Abstract
Mice heavily infected with Mycobacterium bovis BCG rapidly became anergic to cutaneous injection with tuberculin. Evidence is presented suggesting that this anergy reflects an adaptive physiological change within the host in which antigen-reactive Thy-1.2+ cells become sequestered in central lymphoid tissues, with a concomitant reduction in the circulating pool. No evidence could be provided to support the suggestion that anergy was a consequence of an acquired immunosuppressive mechanism.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Reference25 articles.
1. Desensitization III: the role of Iymphokines in the maintenance of the anergic state during desentitation;Baba T.;J. Exp. Pathol.,1983
2. Leprosy: a model of immunological perturbation in chronic infection;Bullock W. E.;J. Infect. Dis.,1978
3. The immunology of tuberculosis;Collins F. M.;Am. Rev. Respir. Dis.,1982
4. The relationship of delayed hypersensitivity to acquired antituberculous immunity. I. Tuberculin sensitivity and resistance to reinfection in BCGvaccinated mice;Collins F. M.;Cell. Immunol.,1970
5. Suppressor T-cells in BCG-infected mice;Collins F. M.;Infect. Immun.,1979
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