CELLULAR MEDIATORS OF ANTI-LISTERIA IMMUNITY AS AN ENLARGED POPULATION OF SHORT-LIVED, REPLICATING T CELLS: KINETICS OF THEIR PRODUCTION

doi:10.1084/jem.138.2.342

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ARTICLE

CELLULAR MEDIATORS OF ANTI-LISTERIA IMMUNITY AS AN ENLARGED POPULATION OF SHORT-LIVED, REPLICATING T CELLS : KINETICS OF THEIR PRODUCTION

Robert J. North ¹

¹ From the Trudeau Institute, Saranac Lake, New York 12983

An intravenous immunizing infection with the facultative, intracellularparasite, Listeria monocytogenes results in the production inthe spleen of a population of immunologically-committed lymphocyteswhich can adoptively immunize normal recipients against a lethalchallenge infection. These cellular mediators of immunity arefirst produced in the spleen between days 2 and 4 of infectionand reach peak production on day 6. Their production then progressivelydecreases until about day 20 when their presence can no longerbe detected.

Increased production of cellular mediators is coincidentwith major increases in cell division, cellularity, and spleenweight. Decreased production of cellular mediators, on the otherhand, is associated with decreases in cell division, cellularity,and spleen weight. Again, the level of delayed sensitivity toListeria antigens expressed by the host at any one time is proportionalto the number of cellular mediators in the spleen.

Increasedproduction of cellular mediators is also associated with majorincreases in the total numbers of replicating T cells and Bcells in the spleen. That the cellular mediators of immunityare part of the replicating T cell population, rather than theB cell population, is evidenced by their susceptibility to anti- $theta$ serum and by their resistance to anti-Ig serum. Furthermore,they can be completely eliminated from the spleen by a briefpulse of the antimitotic drug, vinblastine. This study allowsthe conclusion that the cellular mediators of anti-Listeriaimmunity belong to an expanded population of rapidly dividing,short-lived T cells. It is suggested that they have the sameproperties as the T cell effectors of allograft immunity.

Submitted on March 18, 1973

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