Transfer of immunity against Listeria monocytogenes by T cells purified by a positive selection technique.

Affinity columns prepared with rabbit antibody to the F(ab')(2) fragment of rat immunoglobulin were used to separate rat thoracic duct lymphocytes into sub-populations that differ with respect to the density of their surface membrane immunoglobulin. Using this technique, it was shown that lymphocytes in the DNA synthetic (S) phase of the mitotic cycle are added in increased number to the lymph of rats infected with Listeria monocytogenes. The great majority of these S-phase cells lacked a high density of surface immunoglobulin as indicated by their failure to bind to the immunoabsorbent. Cells which can protect recipient rats against a challenge infection with L. monocytogenes also segregated with nonadherent thoracic duct lymphocytes obtained from Listeria-immune donors. These protective cells realized their full immunological potential only in recipients that shared histocompatibility-gene-coded structures with the immune lymphocyte donors. The above findings accord with the view that immunity to L. monocytogenes is mediated in rats by activated T cells which are formed as part of the animal's cell-mediated response to infection. Although Listeria-protective lymphocytes concentrate in the nonadherent, T-cell-enriched fraction, it was consistently observed that the adherent, B-cell-enriched fractions of immune donor thoracic duct lymphocytes also could transfer a low level of antimicrobial resistance. This immunity was restricted in allogeneic recipients, a finding which implies that the protection afforded by the adherent population is related to its content of T cells. Nonadherent S-phase lymphoblasts moved in substantial numbers from the blood into peritoneal inflammatory exudates induced by L. monocytogenes. The above finding encourages the belief that recently activated T cells realize their protective function locally in centers of infection where they have secondary effects on macrophages.