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.
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