Abstract
Leprosy is a chronic infectious disease caused by Mycobacterium leprae which is estimated to afflict 10–15 million people mainly in developing countries (1). Leprosy has been designated as a “model immunological” disease since the striking variety in clinical symptoms which can develop upon infection in susceptible individuals correlates with the immune response of the host against the parasite (2). The leprosy spectrum ranges from “high resistant” or polar tuberculoid leprosy (TT), characterized by few self-limiting lesions and strong helper T cell (Th) mediated immunity against M. leprae, to “low resistant” or polar lepromatous leprosy (LL) with numerous progressive lesions and M. leprae specific T cell unresponsiveness, presumably as a consequence of M. leprae specific suppression (1). In between those two poles variable degrees of tuberculoid or lepromatous features can be found in borderline leprosy patients (1).
Tom H.M. Ottenhoff and René R.P. de Vries. Submitted for publication in slightly revised form.
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Ottenhoff, T., De Vries, R. (1987). General Discussion: Mycobacterium Leprae Specific Activation of Helper and Suppressor T Cells and its Regulation by HLA Class II Genes and Products. In: Recognition of M. leprae antigens. Developments in Hematology and Immunology, vol 17. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-3327-9_9
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