Abstract

Memory immunity in mice to BCG vaccination is mediated by Thy-1.2 + L3T4 + Lyt-2 − cyclophosphamide-resistant T-lymphocytes. The time required for the emergence of acquired memory immunity was inversely proportional to the BCG inoculum size, although the level of memory expressed, once established, was equivalent regardless of the original dose of BCG administered. In mice given a high intravenous dose (10 8) of BCG, an apparently biphasic memory repsonse was observed, initially peaking on day 15–20, then declining for 10 days or so before increasing again to maximal levels between day 30 and 60 of the infection. This trough in resistance was not due to an active immunosuppressive mechanism; instead, it is suggested that it represents an initial loss or consumption of memory T-cells generated early during the infection which are stimulated to give rise to a state of active immunity as a result of the persisting high mycobacterial load.

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