Different routes of bacterial infection induce long-lived T(H)1 memory cells and short-lived T(H)-17 cells

A sensitive peptide-major histocompatibility complex II (pMHCII) tetramer-based method was used to determine whether CD4(+) memory T cells resemble the T(H)1 and T(H)-17 subsets described in vitro. Intravenous or intranasal Listeria monocytogenes infection induced pMHCII-specific CD4(+) naïve T cells to proliferate and produce effector cells, about 10% of which resembled T(H)1 or T(H)-17 cells, respectively. T(H)1 cells were also present among the memory cells that survived three months post-infection whereas T(H)-17 cells disappeared. The short lifespan of T(H)-17 cells was associated with low amounts of Bcl-2, interleukin 15 receptor, CD27 and little homeostatic proliferation. These results suggest that T(H)1 cells induced by intravenous infection are more efficient at entering the memory pool than T(H)-17 cells induced by intranasal infection.