism of infection of Schwann cells by Mycobacterium leprae. Monocytes carrying M. leprae cross the perineurium in blood vessels and passage through nerves. Leprosy bacilli released from the monocytes bind to the G domain of ₂ chain of laminin 2 in the basal lamina surrounding Schwann cells. In turn, M. leprae binds to -dystroglycan, and its uptake by Schwann cells is mediated by this and other intracellular proteins. T lymphocytes recognize peptides (*) derived from M. leprae proteins presented by HLA molecules on the surface of infected monocytes and possibly Schwann cells. The lymphocytes release Interferon (IFN) Ð and tumour necrosis factor (TNF) causing inflammatory damage to the nerve. IFN, interferon; TNF, tumour necrosis factor.

Figure 2. The clinical–immunopathological spectrum of leprosy. Patients at the tuberculoid pole have strong interferon (IFN) -secreting CD4+ T-cell responses against Mycobacterium leprae and few mycobacteria in affected tissues, whereas patients at the leprosy pole have no measurable T-cell responses and unrestrained replication of M. leprae.

Figure 3. The nerves preferentially infected with Mycobacterium leprae. Nerve trunks (in bold) bearing motor and sensory fibres are infected where they traverse close to the surface. Other superficial sensory nerves (in italics) are also infected. Enlargement of any of these nerves with or without loss of function in their distribution is typical of leprosy.