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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 顧家綺(Chia-Chi Ku) | |
| dc.contributor.author | Chao-Wei Yeh | en |
| dc.contributor.author | 葉昭緯 | zh_TW |
| dc.date.accessioned | 2021-06-15T06:00:42Z | - |
| dc.date.available | 2015-12-16 | |
| dc.date.copyright | 2010-09-09 | |
| dc.date.issued | 2010 | |
| dc.date.submitted | 2010-08-17 | |
| dc.identifier.citation | Alleva, D.G., Kaser, S.B., Monroy, M.A., Fenton, M.J., and Beller, D.I. (1997). IL-15 functions as a potent autocrine regulator of macrophage proinflammatory cytokine production: evidence for differential receptor subunit utilization associated with stimulation or inhibition. J Immunol 159, 2941-2951.
Almeida, A.R., Rocha, B., Freitas, A.A., and Tanchot, C. (2005). Homeostasis of T cell numbers: from thymus production to peripheral compartmentalization and the indexation of regulatory T cells. Semin Immunol 17, 239-249. Altinkilic, B., and Brandner, G. (1988). Interferon inhibits herpes simplex virus-specific translation: a reinvestigation. J Gen Virol 69 ( Pt 12), 3107-3112. Ashcroft, G.S., Lei, K., Jin, W., Longenecker, G., Kulkarni, A.B., Greenwell-Wild, T., Hale-Donze, H., McGrady, G., Song, X.Y., and Wahl, S.M. (2000). Secretory leukocyte protease inhibitor mediates non-redundant functions necessary for normal wound healing. Nat Med 6, 1147-1153. Ashcroft, G.S., Yang, X., Glick, A.B., Weinstein, M., Letterio, J.L., Mizel, D.E., Anzano, M., Greenwell-Wild, T., Wahl, S.M., Deng, C., and Roberts, A.B. (1999). Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response. Nat Cell Biol 1, 260-266. Atamas, S.P., Choi, J., Yurovsky, V.V., and White, B. (1996). An alternative splice variant of human IL-4, IL-4 delta 2, inhibits IL-4-stimulated T cell proliferation. J Immunol 156, 435-441. Becker, T.C., Wherry, E.J., Boone, D., Murali-Krishna, K., Antia, R., Ma, A., and Ahmed, R. (2002). Interleukin 15 is required for proliferative renewal of virus-specific memory CD8 T cells. J Exp Med 195, 1541-1548. Cheng, H., Tumpey, T.M., Staats, H.F., van Rooijen, N., Oakes, J.E., and Lausch, R.N. (2000). Role of macrophages in restricting herpes simplex virus type 1 growth after ocular infection. Invest Ophthalmol Vis Sci 41, 1402-1409. De Creus, A., Van Beneden, K., Stevenaert, F., Debacker, V., Plum, J., and Leclercq, G. (2002). Developmental and functional defects of thymic and epidermal V gamma 3 cells in IL-15-deficient and IFN regulatory factor-1-deficient mice. J Immunol 168, 6486-6493. Dubois, S., Mariner, J., Waldmann, T.A., and Tagaya, Y. (2002). IL-15Ralpha recycles and presents IL-15 In trans to neighboring cells. Immunity 17, 537-547. Engler, H., Zawatzky, R., Kirchner, H., and Armerding, D. (1982). Experimental infection of inbred mice with herpes simplex virus. IV. Comparison of interferon production and natural killer cell activity in susceptible and resistant adult mice. Arch Virol 74, 239-247. Gebhardt, T., Wakim, L.M., Eidsmo, L., Reading, P.C., Heath, W.R., and Carbone, F.R. (2009). Memory T cells in nonlymphoid tissue that provide enhanced local immunity during infection with herpes simplex virus. Nat Immunol 10, 524-530. Grabstein, K.H., Eisenman, J., Shanebeck, K., Rauch, C., Srinivasan, S., Fung, V., Beers, C., Richardson, J., Schoenborn, M.A., Ahdieh, M., and et al. (1994). Cloning of a T cell growth factor that interacts with the beta chain of the interleukin-2 receptor. Science 264, 965-968. Guo, J., Peters, K.L., and Sen, G.C. (2000). Induction of the human protein P56 by interferon, double-stranded RNA, or virus infection. Virology 267, 209-219. Habu, S., Akamatsu, K., Tamaoki, N., and Okumura, K. (1984). In vivo significance of NK cell on resistance against virus (HSV-1) infections in mice. J Immunol 133, 2743-2747. Halford, W.P., Veress, L.A., Gebhardt, B.M., and Carr, D.J. (1997). Innate and acquired immunity to herpes simplex virus type 1. Virology 236, 328-337. Haluszczak, C., Akue, A.D., Hamilton, S.E., Johnson, L.D., Pujanauski, L., Teodorovic, L., Jameson, S.C., and Kedl, R.M. (2009). The antigen-specific CD8+ T cell repertoire in unimmunized mice includes memory phenotype cells bearing markers of homeostatic expansion. J Exp Med 206, 435-448. Hildeman, D.A., Zhu, Y., Mitchell, T.C., Bouillet, P., Strasser, A., Kappler, J., and Marrack, P. (2002). Activated T cell death in vivo mediated by proapoptotic bcl-2 family member bim. Immunity 16, 759-767. Hughes, P.D., Belz, G.T., Fortner, K.A., Budd, R.C., Strasser, A., and Bouillet, P. (2008). Apoptosis regulators Fas and Bim cooperate in shutdown of chronic immune responses and prevention of autoimmunity. Immunity 28, 197-205. Hui, D.J., Bhasker, C.R., Merrick, W.C., and Sen, G.C. (2003). Viral stress-inducible protein p56 inhibits translation by blocking the interaction of eIF3 with the ternary complex eIF2.GTP.Met-tRNAi. J Biol Chem 278, 39477-39482. Hutcheson, J., Scatizzi, J.C., Siddiqui, A.M., Haines, G.K., 3rd, Wu, T., Li, Q.Z., Davis, L.S., Mohan, C., and Perlman, H. (2008). Combined deficiency of proapoptotic regulators Bim and Fas results in the early onset of systemic autoimmunity. Immunity 28, 206-217. Jameson, S.C. (2005). T cell homeostasis: keeping useful T cells alive and live T cells useful. Semin Immunol 17, 231-237. Janas, M.L., Groves, P., Kienzle, N., and Kelso, A. (2005). IL-2 regulates perforin and granzyme gene expression in CD8+ T cells independently of its effects on survival and proliferation. J Immunol 175, 8003-8010. Kennedy, M.K., Glaccum, M., Brown, S.N., Butz, E.A., Viney, J.L., Embers, M., Matsuki, N., Charrier, K., Sedger, L., Willis, C.R., et al. (2000). Reversible defects in natural killer and memory CD8 T cell lineages in interleukin 15-deficient mice. J Exp Med 191, 771-780. Khanna, K.M., Bonneau, R.H., Kinchington, P.R., and Hendricks, R.L. (2003). Herpes simplex virus-specific memory CD8+ T cells are selectively activated and retained in latently infected sensory ganglia. Immunity 18, 593-603. Klonowski, K.D., Williams, K.J., Marzo, A.L., and Lefrancois, L. (2006). Cutting edge: IL-7-independent regulation of IL-7 receptor alpha expression and memory CD8 T cell development. J Immunol 177, 4247-4251. Knickelbein, J.E., Khanna, K.M., Yee, M.B., Baty, C.J., Kinchington, P.R., and Hendricks, R.L. (2008). Noncytotoxic lytic granule-mediated CD8+ T cell inhibition of HSV-1 reactivation from neuronal latency. Science 322, 268-271. Kolumam, G.A., Thomas, S., Thompson, L.J., Sprent, J., and Murali-Krishna, K. (2005). Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection. J Exp Med 202, 637-650. Korte, A., Moricke, A., Beyermann, B., Kochling, J., Taube, T., Kebelmann-Betzing, C., Henze, G., and Seeger, K. (1999). Extensive alternative splicing of interleukin-7 in malignant hematopoietic cells: implication of distinct isoforms in modulating IL-7 activity. J Interferon Cytokine Res 19, 495-503. Kotturi, M.F., Scott, I., Wolfe, T., Peters, B., Sidney, J., Cheroutre, H., von Herrath, M.G., Buchmeier, M.J., Grey, H., and Sette, A. (2008). Naive precursor frequencies and MHC binding rather than the degree of epitope diversity shape CD8+ T cell immunodominance. J Immunol 181, 2124-2133. Le Bon, A., Durand, V., Kamphuis, E., Thompson, C., Bulfone-Paus, S., Rossmann, C., Kalinke, U., and Tough, D.F. (2006). Direct stimulation of T cells by type I IFN enhances the CD8+ T cell response during cross-priming. J Immunol 176, 4682-4689. Le Bon, A., Etchart, N., Rossmann, C., Ashton, M., Hou, S., Gewert, D., Borrow, P., and Tough, D.F. (2003). Cross-priming of CD8+ T cells stimulated by virus-induced type I interferon. Nat Immunol 4, 1009-1015. Leignadier, J., Hardy, M.P., Cloutier, M., Rooney, J., and Labrecque, N. (2008). Memory T-lymphocyte survival does not require T-cell receptor expression. Proc Natl Acad Sci U S A 105, 20440-20445. Manickan, E., and Rouse, B.T. (1995). Roles of different T-cell subsets in control of herpes simplex virus infection determined by using T-cell-deficient mouse-models. J Virol 69, 8178-8179. Marques, J.T., Rebouillat, D., Ramana, C.V., Murakami, J., Hill, J.E., Gudkov, A., Silverman, R.H., Stark, G.R., and Williams, B.R. (2005). Down-regulation of p53 by double-stranded RNA modulates the antiviral response. J Virol 79, 11105-11114. Martin, P., D'Souza, D., Martin, J., Grose, R., Cooper, L., Maki, R., and McKercher, S.R. (2003). Wound healing in the PU.1 null mouse--tissue repair is not dependent on inflammatory cells. Curr Biol 13, 1122-1128. Mittnacht, S., Straub, P., Kirchner, H., and Jacobsen, H. (1988). Interferon treatment inhibits onset of herpes simplex virus immediate-early transcription. Virology 164, 201-210. Mortier, E., Advincula, R., Kim, L., Chmura, S., Barrera, J., Reizis, B., Malynn, B.A., and Ma, A. (2009). Macrophage- and dendritic-cell-derived interleukin-15 receptor alpha supports homeostasis of distinct CD8+ T cell subsets. Immunity 31, 811-822. Murali-Krishna, K., Lau, L.L., Sambhara, S., Lemonnier, F., Altman, J., and Ahmed, R. (1999). Persistence of memory CD8 T cells in MHC class I-deficient mice. Science 286, 1377-1381. Nahmias, A.J., Lee, F.K., and Beckman-Nahmias, S. (1990). Sero-epidemiological and -sociological patterns of herpes simplex virus infection in the world. Scand J Infect Dis Suppl 69, 19-36. Nishimura, H., Washizu, J., Nakamura, N., Enomoto, A., and Yoshikai, Y. (1998). Translational efficiency is up-regulated by alternative exon in murine IL-15 mRNA. J Immunol 160, 936-942. Nishimura, H., Yajima, T., Naiki, Y., Tsunobuchi, H., Umemura, M., Itano, K., Matsuguchi, T., Suzuki, M., Ohashi, P.S., and Yoshikai, Y. (2000). Differential roles of interleukin 15 mRNA isoforms generated by alternative splicing in immune responses in vivo. J Exp Med 191, 157-170. Northrop, J.K., Thomas, R.M., Wells, A.D., and Shen, H. (2006). Epigenetic remodeling of the IL-2 and IFN-gamma loci in memory CD8 T cells is influenced by CD4 T cells. J Immunol 177, 1062-1069. Obar, J.J., Khanna, K.M., and Lefrancois, L. (2008). Endogenous naive CD8+ T cell precursor frequency regulates primary and memory responses to infection. Immunity 28, 859-869. Oberman, F., and Panet, A. (1988). Inhibition of transcription of herpes simplex virus immediate early genes in interferon-treated human cells. J Gen Virol 69 ( Pt 6), 1167-1177. Ohteki, T., Suzue, K., Maki, C., Ota, T., and Koyasu, S. (2001). Critical role of IL-15-IL-15R for antigen-presenting cell functions in the innate immune response. Nat Immunol 2, 1138-1143. Pierce, A.T., DeSalvo, J., Foster, T.P., Kosinski, A., Weller, S.K., and Halford, W.P. (2005). Beta interferon and gamma interferon synergize to block viral DNA and virion synthesis in herpes simplex virus-infected cells. J Gen Virol 86, 2421-2432. Schluns, K.S., Kieper, W.C., Jameson, S.C., and Lefrancois, L. (2000). Interleukin-7 mediates the homeostasis of naive and memory CD8 T cells in vivo. Nat Immunol 1, 426-432. Schluns, K.S., Williams, K., Ma, A., Zheng, X.X., and Lefrancois, L. (2002). Cutting edge: requirement for IL-15 in the generation of primary and memory antigen-specific CD8 T cells. J Immunol 168, 4827-4831. Simmons, A., and Nash, A.A. (1984). Zosteriform spread of herpes simplex virus as a model of recrudescence and its use to investigate the role of immune cells in prevention of recurrent disease. J Virol 52, 816-821. Smith, C.M., Wilson, N.S., Waithman, J., Villadangos, J.A., Carbone, F.R., Heath, W.R., and Belz, G.T. (2004). Cognate CD4(+) T cell licensing of dendritic cells in CD8(+) T cell immunity. Nat Immunol 5, 1143-1148. Spierings, D.C., Lemmens, E.E., Grewal, K., Schoenberger, S.P., and Green, D.R. (2006). Duration of CTL activation regulates IL-2 production required for autonomous clonal expansion. Eur J Immunol 36, 1707-1717. Surh, C.D., Boyman, O., Purton, J.F., and Sprent, J. (2006). Homeostasis of memory T cells. Immunol Rev 211, 154-163. Svennerholm, B., Ziegler, R., and Lycke, E. (1989). Herpes simplex virus infection of the rat sensory neuron. Effects of interferon on cultured cells. Arch Virol 104, 153-156. Szpaderska, A.M., and DiPietro, L.A. (2005). Inflammation in surgical wound healing: friend or foe? Surgery 137, 571-573. Tan, X., and Lefrancois, L. (2006). Novel IL-15 isoforms generated by alternative splicing are expressed in the intestinal epithelium. Genes Immun 7, 407-416. Tsytsikov, V.N., Yurovsky, V.V., Atamas, S.P., Alms, W.J., and White, B. (1996). Identification and characterization of two alternative splice variants of human interleukin-2. J Biol Chem 271, 23055-23060. Tumpey, T.M., Chen, S.H., Oakes, J.E., and Lausch, R.N. (1996). Neutrophil-mediated suppression of virus replication after herpes simplex virus type 1 infection of the murine cornea. J Virol 70, 898-904. van Lint, A., Ayers, M., Brooks, A.G., Coles, R.M., Heath, W.R., and Carbone, F.R. (2004). Herpes simplex virus-specific CD8+ T cells can clear established lytic infections from skin and nerves and can partially limit the early spread of virus after cutaneous inoculation. J Immunol 172, 392-397. Wakim, L.M., Waithman, J., van Rooijen, N., Heath, W.R., and Carbone, F.R. (2008). Dendritic cell-induced memory T cell activation in nonlymphoid tissues. Science 319, 198-202. Wallace, M.E., Keating, R., Heath, W.R., and Carbone, F.R. (1999). The cytotoxic T-cell response to herpes simplex virus type 1 infection of C57BL/6 mice is almost entirely directed against a single immunodominant determinant. J Virol 73, 7619-7626. Weant, A.E., Michalek, R.D., Khan, I.U., Holbrook, B.C., Willingham, M.C., and Grayson, J.M. (2008). Apoptosis regulators Bim and Fas function concurrently to control autoimmunity and CD8+ T cell contraction. Immunity 28, 218-230. Whitmire, J.K., Tan, J.T., and Whitton, J.L. (2005). Interferon-gamma acts directly on CD8+ T cells to increase their abundance during virus infection. J Exp Med 201, 1053-1059. Wojciechowski, S., Jordan, M.B., Zhu, Y., White, J., Zajac, A.J., and Hildeman, D.A. (2006). Bim mediates apoptosis of CD127(lo) effector T cells and limits T cell memory. Eur J Immunol 36, 1694-1706. Wojciechowski, S., Tripathi, P., Bourdeau, T., Acero, L., Grimes, H.L., Katz, J.D., Finkelman, F.D., and Hildeman, D.A. (2007). Bim/Bcl-2 balance is critical for maintaining naive and memory T cell homeostasis. J Exp Med 204, 1665-1675. Yajima, T., Yoshihara, K., Nakazato, K., Kumabe, S., Koyasu, S., Sad, S., Shen, H., Kuwano, H., and Yoshikai, Y. (2006). IL-15 regulates CD8+ T cell contraction during primary infection. J Immunol 176, 507-515. Zehn, D., Lee, S.Y., and Bevan, M.J. (2009). Complete but curtailed T-cell response to very low-affinity antigen. Nature 458, 211-214. Zeng, R., Spolski, R., Finkelstein, S.E., Oh, S., Kovanen, P.E., Hinrichs, C.S., Pise-Masison, C.A., Radonovich, M.F., Brady, J.N., Restifo, N.P., et al. (2005). Synergy of IL-21 and IL-15 in regulating CD8+ T cell expansion and function. J Exp Med 201, 139-148. Zhang, X., Sun, S., Hwang, I., Tough, D.F., and Sprent, J. (1998). Potent and selective stimulation of memory-phenotype CD8+ T cells in vivo by IL-15. Immunity 8, 591-599. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/47457 | - |
| dc.description.abstract | Interleukin-15 (IL-15)是一種多功能的細胞激素，對於宿主的先天性及後天性免疫反應都扮演重要角色。中研院基因突變鼠動物模式核心實驗室 (MMPCF)利用ENU的致突變機制產生出表現顯著多量的IL15選擇性剪接異構體mRNA，簡稱IL-15∆E7的P191品系，在感染第一型疱疹病毒(HSV-1)後，皮膚出現比B6小鼠更為嚴重的傷口，病毒蛋白的表現量較高，cDNA微陣列分析和即時定量PCR的結果也顯示P191皮膚中有顯著高量的IL-1β和IL-6。IL-15∆E7如何影響IL-15的功能，並造成宿主在感染HSV-1後產生更嚴重的發炎反應，還需要進一步的探討。
和MMPCF的結果相符，我們利用流式細胞儀分析P191小鼠淋巴結、脾臟和週邊血中CD8+ T細胞的組成，也發現P191 CD8+ T細胞中表現CD44hiCD122hi的百分比較低。利用Kb-HSV-gB498-505四聚體分子，我們發現具gB抗原特異性的CD8+ T細胞在P191小鼠體內生成的時間比野生型小鼠晚。然而，這組細胞在感染後第十天P191小鼠脾臟中的總細胞數明顯比在B6小鼠還高，顯示這些細胞在感染早期能夠很有效率地在P191的脾臟中增生。當在活體外以gB抗原及IL-2和IL-15刺激CD8+ T細胞時，我們發現P191小鼠的CD8+ T細胞無論在感染前後，接受抗原及IL-15刺激後分裂的能力都比B6小鼠的CD8+ T細胞還差，顯示P191的CD8+ T細胞可能較不具抗原記憶性。利用FlowCytomix檢測B6和P191小鼠脾臟中細胞激素表現的情形，發現在HSV-1感染第七天時，P191小鼠脾臟中IFN-γ表現量顯著低於B6小鼠。P191小鼠脾臟中IFN-γ表現量的下降和具抗原特異性CD8+ T細胞的增生能力是否有任何關聯，仍需要更進一步的研究。 我們的實驗結果顯示P191小鼠在感染HSV-1後，皮膚發炎反應的情形及所產生具抗原特異性CD8+ T細胞的性質都和B6小鼠很不一樣，究竟IL-15異構體如何造成這些變化，是很值得研究的課題。 | zh_TW |
| dc.description.abstract | Interleukin-15 (IL-15) is a pleiotropic cytokine that plays an important role in mediating innate and adaptive immunity in the host. The pedigree 191 (P191) of the ENU-mutagenized mice, generated by the Mouse Mutagenesis Program Core Facility (MMPCF) has been identified and predominantly express an alternatively spliced IL-15 mRNA called IL-15 ∆E7. Infection of P191 mutant mice via flank skin with herpes simplex virus-1 (HSV-1) showed a much more severely disrupted lesional skin than in B6 wildtype mice accompanied with enhanced HSV viral protein expression as well as elevated expressions of IL-1β and IL-6 in P191 lesional skin by cDNA microarray and real-time PCR analysis. How the function of IL-15 is affected and/or regulated by IL-15 ∆E7 and thus results in the altered inflammatory response against HSV-1 infection will be further investigated.
Consistent with the depressed CD44 expression on CD8+ T cells in P191, we also found that the percentages of CD8+ T cells from lymph nodes, spleen and peripheral blood expressing CD44hiCD122hi were reduced in P191 mice by flow cytometric analysis. Using Kb-HSV-gB498-505 tetramer reagent, we found that gB-specific CD8+ T cells were generated in a delayed kinetics in P191 as compared to wildtype mice. However, these gB-specific CD8+ T cells significantly expanded in the spleen of P191 on day 10 after infection and the absolute numbers of gB-specific CD8+ T cells were higher than these in B6 mice, indicating that these cells efficiently proliferated in P191 spleen on early times of infection. In proliferation experiment, CFSE-labeled T cells were stimulated with gB498-505 peptide in rIL-2 and rIL-15. Whereas HSV-primed CD8+ T cells from B6 mice proliferated to gB antigen in vitro, proliferation of HSV-primed CD8+ T cells from P191 was significantly reduced given with sufficient IL-15. This suggested that gB-specific CD8+ T cells generated in P191 were poorly responsive to recall antigen. Using FlowCytomix to profile cytokine expression in B6 and P191 mice after HSV-1 infection, we have found that the level of IFN-γ in spleen was significantly reduced in P191 as compared to B6 spleen. How the reduced production of IFN-γ is associated with less proliferation of antigen-specific CD8+ T cells from P191 requires further investigation. Results from current experiments have shown that inflammatory response in skin and the properties of antigen-specific CD8+ T cells induced by HSV-1 infection are both altered in P191. How expression of IL-15 splice variant is involved in the control of these phenotypes remains to be clarified. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T06:00:42Z (GMT). No. of bitstreams: 1 ntu-99-R97449009-1.pdf: 4156128 bytes, checksum: 5511c5bbb9001a2f883909166f5d56b1 (MD5) Previous issue date: 2010 | en |
| dc.description.tableofcontents | 摘要 i
Abstract ii Table of Contents iv List of Figures vi Chapter I Introduction 1 1. Type I IFNs against HSV-1 infection 2 2. NK cells against HSV-1 infection 3 3. T cell immunity against HSV-1 infection 3 4. CD8+ T cell activation 5 5. Memory CD8+ T cell differentiation and maintenance 7 6. Rationale 9 Chapter II Materials and Methods 11 1. Establishment of HSV-1 zosteriform mouse model 11 2. Histological analysis 13 3. Quantification of tissue cytokine mRNAs 16 4. Quantification of tissue cytokines 19 5. Flow cytometry 20 6. Antibodies 26 7. Enzymes 29 8. Solution recipes 30 9. Chemicals, kits and reagents 33 Chapter III Results 38 1. P191 mice develop more severe lesional skin than B6 mice after HSV-1 infection 38 2. Severe skin inflammation in P191 accompanied by dramatic up-regulation of IL-1β and IL-6 transcripts 39 3. P191 mice exhibit reduced NK and CD44hiCD122hi CD8+ T cells and T cell activation and gB-specific CD8+ T cell generation are delayed after HSV-1 infection 40 4. The kinetics of early generation of gB-specific CD8+ T cells after HSV-1 infection in P191 mice is altered 43 5. CD8+ T cells from P191 spleen are less proliferative in response to in vitro restimulation with gB498-505 peptide, IL-2 and IL-15 45 6. IFN-γ production is reduced in P191 spleen 47 Chapter IV Discussion 49 1. Altered inflammatory responses and lesion resolution in P191 mice 49 2. Skin γδ T cells in inflammation and tissue repairing 51 3. Reduced surface marker up-regulation and generation of gB-specific CD8+ T cells in P191 mice 52 4. Lymph node retention of gB-specific CD8+ T cells 53 5. Antigen recall and IL-15 responsiveness of CD8+ T cells 55 6. Antigen-presenting and IL-15 trans-presenting cells in P191 mice 56 Chapter V Figures 59 Chapter VI References 76 Appendixes 87 Appendix 1. Establishment of HSV-1 infection mouse model via flank skin 87 Appendix 2. Sequences and Tm values of real-time PCR primers 88 Appendix 3. Histological analysis of TCRδc knockout mouse skin on day 7 after HSV-1 infection 89 Appendix 4. CD44hiCD62Lhi central memory CD8+ T cells are selectively reduced in P191 on day 29 after HSV-1 infection. 90 | |
| dc.language.iso | en | |
| dc.title | 利用ENU突變鼠發現IL-15異構體能影響HSV-1感染後皮膚的發炎反應與CD8+ T細胞的生成 | zh_TW |
| dc.title | IL-15 splice variant has effects on skin inflammation and CD8+ T cell activation after HSV-1 infection in an ENU mutagenesis mouse model | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 98-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 孔祥智(John Kung),伍安怡(Betty A. Wu-Hsieh) | |
| dc.subject.keyword | 第一型單純皰疹病毒,N-乙基-N-亞硝基尿素,發炎,CD8 T細胞, | zh_TW |
| dc.subject.keyword | HSV-1,ENU,inflammation,CD8 T cell, | en |
| dc.relation.page | 90 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2010-08-17 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 免疫學研究所 | zh_TW |
| 顯示於系所單位： | 免疫學研究所 | |
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