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            <i>Optimization of Refuse Collection Systems</i>
            ” by Anand V. Chiplunkar, S. L. Mehndiratta, and P. Khanna (December, 1981)

Little information is available about the generation and specificity of the cytotoxic cells that eliminate human monocytes/macrophages infected with mycobacteria. To address this we have developed a cytotoxicity assay in which 51Cr-labeled monocytes pulsed with bacillus Calmette Guerin (BCG) or Mycobacterium leprae, were used as target cells in overnight cytotoxicity assays. As effector cells, peripheral blood mononuclear cells from healthy occupational contacts or from leprosy patients stimulated with antigen for 7 days were used. Cytotoxicity against antigen-pulsed monocytes that could be induced by mycobacterial antigens was proportional to the degree of antigen responsiveness in each individual, as measured in lymphocyte transformation tests. The lepromatous leprosy patients tested were often poor responders to BCG as well as M. leprae, both with regard to induction of cytotoxicity as well as in lympho-proliferation. Killing was significantly higher against antigen-pulsed vs. nonpulsed monocytes, although significant killing was induced against the latter as well and paralleled by induction of natural killer activity against the K-562 target cell. Cross-reactivity was observed between BCG and M. leprae, but not with unrelated antigen (tetanus toxoid) or with endogenous stress proteins induced by heat shock. M. leprae- and BCG-activated cytotoxic cells were found in both the CD4-CD8+ and CD4+CD8- populations, whereas in contrast the soluble antigen, purified protein derivative of M. tuberculosis, generated cytotoxic cells that were exclusively of the CD4+ phenotype. The involvement of both specific T cells as well as nonspecific cells in the killing of human macrophages may be important with respect to protection and immunopathology induced by mycobacterial antigens.

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“…tuberculosis and M . leprue immunized mice [9,12,131. These Tcells were capable of lysing mycobacteria primed BM M@ in an antigen-specific way.…”

Section: Discussionmentioning

confidence: 99%

“…tuberculosis [6,71. Secondly,it has become clear that during infection with intracellular microorganisms not only CD4+CD8-but also CD8+CD4antigen-specific T lymphocytes are generated [4,[8][9][10][11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Mycobacterial‐induced cytotoxic T cells as well as nonspecific killer cells derived from healthy individuals and leprosy patients

et al. 1990

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“…The susceptibility of C57BL/6 and BALB/c mice to infection by high doses of M. avium in the presence of a higher degree of macrophage activation than that observed in the resistant mouse strains may suggest that other effector cells (e.g. cytotoxic T lymphocytes [9]) have impaired functions or that there is an inappropriate activation pathway ofthe macrophage (distinct differentiation mechanisms, heterogeneity of macrophage activation sparing the infected cells). Another possible explanation is that in the susceptible strains there is a macrophage defect in antimycobacterial functions such as a defective triggering of the effector mechanisms that cannot be overcome by macrophage activation.…”

Section: Lepraemuriummentioning

confidence: 99%

“…Although cytotoxic T cells may play a role in protective immunity against mycobacleriosis [9], the main effector mechanism thought to be involved in the control of the mycobacterial infection is the activation of the macrophage by T cell-derived lymphokines [15. 28, 38.…”

mentioning

confidence: 99%

Induction of Non‐Specific Immunosuppression in Mice by Mycobacterial Infections and Its Relationship to Macrophage Activation

Appelberg¹,

Soares²,

Ferreira³

et al. 1989

Scand J Immunol

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The development of non-specific immunosuppression during the infection of different strains of mice with three mycobacterial species was evaluated by studying the immune response to a heterologous antigen (sheep red blood cells) and comparing it with the induction of non-specific resistance to a Listeria monocytogenes challenge. It was shown that early (at 15 days) immunosuppression developed in Mycobacterium avium-susceptible mouse strains infected with a high inoculum dose [2.5 x 10(8) colony forming units (CFU)] of virulent M. avium but not in resistant mice infected with a similar inoculum nor in susceptible mice infected by a smaller inoculum dose (2.5 x 10(6) CFU). In the latter case it developed only during the second month of infection and was of smaller magnitude. An inoculum of M. avium of attenuated virulence did not induce immunosuppression. M. lepraemurium induced a late immunosuppression, which occurred when extensive bacterial proliferation had already taken place. The non-pathogenic M. bovis BCG induced immunosuppression in C57BL/6 mice. The results do not establish a correlation between the development of generalized immunosuppression and susceptibility to infection. It could be seen that the early immunosuppression was observed in those situations where there was extensive macrophage activation as shown by the development of non-specific resistance to a listeria challenge. The late immunosuppression was observed when bacterial proliferation was extensive.

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Closure to “ Optimization of Refuse Collection Systems ” by Anand V. Chiplunkar, S. L. Mehndiratta, and P. Khanna (December, 1981)

Cited by 2 publications

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Mycobacterial‐induced cytotoxic T cells as well as nonspecific killer cells derived from healthy individuals and leprosy patients

Mycobacterial‐induced cytotoxic T cells as well as nonspecific killer cells derived from healthy individuals and leprosy patients

Induction of Non‐Specific Immunosuppression in Mice by Mycobacterial Infections and Its Relationship to Macrophage Activation

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