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Leishmania Major by a Monoclonal ␣␤ T Cell Repertoire1

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Leishmania Major by a Monoclonal ␣␤ T Cell Repertoire1 Control of Leishmania major by a Monoclonal ab T Cell Repertoire1 Steven L. Reiner,2* Deborah J. Fowell,†‡ Naomi H. Moskowitz,* Kevin Swier,* Daniel R. Brown,* Charles R. Brown,* Christoph W. Turck,†§ Phillip A. Scott,2¶ Nigel Killeen,‡ and Richard M. Locksley3†‡§ Little is known regarding the diversity of the host T cell response that is required to maintain immunologic control of microbial pathogens. Leishmania major persist as obligate intracellular parasites within macrophages of the mammalian host. Immunity is dependent upon activation of MHC class II-restricted T cells to an effector state capable of restricting growth and dissemi- nation of the organisms. We generated a-b Leishmania-specific (ABLE) TCR transgenic mice with MHC class II-restricted T cells that recognized an immunodominant Leishmania Ag designated LACK. Naive T cells from ABLE mice proliferated in vitro after incubation with recombinant LACK or with Leishmania-parasitized macrophages and in vivo after injection into infected mice. Infected ABLE mice controlled Leishmania infection almost as well as wild-type mice despite a drastic reduction in the T cell repertoire. ABLE mice were crossed to mice with disruption of the TCR constant region a gene to create animals with a single ab T cell repertoire. Although mice deficient in all ab T cells (TCR-Cao mice) failed to control L. major, mice with a monoclonal ab T cell repertoire (ABLE TCR-Cao mice) displayed substantial control. The immune system is capable of remarkable efficiency even when constrained to recognition of a single epitope from a complex organism. The Journal of Immunology, 1998, 160: 884–889. eishmania major is an obligate intracellular parasite of lesser or better, but generally incomplete, protection when used as macrophages within mammalian hosts; control of infec- vaccines against subsequent challenge with virulent Leishmania L tion is dependent upon the development of effector T lym- (reviewed in Ref. 13). It is unclear whether optimal protection phocytes capable of activating macrophages to a microbicidal state requires a diverse response against numerous parasite Ags or an (1). Much has been learned regarding the host immune response in optimal response against single, dominant, determinants. Such un- inbred mice using mAb depletion or, more recently, gene targeting. derstanding may have important implications for vaccine design. Whereas MHC class II-restricted ab T cells are required for re- We have created TCR transgenic mice with MHC class II-re- sistance (2–4), MHC class I-restricted T cells are dispensable (5). stricted T cells that recognize the LACK4 Ag of Leishmania major by guest on September 30, 2021. Copyright 1998 Pageant Media Ltd. IL-12 (6), IFN-g (7, 8), and inducible (macrophage) nitric oxide (14). LACK is highly conserved among Leishmania species, and synthase (9) are required for host immunity, perhaps reflecting constitutes the immunodominant focus of the early CD41 T cell activities mediated by CD40 ligand-CD40 interactions between T response in vivo (15). Crossing these mice to animals with dis- cells and APC (10–12). These numerous experiments suggest that ruption of the TCR Ca gene (TCR-Cao) (16) created mice with a MHC class II-restricted Th1 effector cells and activated macro- single ab T cell repertoire. These mice were used to assess the phages are necessary and sufficient for control of this intracellular requirements for a diverse pathogen-specific T cell repertoire in a infection. disease controlled by MHC class II-restricted T cells. Although these host determinants have been established, the complexity of the Ags presented by the parasite that are necessary https://www.jimmunol.org Materials and Methods for control of disease remains unknown. Numerous Ags provide Transgenic mice The rearranged a and b TCR genes were isolated from a CD41 Th1 clone, *Department of Medicine, Committee on Immunology and Gwen Knapp Center 9.1-2, that was isolated from a BALB/c mouse that had been immunized for Lupus and Immunology Research, University of Chicago, Chicago, IL 60637; with soluble Ags of L. major (17). Clone 9.1-2 expresses rearranged TCR Departments of †Medicine and ‡Microbiology and Immunology, and §Howard gene segments Va8.2A-JaTA72 and Vb4-Db1-Jb1.6 (15). Primers spe- Hughes Medical Institute, University of California, San Francisco, CA 94143; cific for the 59 region of Va8.2A and Vb4 were used in conjunction with ¶ Downloaded from and Department of Pathobiology, University of Pennsylvania School of Veter- antisense primers from the introns beyond JaTA72 and Jb1.7, respectively, inary Medicine, Philadelphia, PA 19104 to amplify the rearranged V(D)J portions of genomic DNA extracted from Received for publication July 23, 1997. Accepted for publication October clone 9.1-2. The 59 portion of each TCR transgene construct containing the 1, 1997. 59 untranslated and initial coding region of each V gene was subcloned The costs of publication of this article were defrayed in part by the payment of from cosmids obtained from a BALB/c genomic library (provided by K. page charges. This article must therefore be hereby marked advertisement in Wang and L. Hood, California Institute of Technology, Pasadena, CA). accordance with 18 U.S.C. Section 1734 solely to indicate this fact. The 59 portions were spliced into the V(D)J PCR products using unique 1 sites within the V genes of the TCR a- and b-chains (PstI and SalI, re- This work was supported by National Institutes of Health Grants AI30663 and a AI01309, a fellowship from the Juvenile Diabetes Foundation International (to spectively). The TCR -chain transgene was completed by appending a D.J.F.), and a Burroughs Wellcome Fund Scholarship in Molecular Parasitology 9-kb BamHI fragment of the Ca locus (provided by D. Loh, Washington (to R.M.L.). 2 Burroughs Wellcome Fund New Investigator in Molecular Parasitology. 4 Abbreviations used in this paper: LACK, Leishmania homologue of receptor for 3 Address correspondence and reprint requests to Dr. R. M. Locksley, University activated C kinase; ABLE, a/b Leishmania-specific T cell receptor for antigen of California, C-443, 521 Parnassus Ave., San Francisco, CA 94143–0654. transgenic mice; WD, tryptophan-aspartic acid; dull, low level; DN, double neg- E-mail address: [email protected] ative; PE, phycoerythrin. Copyright © 1998 by The American Association of Immunologists 0022-1767/98/$02.00 The Journal of Immunology 885 University, St. Louis, MO) containing 0.8 kb of upstream intron, the entire coding region, and the downstream enhancer to the 39 end of the promoter- V-J-intron construct. The TCR b-chain transgene was completed by ap- pending a Cb1 and downstream b-chain enhancer construct (provided by S. Hedrick, University of California-San Diego) to the 39 end of the pro- moter-V-D-J-intron construct at the Jb-Cb intron using a naturally occur- ring NsiI site. Equimolar concentrations of gel-purified constructs were injected into 3 the pronuclei of [C57BL/6 DBA/2] F1 eggs that had been fertilized by BALB/c males before implantation in pseudopregnant recipients. One of three founders that expressed Vb4 on all peripheral blood T cells was used as the progenitor of the ABLE transgenic line. Progeny were backcrossed to B10.D2 mice. Simultaneously, TCR-Cao mice (16), which lack all ab T cells, were backcrossed to B10.D2 mice. After five generations, mice were intercrossed to yield TCR-Ca1, TCR-Cao, and ABLE TCR-Cao mice on the B10.D2 background. ABLE mice were crossed to the MHC H-2k haplotype as a source of naive donor cells in designated experiments. Reagents Directly fluorescence-conjugated mAbs against CD4, CD8, CD3, Vb4, and CD69 were used for surface immunofluorescent labeling (Caltag, South San Francisco, CA). Anti-MHC class II Abs used in designated experi- ments included mAb M5/114 (rat IgG2b, anti-Ab,d and anti-Ed,k), mAb MKD6 (mouse IgG2a, anti-Ad), or mAb 10–2–16 (mouse IgG2b, anti-Ak). The LACK156–173 peptide from the fourth WD domain of the LACK pro- tein (ICFSPSLEHPIVVSGSWD) (14) was synthesized using an Advanced Chemtech Multiple Peptide Synthesizer (Louisville, KY). Peptides were FIGURE 1. T cell development in ABLE TCR-Cao mice. Six-week- purified by reverse phase HPLC, and their identities were confirmed by old H-2d control (wild-type; left panels) and ABLE TCR-Cao mice analysis with an LCQ mass spectrometer (Finnigan MAT, San Jose, CA). (right panels) were used to evaluate surface expression of T cell mark- Recombinant LACK protein was expressed in Escherichia coli and purified as previously described (14). ers. Thymocytes were stained with anti-CD4-FITC and anti-CD8-PE before flow cytometric analysis (upper panels). Peripheral lymph Parasites and infections nodes were stained with either anti-Vb4-FITC and anti-CD3-PE (mid- L. major (strain WHOM/IR/-/173) was passaged and maintained as previ- dle panels) or anti-CD4-FITC, anti-CD3-PE, and anti-CD8-Tricolor (lower panels). Ten thousand thymocyte-gated (upper panels), lym- ously described (18). Leishmania amazonensis (strain LV-78) was pro- 1 vided by K. P. Chang (Chicago Medical School, Chicago, IL). For the phocyte-gated (middle panels), or CD3 lymphocyte-gated (lower infection of macrophages in vitro, the designated numbers of stationary panels) events are displayed. In the lower panels, numbers next to phase promastigotes were cultured for 24 h with bone marrow-derived boxes represent the percentage of CD31 cells expressing CD4 or CD8. macrophages, prepared as previously described (18), in 96-well, flat-bot- Results represent an individual mouse from each group and are rep- 3 4 tom, microtiter plates containing 5 10 macrophages/well. The mono- resentative of more than eight mice per group. layers were washed extensively to remove extracellular parasites before by guest on September 30, 2021.
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