Leprosy as a Model of Immunity

Yang Degang; Kazuaki Nakamura; Takeshi Akama; Yuko Ishido; Yuqian Luo; Norihisa Ishii; Koichi Suzuki


Future Microbiol. 2014;9(1):43-54. 

In This Article

Abstract and Introduction


Leprosy displays a spectrum of clinical manifestations, such as lepromatous and tuberculoid leprosy, and type I and II lepra reactions, which are thought to be a reflection of the host's immunological response against Mycobacterium leprae. Therefore, differential recognition of M. leprae, as well as its degraded components, and subsequent activation of cellular immunity will be an important factor for the clinical manifestation of leprosy. Although M. leprae mainly parasitizes tissue macrophages in the dermis and the Schwann cells of peripheral nerves, the presence of M. leprae in other organs, such as the liver, may also play important roles in the further modification of seesaw-like bipolar phenotypes of leprosy. Thus, leprosy is an exciting model for investigating the role of the human immune system in host defense and susceptibility to infection.


Leprosy is caused by Mycobacterium leprae, which primarily parasitizes tissue macrophages in the dermis and the Schwann cells of peripheral nerves.[1–4] In many countries, leprosy has been successfully eliminated; however, it still remains a major public health problem in several countries even after multidrug therapy (MDT) was introduced. Thus, although its prevalence has declined over recent decades, 232,857 new cases (four cases/100,000 population) were detected worldwide in 2012.[5] Among WHO regions, the largest amount of cases were reported from southeast Asia (166,445 cases), which includes India (134,752 cases) and Indonesia (18,994 cases). Brazil also reported 33,303 cases in 2012. Both new cases and prevalence of leprosy demonstrate wide variation in numbers reflecting an unequal distribution of the disease. In fact, new cases reported from only 16 countries account for 95% of the total cases in the world.[5]

Leprosy displays a clinical spectrum that is determined by the host immunological response against M. leprae.[6] Differential recognition of viable or dead M. leprae in the natural course or during antibacterial therapy will be one of the factors that determine such immune reactions. In this article, we will briefly overview several aspects of epidemiological and clinical situations of leprosy mainly with regard to immune responses against M. leprae. In particular, we will discuss the potential role of the liver, which may help to understand the clinical manifestation of leprosy as well as open new therapeutic modalities. Perspectives on the new therapy of type II lepra reaction are also included.