請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/99949完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 李建國 | zh_TW |
| dc.contributor.advisor | Chien-Kuo Lee | en |
| dc.contributor.author | 李遠志 | zh_TW |
| dc.contributor.author | Yuan-Chih Lee | en |
| dc.date.accessioned | 2025-09-22T16:06:42Z | - |
| dc.date.available | 2025-09-23 | - |
| dc.date.copyright | 2025-09-22 | - |
| dc.date.issued | 2025 | - |
| dc.date.submitted | 2025-08-11 | - |
| dc.identifier.citation | 1. Swiecki, M. and M. Colonna, The multifaceted biology of plasmacytoid dendritic cells. Nat Rev Immunol, 2015. 15(8): p. 471-85.
2. Reizis, B., Plasmacytoid Dendritic Cells: Development, Regulation, and Function. Immunity, 2019. 50(1): p. 37-50. 3. Cabeza-Cabrerizo, M., et al., Dendritic Cells Revisited. Annu Rev Immunol, 2021. 39: p. 131-166. 4. Nutt, S.L. and M. Chopin, Transcriptional Networks Driving Dendritic Cell Differentiation and Function. Immunity, 2020. 52(6): p. 942-956. 5. Lutz, K., et al., Ly6D(+)Siglec-H(+) precursors contribute to conventional dendritic cells via a Zbtb46(+)Ly6D(+) intermediary stage. Nat Commun, 2022. 13(1): p. 3456. 6. Rodrigues, P.F., et al., Progenitors of distinct lineages shape the diversity of mature type 2 conventional dendritic cells. Immunity, 2024. 57(7): p. 1567-1585 e5. 7. Sulczewski, F.B., et al., Transitional dendritic cells are distinct from conventional DC2 precursors and mediate proinflammatory antiviral responses. Nat Immunol, 2023. 24(8): p. 1265-1280. 8. Leylek, R., et al., Integrated Cross-Species Analysis Identifies a Conserved Transitional Dendritic Cell Population. Cell Rep, 2019. 29(11): p. 3736-3750 e8. 9. Boettcher, S. and M.G. Manz, Regulation of Inflammation- and Infection-Driven Hematopoiesis. Trends Immunol, 2017. 38(5): p. 345-357. 10. Sun, S.J., et al., BCG vaccination impacts the epigenetic landscape of progenitor cells in human bone marrow. bioRxiv, 2023. 11. Sun, S.J., et al., BCG vaccination alters the epigenetic landscape of progenitor cells in human bone marrow to influence innate immune responses. Immunity, 2024. 57(9): p. 2095-2107 e8. 12. Nasiri, K., et al., Spotlight on the impact of viral infections on Hematopoietic Stem Cells (HSCs) with a focus on COVID-19 effects. Cell Commun Signal, 2023. 21(1): p. 103. 13. Rommel, M.G.E., et al., Influenza A virus infection instructs hematopoiesis to megakaryocyte-lineage output. Cell Rep, 2022. 41(1): p. 111447. 14. Cabeza-Cabrerizo, M., et al., Recruitment of dendritic cell progenitors to foci of influenza A virus infection sustains immunity. Sci Immunol, 2021. 6(65): p. eabi9331. 15. Cabeza-Cabrerizo, M., et al., Tissue clonality of dendritic cell subsets and emergency DCpoiesis revealed by multicolor fate mapping of DC progenitors. Sci Immunol, 2019. 4(33). 16. Zhang, S., et al., Transcriptional regulation of dendritic cell development and function. Front Immunol, 2023. 14: p. 1182553. 17. Chauvistre, H. and K. Sere, Epigenetic aspects of DC development and differentiation. Mol Immunol, 2020. 128: p. 116-124. 18. Lin, Q., et al., Epigenetic program and transcription factor circuitry of dendritic cell development. Nucleic Acids Res, 2015. 43(20): p. 9680-93. 19. Yu, V.W.C., et al., Epigenetic Memory Underlies Cell-Autonomous Heterogeneous Behavior of Hematopoietic Stem Cells. Cell, 2017. 168(5): p. 944-945. 20. Berger, S.L., et al., An operational definition of epigenetics. Genes Dev, 2009. 23(7): p. 781-3. 21. Al Aboud, N.M., C. Tupper, and I. Jialal, Genetics, Epigenetic Mechanism, in StatPearls. 2025: Treasure Island (FL). 22. Gillette, T.G. and J.A. Hill, Readers, writers, and erasers: chromatin as the whiteboard of heart disease. Circ Res, 2015. 116(7): p. 1245-53. 23. Moore, L.D., T. Le, and G. Fan, DNA methylation and its basic function. Neuropsychopharmacology, 2013. 38(1): p. 23-38. 24. Ito, S., et al., Tet proteins can convert 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine. Science, 2011. 333(6047): p. 1300-3. 25. Alvarez-Errico, D., et al., Epigenetic control of myeloid cell differentiation, identity and function. Nat Rev Immunol, 2015. 15(1): p. 7-17. 26. Izzo, F., et al., DNA methylation disruption reshapes the hematopoietic differentiation landscape. Nat Genet, 2020. 52(4): p. 378-387. 27. Cong, B., Q. Zhang, and X. Cao, The function and regulation of TET2 in innate immunity and inflammation. Protein Cell, 2021. 12(3): p. 165-173. 28. Jambhekar, A., A. Dhall, and Y. Shi, Roles and regulation of histone methylation in animal development. Nat Rev Mol Cell Biol, 2019. 20(10): p. 625-641. 29. Lawrence, M., S. Daujat, and R. Schneider, Lateral Thinking: How Histone Modifications Regulate Gene Expression. Trends Genet, 2016. 32(1): p. 42-56. 30. Bannister, A.J. and T. Kouzarides, Regulation of chromatin by histone modifications. Cell Res, 2011. 21(3): p. 381-95. 31. Nicetto, D. and K.S. Zaret, Role of H3K9me3 heterochromatin in cell identity establishment and maintenance. Curr Opin Genet Dev, 2019. 55: p. 1-10. 32. Padeken, J., S.P. Methot, and S.M. Gasser, Establishment of H3K9-methylated heterochromatin and its functions in tissue differentiation and maintenance. Nat Rev Mol Cell Biol, 2022. 23(9): p. 623-640. 33. Kennedy, D.R., et al., Phosphorylation of HP1/Swi6 relieves competition with Suv39/Clr4 on nucleosomes and enables H3K9 trimethyl spreading. bioRxiv, 2024. 34. Pace, L., et al., The epigenetic control of stemness in CD8(+) T cell fate commitment. Science, 2018. 359(6372): p. 177-186. 35. Jiang, L., L. Huang, and W. Jiang, H3K27me3-mediated epigenetic regulation in pluripotency maintenance and lineage differentiation. Cell Insight, 2024. 3(4): p. 100180. 36. Saeed, S., et al., Epigenetic programming of monocyte-to-macrophage differentiation and trained innate immunity. Science, 2014. 345(6204): p. 1251086. 37. Kleinnijenhuis, J., et al., Bacille Calmette-Guerin induces NOD2-dependent nonspecific protection from reinfection via epigenetic reprogramming of monocytes. Proc Natl Acad Sci U S A, 2012. 109(43): p. 17537-42. 38. Jambhekar, A., A. Dhall, and Y. Shi, Author Correction: Roles and regulation of histone methylation in animal development. Nat Rev Mol Cell Biol, 2020. 21(1): p. 59. 39. Panigrahi, A.K. and D. Pati, Higher-order orchestration of hematopoiesis: is cohesin a new player? Exp Hematol, 2012. 40(12): p. 967-73. 40. Vecera, J., et al., HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals. J Cell Physiol, 2018. 233(1): p. 530-548. 41. Hezroni, H., et al., H3K9 histone acetylation predicts pluripotency and reprogramming capacity of ES cells. Nucleus, 2011. 2(4): p. 300-9. 42. Karmodiya, K., et al., H3K9 and H3K14 acetylation co-occur at many gene regulatory elements, while H3K14ac marks a subset of inactive inducible promoters in mouse embryonic stem cells. BMC Genomics, 2012. 13: p. 424. 43. Chauvistre, H., et al., Dendritic cell development requires histone deacetylase activity. Eur J Immunol, 2014. 44(8): p. 2478-88. 44. Zhang, Y., et al., Regulation of pDC fate determination by histone deacetylase 3. Elife, 2023. 12. 45. De Sa Fernandes, C., et al., The histone deacetylase HDAC1 controls dendritic cell development and anti-tumor immunity. Cell Rep, 2024. 43(6): p. 114308. 46. Whyte, W.A., et al., Master transcription factors and mediator establish super-enhancers at key cell identity genes. Cell, 2013. 153(2): p. 307-19. 47. Long, H.K., S.L. Prescott, and J. Wysocka, Ever-Changing Landscapes: Transcriptional Enhancers in Development and Evolution. Cell, 2016. 167(5): p. 1170-1187. 48. Grajales-Reyes, G.E., et al., Batf3 maintains autoactivation of Irf8 for commitment of a CD8alpha(+) conventional DC clonogenic progenitor. Nat Immunol, 2015. 16(7): p. 708-17. 49. Kurotaki, D., et al., IRF8 inhibits C/EBPalpha activity to restrain mononuclear phagocyte progenitors from differentiating into neutrophils. Nat Commun, 2014. 5: p. 4978. 50. Bagadia, P., et al., An Nfil3-Zeb2-Id2 pathway imposes Irf8 enhancer switching during cDC1 development. Nat Immunol, 2019. 20(9): p. 1174-1185. 51. Kashiwada, M., et al., NFIL3/E4BP4 is a key transcription factor for CD8alpha(+) dendritic cell development. Blood, 2011. 117(23): p. 6193-7. 52. Seillet, C., et al., CD8alpha+ DCs can be induced in the absence of transcription factors Id2, Nfil3, and Batf3. Blood, 2013. 121(9): p. 1574-83. 53. Wu, X., et al., Transcription factor Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate. Proc Natl Acad Sci U S A, 2016. 113(51): p. 14775-14780. 54. Hnisz, D., et al., Super-enhancers in the control of cell identity and disease. Cell, 2013. 155(4): p. 934-47. 55. Blayney, J.W., et al., Super-enhancers include classical enhancers and facilitators to fully activate gene expression. Cell, 2023. 186(26): p. 5826-5839 e18. 56. Durai, V., et al., Cryptic activation of an Irf8 enhancer governs cDC1 fate specification. Nat Immunol, 2019. 20(9): p. 1161-1173. 57. Yamasaki, T., et al., Physical and functional interaction among Irf8 enhancers during dendritic cell differentiation. Cell Rep, 2024. 43(4): p. 114107. 58. Sichien, D., et al., IRF8 Transcription Factor Controls Survival and Function of Terminally Differentiated Conventional and Plasmacytoid Dendritic Cells, Respectively. Immunity, 2016. 45(3): p. 626-640. 59. Henikoff, S., et al., Efficient chromatin accessibility mapping in situ by nucleosome-tethered tagmentation. Elife, 2020. 9. 60. Ernst, J. and M. Kellis, Chromatin-state discovery and genome annotation with ChromHMM. Nat Protoc, 2017. 12(12): p. 2478-2492. 61. Marroquin-Rivera, A., et al., Immune-related transcriptomic and epigenetic reconfiguration in BV2 cells after lipopolysaccharide exposure: an in vitro omics integrative study. Inflamm Res, 2024. 73(2): p. 211-225. 62. Heinz, S., et al., Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identities. Mol Cell, 2010. 38(4): p. 576-89. 63. Aibar, S., et al., SCENIC: single-cell regulatory network inference and clustering. Nat Methods, 2017. 14(11): p. 1083-1086. 64. Minutti, C.M., et al., Distinct ontogenetic lineages dictate cDC2 heterogeneity. Nat Immunol, 2024. 25(3): p. 448-461. 65. Medina, K.L., et al., Separation of plasmacytoid dendritic cells from B-cell-biased lymphoid progenitor (BLP) and Pre-pro B cells using PDCA-1. PLoS One, 2013. 8(10): p. e78408. 66. Cytlak, U., et al., Ikaros family zinc finger 1 regulates dendritic cell development and function in humans. Nat Commun, 2018. 9(1): p. 1239. 67. Liu, W., et al., CUX1 regulates human hematopoietic stem cell chromatin accessibility via the BAF complex. Cell Rep, 2024. 43(5): p. 114227. 68. Platzer, B., et al., RelB regulates human dendritic cell subset development by promoting monocyte intermediates. Blood, 2004. 104(12): p. 3655-63. 69. Geiselhoringer, A.L., et al., Dominant immune tolerance in the intestinal tract imposed by RelB-dependent migratory dendritic cells regulates protective type 2 immunity. Nat Commun, 2024. 15(1): p. 9143. 70. Lau, C.M., et al., Transcription factor Etv6 regulates functional differentiation of cross-presenting classical dendritic cells. J Exp Med, 2018. 215(9): p. 2265-2278. 71. Attwooll, C., E. Lazzerini Denchi, and K. Helin, The E2F family: specific functions and overlapping interests. EMBO J, 2004. 23(24): p. 4709-16. | - |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/99949 | - |
| dc.description.abstract | 樹突細胞 (Dendritic cells, DCs)，包含漿狀樹突細胞 (plasmacytoid DCs, pDCs) 與傳統樹突細胞 (conventional DCs, cDCs)是免疫反應的關鍵調節者。這群細胞的生命週期短，而且不斷地由造血幹細胞與先驅細胞 (HSPCs) 持續補充。先前我們發現，Flt3 配體 (Flt3 ligand, FL) 在穩定狀態下會促進共同淋巴先驅細胞 (common lymphoid progenitors, CLPs) 優先分化成 pDC 。然而，當使用 TLR7 促效劑 R848刺激或感染流感病毒時，無論在體內或體外，反而會促進 cDC 的發育但抑制 pDC 的生成。對 CLPs 下游的 DC 前驅細胞進行分析後發現，R848 的刺激會阻斷所有淋巴先驅細胞 (ALPs) 向 pre-pDCs 的分化進程，並將這些先驅細胞的發育命運轉向 cDC。轉錄組分析顯示，由 TLR7 訊息傳遞所引發的前 100 個下調基因中，有 70% 是 pDC 的專一表達基因，包括關鍵轉錄因子Tcf4、Runx2 和 Irf8。由於表觀遺傳(Epigenetic)調控在發育過程中對基因表現的活化(Transcriptionally active)或靜默異染色質(Silencing heterochromatin)扮演關鍵的角色，我們假設它也參與了TLR7訊息傳遞所誘導的DC發育重塑。整體的表觀遺傳分析顯示，與單獨使用 FL 相比，R848 刺激 6 小時後，CLPs 中的 H3K27ac、H3K27me3、H3K9ac 和 H3K9me3 組蛋白標記皆顯著增強。然而，只有H3K9ac和H3K9me3的標記在R848處理 24小時後仍然持續增加，這暗示了與轉錄活化或靜默異染色質相關的H3K9ac及H3K9me3標記可能參與其中。有趣的是，調控H3K9me3 的數個表觀遺傳修飾因子的轉錄程度，包括甲基轉移酶(Methyltransferase)如 Setdb1、Setdb2 以及組蛋白讀取蛋白(Reader)如 Cbx1，在 R848 刺激 6 小時後均顯著上調。我們結合不同組蛋白標記的 CUT&Tag 數據，並使用ChromHMM 對「染色質狀態」進行了綜合分析。最佳化後的14 種狀態ChromHMM 模型顯示，TLR7 誘導的表觀遺傳的重編程在6小時便在 pDC 相關的專一基因位點建立了抑制性的染色質狀態。相反的，在cDC 相關專一基因上則誘導產生活化性的染色質狀態。而此時的CUTAC分析顯示，pDC 與 cDC 基因位點的染色質開放區域與 48 小時的轉錄組分析結果呈現正相關，這些結果顯示 TLR7 誘導的表觀遺傳重塑在早期就已確立了發育的路徑。透過 ROSE 演算法從 CUT&Tag 數據中鑑定出的超級增強子 (super enhancer) 顯示，H3K9ac及H3K27ac 超級增強子可能各自主導了 DC 發育重塑的不同迴路。最後，利用 SCENIC （單細胞調控網絡推斷與聚類） 從single-cell RNA sequencing推斷出的基因調控網路 (GRNs)，以及從 CUT&Tag 預測的 DNA 結合序列皆顯示存在數群細胞類型特異性的 GRNs 可能引導了此發育重塑。總體而言，我們的研究結果強調，TLR7 訊息傳遞誘導的 CLPs 發育重塑可能是由表觀遺傳重編所驅動，而此過程又可能受到不同超級增強子群集與細胞類型特異性 GRNs 之間的交互作用來調控。 | zh_TW |
| dc.description.abstract | Dendritic cells (DCs), comprising plasmacytoid DCs (pDCs) and conventional DCs (cDCs), are essential mediators of the immune response. These short-lived cells are continuously replenished from hematopoietic stem and progenitor cells (HSPCs). Previously, we found that Flt3 ligand (FL) preferentially promoted pDC development from common lymphoid progenitors (CLPs) at steady state. However, the administration of a TLR7 agonist R848 or infection with influenza viruses favored cDC development but suppressed pDC generation from CLPs in vitro and in vivo. Analysis of the DC precursors downstream of CLPs revealed that the progression of all lymphoid progenitors (ALPs) to pre-pDCs was blocked, and the developmental fate of these progenitors was also skewed toward cDCs upon R848 stimulation. Transcriptomic profiling revealed that 70% of the TLR7 signaling-induced top 100 downregulated genes were pDC-specific, including key transcription factors Tcf4, Runx2, and Irf8. Since epigenetic regulation plays a critical role in activating or silencing gene expression during development, we hypothesized that it may also be involved in TLR7 signaling-induced reprogramming of DC development from CLPs. Total epigenetic profiling revealed that FL plus R848 stimulation enhanced the establishment of histone marks H3K27ac, H3K27me3, H3K9ac, and H3K9me3 in CLPs after 6 h of treatment compared to FL treatment alone. However, only H3K9ac, H3K9me3, but not H3K27ac or H3K27me3, were maintained for up to 24 h post-treatment, suggesting that H3K9ac and H3K9me3, a mark known to induce transcriptionally active regions and silent heterochromatin, respectively, may play a role in this process. Interestingly, the transcriptional levels of several epigenetic modifiers for H3K9me3, including a methyltransferase Setdb1 and Setdb2, and histone readers Cbx1, were significantly upregulated by R848 stimulation at 6 h. A comprehensive analysis of the “chromatin state” was performed by combining the CUT&Tag of different histone marks by using the chromatin hidden Markov model (ChromHMM). The optimized 14-state ChromHMM model revealed that the TLR7-induced epigenetic reprogramming established the suppressive chromatin states on pDC-specific gene loci and induced the active chromatin states on cDC-specific gene loci at 6 h. Chromatin accessible data on pDC and cDC gene loci from cleavage under targeted accessible chromatin (CUTAC) at 6 h post-treatment showed a positive correlation with transcriptomic profiling at 48 h post-treatment, suggesting that TLR7-induced epigenetic reprogramming establishes the developmental pathway early on. Moreover, we identified the super enhancers of the CUT&Tag dataset by Rank Ordering of Super-Enhancers (ROSE). We found that H3K9ac/H3K27ac super enhancer may govern different circuits of reprogrammed DC development from CLPs. Gene regulatory networks (GRNs) inferred from single-cell RNA sequencing using the single-cell regulatory network inference and clustering (SCENIC) and DNA binding motif predicted from CUT&Tag demonstrated the presence of groups of cell-type-specific GRNs that may guide the reprogrammed DC development. Together, our findings emphasize that TLR7 signaling-induced reprogrammed DC development from CLPs is driven by epigenetic reprogramming, which is governed by the interaction between various clusters of super enhancers and cell-type-specific GRNs. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2025-09-22T16:06:42Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2025-09-22T16:06:42Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 致謝 i
摘要 ii Abstract iv Contents vii Chapter 1 Introduction 1 1.1 Development of dendritic cells 1 1.2 Inflammation alters the cell fate in hematopoiesis 2 1.3 Epigenetic regulation in dendritic cell development 3 1.4 Histone methylation in cell fate determination 5 1.5 Histone acetylation in cell fate determination 6 1.6 Crosstalk between epigenetics and transcription factors in dendritic cell development 8 1.7 Rationale and specific aims 9 Chapter 2 Materials and Methods 11 2.1 Mice 11 2.2 CLP cells sorting using fluorescence-activated cell sorting (FACS) 11 2.3 Intracellular staining 12 2.4 RT-qPCR 12 2.5 Cleavage Under Target and Tagmentation (CUT&Tag) 13 2.6 Cleavage Under Targeted Accessible Chromatin (CUTAC) 13 2.7 CUT&Tag sequencing data pre-processing 14 2.8 Chromatin state annotation using ChromHMM 14 2.9 Identification of super enhancers from the CUT&Tag data using ROSE 15 2.10 Identification of DNA binding motif from the CUT&Tag data using HOMER 16 2.11 Gene Regulatory Network (GRNs) inference of scRNA-seq using SCENIC 17 2.12 Statistical analysis 18 2.13 Antibody list 18 2.14 Primer list 19 Chapter 3 Results 21 3.1 Setdb1 & Setdb2 are upregulated in CLPs upon R848 stimulation 21 3.2 Histone modification of H3K9 but not H3K27 are induced and maintained in CLPs upon R848 stimulation 22 3.3 Global cDC-and pDC-specific gene histone mark enrichment near TSS is profiled using CUT&Tag 23 3.4 Chromatin accessibility established in early CLP-dependent DC development positively correlates with a later stage of transcriptional profile in bulk RNA-seq of CLPs 24 3.5 Chromatin state discovery and characterization for the epigenetic landscapes of CLPs upon stimulation by ChromHMM 25 3.6 TLR7 signaling induces repressive epigenetic marks in pDC-specific gene loci and active marks in cDC-specific gene loci 26 3.7 SCENIC algorithm predicts cell-type-specific GRNs in CLP-derived DC development inferred from scRNA-seq 27 3.8 H3K9ac and H3K27ac super enhancers may govern different circuits of reprogrammed DC development from CLP-specific gene loci 29 Chapter 4 Discussion 30 4.1 The potential roles of H3K9me3 and H3K9ac in reprogramming of pDC and cDC from CLPs in response to TLR7 stimulation 30 4.2 Epigenetic reprogramming involved in the CLP-derived DC development 30 4.3 Chromatin states annotated by ChromHMM 31 4.4 The inconsistency between SCENIC from scRNA-seq and ROSE analysis from CUT&Tag 32 Chapter 5 Figures 33 Chapter 6 References 55 Chapter 7 Appendix 60 | - |
| dc.language.iso | en | - |
| dc.subject | 共同淋巴前驅細胞 | zh_TW |
| dc.subject | 表觀遺傳 | zh_TW |
| dc.subject | 發炎 | zh_TW |
| dc.subject | 樹突細胞發育 | zh_TW |
| dc.subject | dendritic cell development | en |
| dc.subject | inflammation | en |
| dc.subject | common lymphoid progenitors | en |
| dc.subject | epigenetic | en |
| dc.title | TLR7訊號所驅動的表觀遺傳重塑源自共同淋巴前驅細胞的樹突細胞發育 | zh_TW |
| dc.title | TLR7 signaling induces epigenetic reprogramming of dendritic cell development from common lymphoid progenitors | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 113-2 | - |
| dc.description.degree | 碩士 | - |
| dc.contributor.oralexamcommittee | 林國儀;許家郎 | zh_TW |
| dc.contributor.oralexamcommittee | Kuo-I Lin;Chia-Lang Hsu | en |
| dc.subject.keyword | 表觀遺傳,共同淋巴前驅細胞,樹突細胞發育,發炎, | zh_TW |
| dc.subject.keyword | epigenetic,common lymphoid progenitors,dendritic cell development,inflammation, | en |
| dc.relation.page | 70 | - |
| dc.identifier.doi | 10.6342/NTU202504380 | - |
| dc.rights.note | 同意授權(限校園內公開) | - |
| dc.date.accepted | 2025-08-11 | - |
| dc.contributor.author-college | 醫學院 | - |
| dc.contributor.author-dept | 免疫學研究所 | - |
| dc.date.embargo-lift | 2030-08-11 | - |
| 顯示於系所單位： | 免疫學研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-113-2.pdf 未授權公開取用 | 6.81 MB | Adobe PDF | 檢視/開啟 |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。