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The immunobiology of leprosy.
Int Rev Exp Pathol. 1986; 28:45-78.IR

Abstract

Leprosy, a chronic infectious disease of man, is caused by the obligate intracellular bacterium M. leprae. Infection with M. leprae affects the peripheral nerves and the dermis, causing an accumulation of macrophages and other immune cells at the infected sites. Host resistance to the bacterium determines the extent of local inflammatory reactions and its resulting damage to the affected tissues. In lepromatous disease little if any cellular immunity develops. Bacterial multiplication is uncontrolled and M. leprae disseminate throughout most of the dermis. In tuberculoid disease, marked cellular immunity is observed and bacterial growth and dissemination are controlled. The depression of cellular immunity in lepromatous patients is not fully understood. Since M. leprae cannot be grown in vitro, and a suitable animal model has not yet been developed, the study of host immunity to the pathogen is limited primarily to investigations of the cutaneous lesions of patients and to in vitro responses of the peripheral blood leukocytes to M. leprae. While the blood monocytes of leprosy patients appear to be activated normally by lymphokines, T cell proliferation and production of lymphokines in response to M. leprae are impaired in lepromatous patients. Attempts to restore responsiveness in cells from these patients have been unsuccessful in our hands. The addition of exogenous IL-2 to leukocyte cultures does not appear to restore responsiveness to M. leprae in cells from nonresponsive patients. Rather, some enhancement, often not antigen specific, is observed in cells from patients with a preexisting response. Similarly, depletion of monocytes does not restore responsiveness to M. leprae in nonresponder patients, but a nonspecific enhancement of proliferation is observed in monocyte-free cultures from patients that do respond to M. leprae. Thus, the defect in lepromatous nonresponder patients does not result from a simple lack of IL-2 production or suppression by monocytes and/or their products. Possibly, there is a low level or lack of M. leprae-responsive T cells in the circulation of these patients. Attempts to overcome the defect in immunity of patients with lepromatous leprosy by immunoprophylaxis and immunotherapy are being investigated. This approach has become of major importance since the development of widespread drug resistance to Dapsone as well as to the other chemotherapeutic agents used to control leprosy.

Authors

No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

3516911

Citation

Kaplan, G, and Z A. Cohn. "The Immunobiology of Leprosy." International Review of Experimental Pathology, vol. 28, 1986, pp. 45-78.
Kaplan G, Cohn ZA. The immunobiology of leprosy. Int Rev Exp Pathol. 1986;28:45-78.
Kaplan, G., & Cohn, Z. A. (1986). The immunobiology of leprosy. International Review of Experimental Pathology, 28, 45-78.
Kaplan G, Cohn ZA. The Immunobiology of Leprosy. Int Rev Exp Pathol. 1986;28:45-78. PubMed PMID: 3516911.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The immunobiology of leprosy. AU - Kaplan,G, AU - Cohn,Z A, PY - 1986/1/1/pubmed PY - 1986/1/1/medline PY - 1986/1/1/entrez SP - 45 EP - 78 JF - International review of experimental pathology JO - Int Rev Exp Pathol VL - 28 N2 - Leprosy, a chronic infectious disease of man, is caused by the obligate intracellular bacterium M. leprae. Infection with M. leprae affects the peripheral nerves and the dermis, causing an accumulation of macrophages and other immune cells at the infected sites. Host resistance to the bacterium determines the extent of local inflammatory reactions and its resulting damage to the affected tissues. In lepromatous disease little if any cellular immunity develops. Bacterial multiplication is uncontrolled and M. leprae disseminate throughout most of the dermis. In tuberculoid disease, marked cellular immunity is observed and bacterial growth and dissemination are controlled. The depression of cellular immunity in lepromatous patients is not fully understood. Since M. leprae cannot be grown in vitro, and a suitable animal model has not yet been developed, the study of host immunity to the pathogen is limited primarily to investigations of the cutaneous lesions of patients and to in vitro responses of the peripheral blood leukocytes to M. leprae. While the blood monocytes of leprosy patients appear to be activated normally by lymphokines, T cell proliferation and production of lymphokines in response to M. leprae are impaired in lepromatous patients. Attempts to restore responsiveness in cells from these patients have been unsuccessful in our hands. The addition of exogenous IL-2 to leukocyte cultures does not appear to restore responsiveness to M. leprae in cells from nonresponsive patients. Rather, some enhancement, often not antigen specific, is observed in cells from patients with a preexisting response. Similarly, depletion of monocytes does not restore responsiveness to M. leprae in nonresponder patients, but a nonspecific enhancement of proliferation is observed in monocyte-free cultures from patients that do respond to M. leprae. Thus, the defect in lepromatous nonresponder patients does not result from a simple lack of IL-2 production or suppression by monocytes and/or their products. Possibly, there is a low level or lack of M. leprae-responsive T cells in the circulation of these patients. Attempts to overcome the defect in immunity of patients with lepromatous leprosy by immunoprophylaxis and immunotherapy are being investigated. This approach has become of major importance since the development of widespread drug resistance to Dapsone as well as to the other chemotherapeutic agents used to control leprosy. SN - 0074-7718 UR - https://www.unboundmedicine.com/medline/citation/3516911/The_immunobiology_of_leprosy_ L2 - https://medlineplus.gov/mycobacterialinfections.html DB - PRIME DP - Unbound Medicine ER -