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Early Infection Termination Affects Number of CD8⁺ Memory T Cells and Protective Capacities in Listeria monocytogenes-Infected Mice upon Rechallenge ¹

Kuo-En Tseng^2,*, Cheng-Yu Chung^2,, Weng Siong H’ng^* and Shih-Lien Wang^3,*

^* Graduate Institute of Microbiology, Immunology and Molecular Medicine, and Department of Life Science, Tzu-Chi University, Hualien, Taiwan

Here, we reevaluate the effects of early termination of infection on primary T cell expansion, subsequent memory cell development, and protective immunity. Using a murine Listeria monocytogenes (LM) infection model, we found the primary expansions of both CD4⁺ and CD8⁺ T cells were affected even when ampicillin was given as late as 60 h postinfection (p.i.). Subsequent development of CD8⁺ memory T cells was also impaired, although to a lesser extent, and only mice that received ampicillin at 24 h p.i. revealed a significant decrease in memory CD8⁺ T cells. Upon rechallenge with 1 x 10⁵ CFU of LM, all ampicillin-treated mice cleared LM as effectively, and they generated similar amounts of Ag-specific CD8⁺ T cells as with untreated mice. However, mice that received ampicillin at 24 h p.i. lost their protective abilities when rechallenged with 7.5 x 10⁵ CFU of LM. Ampicillin treatment also revealed early down-regulation of B7.1 and B7.2, but not CD40, on dendritic cells 72 h p.i. Our results have several important implications: 1) they argue against the hypothesis that brief exposure of T cells to an Ag is sufficient for full-fledged primary T cell responses and subsequent memory T cell development in vivo; 2) they suggest the existence of a reservoir of memory T cells, more than the immune system can possibly expand during secondary infection; and 3) they suggest that protective capacity is correlated with the number of preexisting memory T cells and that secondary expanding T cells play a limited role, at least in murine LM infection.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was support by Grant 94–2320-B-320–012 and Grant 96–2320-B-320–003 from the National Science Council, Taiwan (to S.-L.W.).

² K.-E.T. and C.-Y.C. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Shih-Lien Wang, Graduate Institute of Microbiology, Immunology, and Molecular Medicine, Tzu-Chi University, No. 701, Section 3, Chung-Yan Road, Hualien 970, Taiwan. E-mail address: wangsltw{at}mail.tcu.edu.tw

⁴ Abbreviations used in this paper: LM, Listeria monocytogenes; Amp, ampicillin; DC, dendritic cells; LLO, listeriolysin O; Moxi, moxifloxacin; p.i., postinfection; SEB, staphylococcal enterotoxin B.

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