Immunological unresponsiveness in leprosy - PubMed (original) (raw)

Review

Immunological unresponsiveness in leprosy

B R Bloom et al. Immunol Rev. 1984 Aug.

Abstract

The various forms of leprosy form a clinical and immunological spectrum which offers extraordinary possibilities for insight into immunoregulatory mechanisms in man. At one pole, tuberculoid leprosy, patients develop high levels of cell-mediated immunity which ultimately results in killing of bacilli in the tissues, albeit often with damage to nerves. At the lepromatous pole, patients exhibit selective immunological unresponsiveness to antigens of M. leprae. Even though all currently known protein species of M. leprae and BCG are cross-reactive, lepromatous patients unreactive to M. leprae antigens frequently respond strongly to tuberculin. In vitro experiments suggest the existence of lepromin-induced suppressor activity, mediated by both monocytes and T cells. The T suppressor cells have the T8 phenotype of which 50% express the activation markers, Ia and FcR. The one unique species of antigen of the leprosy bacillus is a phenolic glycolipid, and it appears that the TS cells largely recognize the terminal trisaccharide of this unique antigen. Depletion of the TS cells restores in vitro reactivity of lymphocytes to lepromin in a portion of lepromatous patients, and addition of IL-2-containing supernatants partially restores responsiveness to M. leprae antigens. Vaccination of lepromatous patients with a mixture of M. leprae and live BCG restores cell-mediated immunity in the majority of lepromatous patients, and concomitantly reduces the in vitro suppressor activity and number of activated T8 cells. These experiments suggest the existence of stage-of-disease related suppressor cells in leprosy which appear to block the responsiveness of TH capable of responding to either specific or cross-reactive mycobacterial antigens. The mode of action of these TS appears to be the inhibition of production of IL-2 and other lymphokines. Successful immunotherapeutic vaccination appears to overcome this block in the majority of patients.

PubMed Disclaimer

Cited by

Immunopathology of leprosy granulomas.
Modlin RL, Rea TH. Modlin RL, et al. Springer Semin Immunopathol. 1988;10(4):359-74. doi: 10.1007/BF02053846. Springer Semin Immunopathol. 1988. PMID: 3065952 Review. No abstract available.
Definition of a human suppressor T-cell epitope.
Mutis T, Cornelisse YE, Datema G, van den Elsen PJ, Ottenhoff TH, de Vries RR. Mutis T, et al. Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9456-60. doi: 10.1073/pnas.91.20.9456. Proc Natl Acad Sci U S A. 1994. PMID: 7524076 Free PMC article.
Mycobacterial disease, immunosuppression, and acquired immunodeficiency syndrome.
Collins FM. Collins FM. Clin Microbiol Rev. 1989 Oct;2(4):360-77. doi: 10.1128/CMR.2.4.360. Clin Microbiol Rev. 1989. PMID: 2680057 Free PMC article. Review.
Dominant cell wall proteins of Mycobacterium leprae recognized by monoclonal antibodies.
Britton WJ, Hellqvist L, Garsia RJ, Basten A. Britton WJ, et al. Clin Exp Immunol. 1987 Jan;67(1):31-42. Clin Exp Immunol. 1987. PMID: 3304738 Free PMC article.
The mechanism of action of the factor in leprosy serum that inhibits the growth of mitogen-stimulated normal human lymphocytes.
Hussein YM, Kerr MA, Beck JS. Hussein YM, et al. Immunology. 1987 Jun;61(2):125-9. Immunology. 1987. PMID: 3496268 Free PMC article.

Immunological unresponsiveness in leprosy - PubMed (original) (raw)