Noncompetitive expansion of cytotoxic T lymphocytes specific for differentantigens during bacterial infection

Listeria monocytogenes is an intracellular bacterium that elicits complex c ytotoxic T-lymphocyte (CTL) responses in infected mice. The responses of CT L, populations that differ in antigen specificity range in magnitude from l arge, dominant responses to small, subdominant responses. To test the hypot hesis that dominant T-cell responses inhibit subdominant responses, we elim inated the two dominant epitopes of L. monocytogenes by anchor residue muta genesis and measured the T-cell responses to the remaining subdominant epit opes. Surprisingly, the loss of dominant T-cell responses did not enhance s ubdominant responses. While mice immunized with bacteria lacking dominant e pitopes developed L. monocytogenes-specific immunity, their ability to resp ond to dominant epitopes upon rechallenge with wild-type bacteria was marke dly diminished. Recall responses in mice immunized with wild-type or epitop e-deficient L. monocytogenes showed that antigen presentation during recall infection is sufficient for activating memory cells yet insufficient for o ptimal priming of naive T lymphocytes. Our findings suggest that T-cell pri ming to different epitopes during L. monocytogenes infection is not competi tive. Rather, T-cell populations specific for different antigens but the sa me pathogen expand independently.