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Rapid Development of T Cell Memory Phillip Wong, María Lara-Tejero, Alexander Ploss, Ingrid Leiner and Eric G

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Rapid Development of T Cell Memory Phillip Wong, María Lara-Tejero, Alexander Ploss, Ingrid Leiner and Eric G Rapid Development of T Cell Memory Phillip Wong, María Lara-Tejero, Alexander Ploss, Ingrid Leiner and Eric G. Pamer This information is current as J Immunol 2004; 172:7239-7245; ; of October 1, 2021. doi: 10.4049/jimmunol.172.12.7239 http://www.jimmunol.org/content/172/12/7239 References This article cites 30 articles, 12 of which you can access for free at: Downloaded from http://www.jimmunol.org/content/172/12/7239.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision http://www.jimmunol.org/ • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: by guest on October 1, 2021 http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2004 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Rapid Development of T Cell Memory1 Phillip Wong,* Marı´a Lara-Tejero,* Alexander Ploss,*† Ingrid Leiner,* and Eric G. Pamer2* Prime-boost immunization is a promising strategy for inducing and amplifying pathogen- or tumor-specific memory CD8 T cell responses. Although expansion of CD8 T cell populations following the second Ag dose is integral to the prime-boost strategy, it remains unclear when, after priming, memory T cells become competent to proliferate. In this study, we show that Ag-specific CD8 T cells with the capacity to undergo extensive expansion are already present at the peak of the primary immune response in mice. These early memory T cells represent a small fraction of the primary immune response and, at early time points, their potential to proliferate is obscured by large effector T cell populations that rapidly clear Ag upon reimmunization. With sufficient Ag boosting, however, secondary expansion of these memory cells can be induced as early as 5–7 days following primary immuni- zation. Importantly, both early and delayed boosting result in similar levels of protective immunity to subsequent pathogen challenge. Early commitment and differentiation of memory T cells during primary immunization suggest that a short duration between priming and boosting is feasible, providing potential logistic advantages for large-scale prime-boost vaccination of human populations. The Journal of Immunology, 2004, 172: 7239–7245. Downloaded from emory CD8 T cells are essential for immunity to many erate upon re-encountering Ag for 3 wk following priming (13). viral, bacterial, and protozoal pathogens (1). Upon pri- LCMV infection, however, induces extraordinarily large primary M mary activation by foreign Ag, CD8 T cells follow a immune responses (2, 3), and therefore may not reflect the type of program of proliferation and differentiation into CTL armed with T cell priming that occurs with vaccines. effector functions that enable pathogen clearance or containment To explore the kinetics of memory development and the factors http://www.jimmunol.org/ (2–8). After the expansion phase, the majority of Ag-specific CD8 that influence the magnitude of memory cell expansion in the set- T cells undergo programmed cell death, leaving a population of ting of a more typical CD8 T cell response, we examined mice memory CD8 T cells that swiftly proliferate upon secondary an- infected with the intracellular bacterial pathogen Listeria monocy- tigenic challenge. Substantial evidence suggests that CD8 T cells togenes. Peak CD8 T cell responses to L. monocytogenes infection transit through the effector phase before entering the memory pool occur 8 days following bacterial inoculation; subsequently, T cells (9, 10), but it remains unclear when, during the primary immune contract into stable memory populations within 14–21 days (14). response, effector T cells differentiate into long-lived memory In this study, we show that a subset of Ag-specific CD8 T cells can cells. A recent report showed that surface expression of the IL-7R undergo recall proliferative responses upon secondary encounter by guest on October 1, 2021 ␣-chain (IL-7R␣) distinguishes a small population of CD8 effector with Ag within 5–7 days of primary infection, even before the T cells at the peak of the primary response that gives rise to long- primary T cell response begins to subside. Interestingly, we find term memory cells (11); however, it remains unclear when, fol- that the rapid elimination of Ag by effector cells during an ongoing lowing priming, memory T cells acquire the ability to undergo immune response prevents the activation and proliferation of extensive proliferation in response to Ag. Although it was previ- memory cells, explaining the apparent lack of functional memory ously demonstrated that increased CD8 T cell proliferation can be CD8 T cells at early time points after primary immunization. The induced by additional Ag administration within 1 wk following ability of memory T cells to proliferate is revealed, however, when primary bacterial infection (12), a more recent report analyzing the the boosting dose of Ag exceeds the clearance capacity of effector CD8 T cell response to lymphocytic choriomeningitis virus T cells. Remarkably, boosting at early or late time points following (LCMV)3 infection concluded that memory T cells do not prolif- priming is similarly effective at enhancing both the size of sec- ondary memory T cell populations and protective immunity to sub- sequent pathogen challenge. These findings have significant im- *Infectious Diseases Service, Immunology Program, Department of Medicine, Sloan- plications for the design and delivery of prime-boost vaccines. Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10021; and †Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY 10021 Materials and Methods Mice, bacteria, and viruses Received for publication December 5, 2003. Accepted for publication March 25, 2004. BALB/cJ were obtained from The Jackson Laboratory (Bar Harbor, ME). The costs of publication of this article were defrayed in part by the payment of page BALB/c Thy-1.1-congenic mice were provided by C. Surh (Scripps Re- charges. This article must therefore be hereby marked advertisement in accordance search Foundation, La Jolla, CA). Wild-type (WT) L. monocytogenes strain with 18 U.S.C. Section 1734 solely to indicate this fact. 10403S, the ActAϪ/Ϫ strain of L. monocytogenes (15) (both provided by D. 1 This work was supported by National Institutes of Health Grants AI-39031 and Portnoy, University of California, Berkeley, CA), and the LLO92Ser mutant AI-42135, an Arthritis Foundation postdoctoral fellowship (to P.W.), and a Cancer strain of L. monocytogenes (mutation of the tyrosine in position 92 of Research Institute predoctoral fellowship (to A.P.). M.L.-T. is a Rosenwald Family/ listeriolysin to a serine (16)) were grown in brain-heart infusion (BHI) DeVaan-Irvington Institute postdoctoral fellow. broth (BD Biosciences, Sparks, MD). Vesicular stomatitis virus (VSV) 2 Address correspondence and reprint requests to Dr. Eric G. Pamer, Memorial Sloan- expressing the L. monocytogenes listeriolysin O (LLO) and p60 epitopes Kettering Cancer Center, 1275 York Avenue, New York, NY 10021. E-mail address: was generated by cloning a PCR-amplified fragment of the L. monocyto- [email protected] genes p60 protein encompassing the p60217–225 and p60449–457 epitopes 3 Abbreviations used in this paper: LCMV, lymphocytic choriomeningitis virus; into pVSV-XN2 (kindly provided by J. Rose, Yale University, New Haven, BHI, brain-heart infusion; LLO, listeriolysin O; VSV, vesicular stomatitis virus; WT, CT) using its unique XhoI and NheI sites. A 64-bp linker encoding wild type. LLO91–99 was then ligated in frame with the p60 fragment at the XhoI site Copyright © 2004 by The American Association of Immunologists, Inc. 0022-1767/04/$02.00 7240 RAPID DEVELOPMENT OF T CELL MEMORY to generate a fusion LLO-p60 protein in pVSV-XN2. Recombinant VSV- immunization (13), an alternative explanation is that the secondary LLO-p60 viruses were then obtained, as previously described (17). Briefly, bacterial challenge is cleared with different kinetics at early and the LLO-p60-containing plasmid was transfected along with pBS-N, late time points following primary infection. Indeed, recent studies pBS-P, and pBS-L helper plasmids into baby hamster kidney cells infected with recombinant vaccinia virus expressing T7 polymerase (vTF7-3). Su- demonstrated that swift activation of Ag-specific T cells following pernatants were recovered 48 h later, spun down to remove debris, and primary infection rapidly eliminates APCs, thereby restricting ad- filtered through a 0.2-␮m filter to remove vTF7-3. The cleared supernatants ditional T cell priming (20, 21). To explore this possibility, we were used to infect baby hamster kidney monolayers. Supernatants were measured in vivo CTL activity using LLO -coated target cells recovered 48 h after the secondary infection, aliquoted, and stored at 91–99 Ϫ80°C. Viral titers were determined by plaque assay. at intervals after primary L. monocytogenes
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