Different routes of bacterial infection induce long-lived TH1 memory cells and short-lived TH-17 cells

• Published in: Nature immunology Vol. 11; no. 1; pp. 83 - 89
• Main Authors: Pepper, Marion, Linehan, Jonathan L, Pagán, Antonio J, Zell, Traci, Dileepan, Thamotharampillai, Cleary, P. Patrick, Jenkins, Marc K
• Format: Journal Article
• Language: English
• Published: 22.11.2009
• ISSN: 1529-2908; 1529-2916
• DOI: 10.1038/ni.1826

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.