BriefDefinitive Report ACQUIRED RESISTANCE TO LISTERIA MONOCYTOGENES IS MEDIATED BY Lyt-2+ T CELLS INDEPENDENTLY OF THE INFLUX OF MONOCYTES INTO GRANULOMATOUS LESIONS

Infections by facultative intracellular bacteria result in inflammatory tissue responses, such as delayed-type hypersensitivity (DTH), and the focal accumulation of mononuclear cells within granulomatous lesions (1, 2) . Both DTH and granuloma formation depend on an intact T cell response and have so far been accepted to be indispensable for protection against facultative intracellular bacteria, including Listeria monocytogenes . As recently shown (3), however, DTH and protective immunity can be dissociated from each other in secondarily infected mice . Thus, whereas DTH critically depended on the presence of L3T4+ T lymphocytes, Lyt-2+ T cells proved necessary and sufficient for the rapid elimination of Listeria . Although the protective capacity of Lyt-2+ T cells in murine listeriosis has been demonstrated also at the clonal level (4), the mode of action of these cells is still unclear. Two different mechanisms were proposed (5): (a) the direct activation of infected macrophagesby lymphokines; and (b) the lysis of infected, but insufficiently microbicidal/host cells followed by the attraction and activation of blood-borne monocytes . This report summarizes data from an immunohistochemical study of T cell subset-depleted mice suffering from a secondary Listeria infection . The data show that protection against a lethal challenge with L. monocytogenes in immune mice can be achieved by Lyt-2+ T cells in the absence of invading blood-borne monocytes . The results, therefore, support the hypothesis that CD8+ T cells mediate protection by directly activating resident macrophages.