Different routes of bacterial infection induce long-lived [T.sub.H]1 memory cells and short-lived [T.sub.H] 17 cells

• Published in: Nature immunology Vol. 11; no. 1; pp. 83 - 90
• Main Authors: Pepper, Marion, Linehan, Jonathan L, Pagan, Antonio J, Zell, Traci, Dileepan, Thamotharampillai, Cleary, P. Patrick, Jenkins, Marc K
• Format: Journal Article
• Language: English
• Published: Nature Publishing Group 01.01.2010
• Subjects: Bacterial infections; CD8 lymphocytes; Health aspects; MHC antibodies; Prevention; United States
• ISSN: 1529-2908; 1529-2916
• DOI: 10.1038/ni.1826

We used a sensitive method based on tetramers of peptide and major histocompatibility complex II (pMHCII) to determine whether [CD.sup.4+] memory T cells resemble the T helper type 1 ([T.sub.H]1) and interleukin 17 (IL-17)-producing T helper ([T.sub.H]17) subsets described in vitro. Intravenous or intranasal infection with Listeria monocytogenes induced pMHCII-specific [CD4.sup.+] naive T cells to proliferate and produce effector cells, about 10% of which resembled [T.sub.H] or [T.sub.H]17 cells, respectively. TO cells were also present among the memory cells that survived 3 months after infection, whereas [T.sub.H]17 cells disappeared. The short lifespan of [T.sub.H]17 cells was associated with small amounts of the antiapoptotic protein Bcl-2, the IL-15 receptor and the receptor CD27, and little homeostatic proliferation. These results suggest that TO cells induced by intravenous infection are more efficient at entering the memory pool than are [T.sub.H]17 cells induced by intranasal infection.