Abstract
The inhibition of activated T cells by products of the humoral immune response is almost abolished by systemic infection with BCG. As a result, BCG-infected mice develop very high levels of delayed-type hypersensitivity (DTH) in response to doses of sheep red blood cells (SRBC) that cause complete suppression of DTH in normal mice. This systemic effect of BCG is dose-dependent, and lasts for about 3 wk. Its main effect is to counteract the inhibition of T cells by products of the humoral response. As a result, and in contrast to the T-cell-potentiating effects of cyclophosphamide (CY) which depend on a diminished production of antibodies, increased levels of DTH in BCG-infected mice are associated with increased antibody production. Since BCG and CY act in different ways, their effects are additive. Very remarkable levels of DTH are achieved when they are used in combination.
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Selected References
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