Different routes of bacterial infection induce long-lived T _H1 memory cells and short-lived T _H-17 cells

Abstract

A sensitive peptide-major histocompatibility complex II (pMHCII) tetramer-based method was used to determine whether CD4 ⁺ memory T cells resemble the T _H1 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 _H1 or T _H-17 cells, respectively. T _H1 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 _H1 cells induced by intravenous infection are more efficient at entering the memory pool than T _H-17 cells induced by intranasal infection.