Abstract
Leprosy is a chronic infectious disease caused by Mycobacterium leprae. A characteristic feature of the disease is its remarkable spectrum of clinical symptoms correlating with the cellular immune responsiveness of the patient1. At one pole of this spectrum are tuberculoid patients displaying both acquired cell-mediated immunity and delayed type hypersensitivity against the bacillus2–4.At the other pole are lepromatous patients which show a specific T-cell unresponsiveneess against M.leprae5. In between those two poles variable degrees of tuberculoid and lepromatous features may be seen in borderline leprosy patients. Thus far, studies on the mechanism of the antigen specific unresponsiveness in lepromatous leprosy have been contradictory and difficult to interpret, probably because of the use of heterogeneous cell populations in those experiments6–10. We have now succeeded in cloning M. leprae stimulated T-helper (TH) as well as T-suppressor (Ts) cells from a borderline lepromatous patient. The Ts-clones of this patient specifically suppress reponses of peripheral TH cells as well as TH clones induced by both M. leprae and other mycobacteria, but not unrelated antigen or mitogen. These Ts cells also completely suppress TH cell responses against aM. leprae specific protein with a relative molecular mass of 36,000 (36K), suggesting the presence of a suppression inducing determinant on this 36K M. leprae protein.
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Ottenhoff, T., Elferink, D., Klatser, P. et al. Cloned suppressor T cells from a lepromatous leprosy patient suppress Mycobacterium leprae reactive helper T cells. Nature 322, 462–464 (1986). https://doi.org/10.1038/322462a0
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DOI: https://doi.org/10.1038/322462a0
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