Enhanced primary resistance to Listeria monocytogenes in T cell-deprived mice.

The present studies reinvestigate the role of the T cell in the development of resistance to . Doubly thymus-deprived adult thymectomized irradiated bone marrow-reconstituted mice (D-AT × BM) were prepared using anti-theta serum-treated bone marrow from AT × BM donors for reconstitution. The growth of the bacteria in spleens and livers of D-AT × BM was inhibited and such animals survived infection with doses which were lethal to normal mice. Since the D-AT × BM animals were T cell-depleted, as evidenced by (a) absence of theta-positive cells in their spleens; (b) inability to mount a primary humoral response to a T-dependent antigen and (c) failure to reject H-2 incompatible skin allografts, their antibacterial resistance was not due to the presence of a residual T-cell population. Further evidence of T-cell depletion in these animals was furnished by the findings that, despite their resistance to , they failed to exhibit a delayed hypersensitivity reaction to antigens, their splenocytes were unable to transfer resistance to naïve hosts and they did not develop an anamnestic response upon secondary challenge. We concluded from these findings that primary antibacterial resistance to need not necessarily depend on the development of specific cell-mediated immunity although under normal circumstances these two processes develop in chronological association. The increased resistance of D-AT × BM animals is interpreted as being due to the enhancement of bactericidal activity of mononuclear phagocytes, possibly caused by the removal of a regulatory T-cell population. This population seems to be radiosensitive and spleen-seeking and requires an intact spleen to mediate its effect.