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

Marion Pepper, Jonathan L. Linehan, Antonio J. Pagán, Traci Zell, Dileepan T, P. Patrick Cleary, Marc Jenkins

Research output: Contribution to journalArticlepeer-review

219 Scopus citations

Abstract

We used a sensitive method based on tetramers of peptide and major histocompatibility complex II (pMHCII) to determine whether CD4 + memory T cells resemble the T helper type 1 (T H 1) and interleukin 17 (IL-17)-producing T helper (T H 17) subsets described in vitro. Intravenous or intranasal infection with Listeria monocytogenes induced pMHCII-specific CD4 + naive 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 3 months after infection, whereas T H 17 cells disappeared. The short lifespan of T 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 T H 1 cells induced by intravenous infection are more efficient at entering the memory pool than are T H 17 cells induced by intranasal infection.

Original languageEnglish (US)
Pages (from-to)83-89
Number of pages7
JournalNature immunology
Volume11
Issue number1
DOIs
StatePublished - Jan 2010

Bibliographical note

Funding Information:
We thank S. Jameson, H. Chu and J. Taylor for reviewing the manuscript; J. Walter, J. McLachlan and A. Schmidt for technical assistance; and P. Champoux and N. Shah for flow cytometry sorting. Supported by the US National Institutes of Health (AI39614, AI66016 and AI27998 to M.K.J.; T32-AI07313 to A.J.P.; and T32-CA9138 to M.P.).

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