Journal articles: 'Memory Cell'

1

Wells, William. "Cell memory." Genome Biology 1 (2000): spotlight—20000508–01. http://dx.doi.org/10.1186/gb-spotlight-20000508-01.

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Bell, Eric B., and Jürgen Westermann. "CD4 memory T cells on trial: immunological memory without a memory T cell." Trends in Immunology 29, no. 9 (2008): 405–11. http://dx.doi.org/10.1016/j.it.2008.06.002.

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Schoenberger, Stephen P. "T cell memory." Seminars in Immunology 21, no. 2 (2009): 51–52. http://dx.doi.org/10.1016/j.smim.2009.02.007.

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Dutton, R. W., L. M. Bradley, and S. L. Swain. "T CELL MEMORY." Annual Review of Immunology 16, no. 1 (1998): 201–23. http://dx.doi.org/10.1146/annurev.immunol.16.1.201.

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Powell, Daniel J. "Abstract 1366: A novel stem cell memory T cell subpopulation intermediate to canonical stem cell memory and central memory T cells in human cancer." Cancer Research 82, no. 12_Supplement (2022): 1366. http://dx.doi.org/10.1158/1538-7445.am2022-1366.

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Abstract Stem memory T cells (Tscm) are integral for effective immunotherapy and antitumor responses, but little is known about Tscm immunobiology in solid human tumors. Here we identify self-renewing and multipotent Tscm tumor-infiltrating lymphocytes (TILs) in human cancer and present a novel Tscm subset which expresses CD45RO, is derived from CD45RO- Tscm T cells, and is capable of self-renewal and multipotency. From the analysis of CD45RO+ Tscm differentiation, phenotyping, gene expression, and the broader TCR repertoire, we find that CD45RO+ Tscm cells are hierarchically positioned in between canonical CD45RO- Tscm cells and central memory T cells. Notably, CD45RO+ Tscm cells exhibit a gene expression profile consistent with effector capabilities and a tumor-specific phenotype that is more similar to T cells associated with successful immunotherapy than canonical Tscm. Thus, we describe a novel Tscm subset in human cancer which has distinct phenotypic, transcriptional, and effector-like attributes that position it as an attractive subset for future basic and clinical research in the setting of cancer immunotherapy. Citation Format: Daniel J. Powell. A novel stem cell memory T cell subpopulation intermediate to canonical stem cell memory and central memory T cells in human cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1366.

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Defrance, Thierry, Morgan Taillardet, and Laurent Genestier. "T cell-independent B cell memory." Current Opinion in Immunology 23, no. 3 (2011): 330–36. http://dx.doi.org/10.1016/j.coi.2011.03.004.

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Wang, Shiyu, Longlong Wang, Yang Liu, Yonggang Zhu, and Ya Liu. "Characteristics of T-cell receptor repertoire of stem cell-like memory CD4+ T cells." PeerJ 9 (August 25, 2021): e11987. http://dx.doi.org/10.7717/peerj.11987.

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Stem cell-like memory T cells (Tscm) combine phenotypes of naïve and memory. However, it remains unclear how T cell receptor (TCR) characteristics contribute to heterogeneity in Tscm and other memory T cells. We compared the TCR-beta (TRB) repertoire characteristics of CD4+ Tscm with those of naïve and other CD4+ memory (Tm) in 16 human subjects. Compared with Tm, Tscm had an increased diversity across all stretches of TRB repertoire structure, a skewed gene usage, and a shorter length distribution of CDR3 region. These distinctions between Tscm and Tm were enlarged in top1000 abundant clonotypes. Furthermore, top1000 clonotypes in Tscm were more public than those in Tm and grouped in more clusters, implying more epitope types recognized by top1000 clonotypes in Tscm. Importantly, self-reactive clonotypes were public and enriched in Tscm rather than Tm, of type one diabetes patients. Therefore, this study highlights the unique features of Tscm different from those of other memory subsets and provides clues to understand the physiological and pathological functions of Tscm.

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8

Visan, Ioana. "Memory B cell induction." Nature Immunology 22, no. 6 (2021): 672. http://dx.doi.org/10.1038/s41590-021-00952-y.

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Paust, Silke, and Ulrich H. von Andrian. "Natural killer cell memory." Nature Immunology 12, no. 6 (2011): 500–508. http://dx.doi.org/10.1038/ni.2032.

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Wang, Xianwei, Hui Peng, and Zhigang Tian. "Innate lymphoid cell memory." Cellular & Molecular Immunology 16, no. 5 (2019): 423–29. http://dx.doi.org/10.1038/s41423-019-0212-6.

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Stockinger, Brigitta, George Kassiotis, and Christine Bourgeois. "CD4 T-cell memory." Seminars in Immunology 16, no. 5 (2004): 295–303. http://dx.doi.org/10.1016/j.smim.2004.08.010.

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Rocha, B., and C. Tanchot. "CD8 T cell memory." Seminars in Immunology 16, no. 5 (2004): 305–14. http://dx.doi.org/10.1016/j.smim.2004.08.011.

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Dolinšek, J., M. Feuerbacher, M. Jagodič, Z. Jagličić, M. Heggen, and K. Urban. "A thermal memory cell." Journal of Applied Physics 106, no. 4 (2009): 043917. http://dx.doi.org/10.1063/1.3207791.

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Snape, Alison. "Methylation and cell memory." Trends in Genetics 17, no. 6 (2001): 315. http://dx.doi.org/10.1016/s0168-9525(01)02352-6.

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15

Lanzavecchia, Antonio, and Federica Sallusto. "Human B cell memory." Current Opinion in Immunology 21, no. 3 (2009): 298–304. http://dx.doi.org/10.1016/j.coi.2009.05.019.

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O’Sullivan, Timothy E., Joseph C. Sun, and Lewis L. Lanier. "Natural Killer Cell Memory." Immunity 43, no. 4 (2015): 634–45. http://dx.doi.org/10.1016/j.immuni.2015.09.013.

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17

Anjamrooz, Seyed Hadi. "Cell memory‐based therapy." Journal of Cellular and Molecular Medicine 19, no. 11 (2015): 2682–89. http://dx.doi.org/10.1111/jcmm.12646.

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18

Mantovani, Alberto. "Investigating T-cell memory." Nature 407, no. 6800 (2000): 40. http://dx.doi.org/10.1038/35024159.

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Visan, Ioana. "Epithelial stem cell memory." Nature Immunology 18, no. 12 (2017): 1287. http://dx.doi.org/10.1038/ni.3877.

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Rosenblum, Michael D., Sing Sing Way, and Abul K. Abbas. "Regulatory T cell memory." Nature Reviews Immunology 16, no. 2 (2015): 90–101. http://dx.doi.org/10.1038/nri.2015.1.

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21

Bell, Elaine. "SAPping B-cell memory." Nature Reviews Immunology 3, no. 2 (2003): 93. http://dx.doi.org/10.1038/nri1009.

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Chen, G. J., P. A. Rosenthal, and M. R. Beasley. "Kinetic inductance memory cell." IEEE Transactions on Appiled Superconductivity 2, no. 2 (1992): 95–100. http://dx.doi.org/10.1109/77.139225.

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23

McLean, Angela R. "Modelling T Cell Memory." Journal of Theoretical Biology 170, no. 1 (1994): 63–74. http://dx.doi.org/10.1006/jtbi.1994.1168.

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24

Klinman, Norman. "Introduction: B-cell memory." Seminars in Immunology 9, no. 4 (1997): 217. http://dx.doi.org/10.1006/smim.1997.0074.

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Lee, Kwangseok, and Woo Young Choi. "Nanoelectromechanical Memory Cell (T Cell) for Low-Cost Embedded Nonvolatile Memory Applications." IEEE Transactions on Electron Devices 58, no. 4 (2011): 1264–67. http://dx.doi.org/10.1109/ted.2010.2104154.

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26

Levack, Russell C., Kevin J. Kenderes, Berenice Cabrera-Martinez, and Gary Winslow. "Stem cell-like T-bet+ IgM memory cells generate multi-lineage effector B cells." Journal of Immunology 200, no. 1_Supplement (2018): 48.6. http://dx.doi.org/10.4049/jimmunol.200.supp.48.6.

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Abstract Our laboratory has been studying the differentiation of CD11c+ T-bet+ IgM memory B cells during secondary ehrlichial infection. These cells are closely related to B cells that have been described in a range of other contexts, including hepatitis, AIDs, malaria, SLE, and age-related autoimmunity. Following secondary infection, IgM memory cells, as a population, undergo self-renewal, and differentiate into effector cells, including splenic and bone marrow antibody secreting cells (ASC). Moreover, IgM memory cells enter germinal centers, where they undergo class-switch recombination and give rise to class-switched memory and effector cells. Although these data suggest that a single memory cell has multi-lineage potential, we sought to formally address this question by searching for shared clones among IgM memory cell-derived effector cells. Among the IgM memory cell-derived subsets, we identified several clones common to all effector cell populations. The number of common clones varied for each pairwise comparison of effector cells and suggested lineal relationships. IgM memory cells accumulated mutations following rechallenge; although all memory cell-derived subsets displayed similar numbers of V region mutations. Lineage analysis demonstrated that the effector cell subsets underwent varying degrees of clonal diversification, although this was clone-dependent. These studies reveal that a single IgM memory cell clone can give rise to different memory and effector cell subsets, that is, they exhibit stem cell properties. This property distinguishes these T-bet+ IgM memory cells as a unique memory cell subset.

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27

Croft, M., L. M. Bradley, and S. L. Swain. "Naive versus memory CD4 T cell response to antigen. Memory cells are less dependent on accessory cell costimulation and can respond to many antigen-presenting cell types including resting B cells." Journal of Immunology 152, no. 6 (1994): 2675–85. http://dx.doi.org/10.4049/jimmunol.152.6.2675.

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Abstract Secondary responses to Ag in vivo are characterized by more rapid kinetics and greatly enhanced magnitude compared with primary responses. For CD4+ T cells, this is in part due to a greater frequency of Ag-specific memory cells, and may also reflect differences in responsiveness of memory vs naive cells to stimulation. To compare activation requirements and the role of accessory cells, naive and memory cells were stimulated with immobilized anti-CD3 in the presence or absence of APC. With anti-CD3 alone, naive cells proliferated slightly but produced no detectable IL-2, whereas memory cells proliferated well with significant IL-2 production. Increasing numbers of T-depleted APC greatly enhanced responses of naive cells to levels equivalent to those of memory cells, whereas for memory cells only IL-2 production increased slightly. The response of naive cells was equivalent in magnitude and kinetics to that of memory cells when low density APC, enriched in dendritic cells and depleted of resting B cells, were used with anti-CD3. To directly compare naive and memory responses in an Ag-specific model, we examined CD4+ cells specific for a peptide of pigeon cytochrome c fragment isolated from TCR-alpha beta transgenic mice. Naive cells were compared with 4-day activated blasts (effectors) and memory cells generated by adoptive transfer of effectors to adult thymectomized bone marrow reconstituted mice, in which the cells return to a resting state but still respond to recall Ag. Naive cells responded to Ag on dendritic cells and activated B cells but not on resting B cells or macrophages. In contrast, both memory cells and effectors were stimulated by all APCs, including resting B cells and macrophage to a limited extent. The ability of memory cells to respond to all APC types was confirmed using Ag-specific cells generated by in vivo priming with keyhole limpet hemocyanin. These results suggest that memory cells are considerably less dependent on accessory cell costimulation than naive cells, but that naive cells can respond equivalently in both magnitude and kinetics if Ag is presented on costimulatory APCs such as dendritic cells. In addition, these studies suggest that the enhanced secondary T cell response is due to a combination of the increased frequency of Ag-specific cells and their ability to react to Ag presented on a wider range of APC types, rather than an inherent capacity of memory T cells to respond better and faster.

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28

Highton, Andrew J., Madeleine E. Zinser, Lian Ni Lee, et al. "Single-cell transcriptome analysis of CD8+ T-cell memory inflation." Wellcome Open Research 4 (May 9, 2019): 78. http://dx.doi.org/10.12688/wellcomeopenres.15115.1.

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Background: Persistent viruses such as murine cytomegalovirus (MCMV) and adenovirus-based vaccines induce strong, sustained CD8+ T-cell responses, described as memory “inflation”. These retain functionality, home to peripheral organs and are associated with a distinct transcriptional program. Methods: To further define the nature of the transcriptional mechanisms underpinning memory inflation at different sites we used single-cell RNA sequencing of tetramer-sorted cells from MCMV-infected mice, analyzing transcriptional networks in virus-specific populations in the spleen and gut intra-epithelial lymphocytes (IEL). Results: We provide a transcriptional map of T-cell memory and define a module of gene expression, which distinguishes memory inflation in spleen from resident memory T-cells (TRM) in the gut. Conclusions: These data indicate that CD8+ T-cell memory in the gut epithelium induced by persistent viruses and vaccines has a distinct quality from both conventional memory and “inflationary” memory which may be relevant to protection against mucosal infections.

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Welsh, Raymond M., Susan E. Stepp, and Eva Szomolanyi-Tsuda. "B cell memory: Sapping the T cell." Nature Medicine 9, no. 2 (2003): 164–66. http://dx.doi.org/10.1038/nm0203-164.

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McHeyzer-Williams, Louise J., Melinda Cool, and Michael G. McHeyzer-Williams. "Antigen-Specific B Cell Memory." Journal of Experimental Medicine 191, no. 7 (2000): 1149–66. http://dx.doi.org/10.1084/jem.191.7.1149.

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The mechanisms that regulate B cell memory and the rapid recall response to antigen remain poorly defined. This study focuses on the rapid expression of B cell memory upon antigen recall in vivo, and the replenishment of quiescent B cell memory that follows. Based on expression of CD138 and B220, we reveal a unique and major subtype of antigen-specific memory B cells (B220−CD138−) that are distinct from antibody-secreting B cells (B220+/−CD138+) and B220+CD138− memory B cells. These nonsecreting somatically mutated B220− memory responders rapidly dominate the splenic response and comprise >95% of antigen-specific memory B cells that migrate to the bone marrow. By day 42 after recall, the predominant quiescent memory B cell population in the spleen (75–85%) and the bone marrow (>95%) expresses the B220− phenotype. Upon adoptive transfer, B220− memory B cells proliferate to a lesser degree but produce greater amounts of antibody than their B220+ counterparts. The pattern of cellular differentiation after transfer indicates that B220− memory B cells act as stable self-replenishing intermediates that arise from B220+ memory B cells and produce antibody-secreting cells on rechallenge with antigen. Cell surface phenotype and Ig isotype expression divide the B220− compartment into two main subsets with distinct patterns of integrin and coreceptor expression. Thus, we identify new cellular components of B cell memory and propose a model for long-term protective immunity that is regulated by a complex balance of committed memory B cells with subspecialized immune function.

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Pordes, Aniko Ginta, Christina Hausl, Peter Allacher, et al. "Requirements for Co-Stimulation in T-Cell Dependent and T-Cell Independent Re-Stimulation of FVIII-Specific Memory B Cells." Blood 112, no. 11 (2008): 238. http://dx.doi.org/10.1182/blood.v112.11.238.238.

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Abstract Memory B cells specific for factor VIII (FVIII) are critical for maintaining FVIII inhibitors in patients with hemophilia A. They are precursors of anti-FVIII antibody-producing plasma cells and are highly efficient antigen-presenting cells for the activation of T cells. The eradication of FVIII-specific memory B cells will be a prerequisite for any successful new approach to induce immune tolerance in patients with FVIII inhibitors. Little is known about the regulation of these cells. Previously we showed that ligands for toll-like receptors (TLR) 7 and 9 are able to re-stimulate FVIII-specific memory B cells in the absence of T-cell help. However, alternative “helper cells” such as dendritic cells are essential for providing help to memory B cells under such conditions. Based on these findings, we asked which co-stimulatory interactions are required for the restimulation of memory B cells in the presence of dendritic cells and ligands for TLR and whether these co-stimulatory interactions are the same as those required for the restimulation of memory B cells in the presence of activated T cells. We used spleen cells from hemophilic mice treated with human FVIII to generate highly purified populations of memory B cells, CD4+ T cells and dendritic cells. The required purity was achieved by a combination of magnetic bead separation and fluorescence-activated cell sorting. The memory B cell compartment was specified by the expression of CD19 together with IgG and the absence of surface IgM and IgD. Memory B cells were cultured in the presence of FVIII to stimulate their differentiation into anti-FVIII antibody-producing plasma cells. Different combinations of CD4+ T cells, ligands for TLR 7 and 9 and dendritic cells were added to the memory-B-cell cultures. Blocking antibodies and competitor proteins were used to specify the co-stimulatory interactions required for the re-stimulation of memory B cells in the presence of either CD4+ T cells or dendritic cells and ligands for TLR 7 and 9. Our results demonstrate that the blockade of B7-1 and B7-2 as well as the blockade of CD40L inhibit the re-stimulation of FVIII-specific memory B cells and their differentiation into anti-FVIII antibody-producing plasma cells in the presence of T-cell help. Similar requirements apply for the re-stimulation of memory B cells in the presence of dendritic cells and ligands for TLR 7 or 9. Dendritic cells in the absence of ligands for TLR are not able to provide help for the re-stimulation of memory B cells, which indicates that dendritic cells need to be activated. Furthermore, ligands for TLR 7 or 9 were not able to re-stimulate memory B cells in the complete absence of dendritic cells. Based on these results we conclude that dendritic cells activated by ligands for TLR 7 or 9 can substitute for activated CD4+ T cells in providing co-stimulatory help for memory-B-cell re-stimulation. CD40-CD40L interactions seem to be the most important co-stimulatory interactions for the re-stimulation of memory B cells, not only in the presence of activated CD4+ T cells but also in the presence of ligands for TLR and dendritic cells.

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32

Jacob, Joshy, and David Baltimore. "Modelling T-cell memory by genetic marking of memory T cells in vivo." Nature 399, no. 6736 (1999): 593–97. http://dx.doi.org/10.1038/21208.

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33

Gage, Emily, Neal Van Hoeven, and Rhea Coler. "Memory CD4+ T cells guide memory B cell adaptability to drifting influenza vaccination." Journal of Immunology 200, no. 1_Supplement (2018): 125.12. http://dx.doi.org/10.4049/jimmunol.200.supp.125.12.

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Abstract Influenza A annually infects 5–10% of the world’s human population resulting in an estimated one million deaths. Unlike other infectious agents, where either infection or vaccination against the disease confers long-term immunity, influenza causes annual epidemics and re-infects previously exposed individuals as a result of antigenic drift in the surface glycoprotein hemagglutinin (HA). Due to antigenic drift, the human immune system is simultaneously exposed to both novel and conserved parts of the influenza virus through vaccination and/or infection multiple times throughout life. Preexisting immunity by infection or vaccination influences subsequent neutralizing antibody responses, the correlate of protection for influenza. To understand how preexisting immunity augments future responses to drifted influenza immunization, we established mouse models, sequentially infecting mice with a H1N1 strain and then immunizing with a second drifted H1N1 strain. Mice previously infected with A/CA have increased neutralizing antibody response (nAb) to A/PR upon immunization with A/PR HA. This increase in nAbs was dependent on CD4+ T cell and memory B cell, correlating with CD4+ T cell reactivity conserved across both influenza HA’s. We also found increased germinal center PR8-specific B and T follicular helper cells post vaccination in the draining lymph node. These results suggest conserved MHC Class II restricted epitopes within HA are critical for B cells to adapt to drifting influenza and could be leveraged to boost out subsequent neutralizing antibody responses. Understanding the mechanism by which preexisting immune responses shape future responses is essential to optimize and leverage vaccination strategies.

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34

Bradley, Linda M. "CD4+ cell memory: the enigma of Th1 cells." Trends in Molecular Medicine 9, no. 5 (2003): 186–88. http://dx.doi.org/10.1016/s1471-4914(03)00053-4.

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35

Ghanimi, Hussein A., Waleed Khaled Younis Albahadly, Arash Abdolmaleki, Ali Roohbakhsh, and Nosaibeh Riahi Zaniani. "Assessment of Hippocampal Cell Death and Memory Deficits in Rats Following Neonatal Stress." NeuroQuantology 20, no. 4 (2022): 434–42. http://dx.doi.org/10.14704/nq.2022.20.4.nq22256.

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Objective: Neonatal stress (NS) has harmful effects on the hippocampal neurons of rat neonates. It has been reported to enhance neuronal cell death and impair memory behaviors. The researchers conducted this study in order to assess NS’s effects on hippocampal apoptosis and memory deficits in rat neonates’ hippocampus. Methods: Three groups of male Wistar rat neonates exposed to NS; rat neonates reared with 1 hour neonatal isolation (NI) for 8 consecutive days (P2-P9), rat neonates exposed to febrile seizure (FS) at day 10 (P10) and rat neonates reared with both NI plus FS (NI-FS). Control group was reared normally. Novel object recognition test (NORT) carried out to evaluate the effects of NI, FS and NI-FS on memory deficits. At day 22 (P22), Terminal deoxynucleotidyl transferase- mediated dUTP nick end labeling (TUNEL) assay was done. Results: NORT demonstrated that rat neonates exposed to NI-FS had short-term and long-term memory deficits (P<0.01 and P<0.001). Rat neonates experienced NI had long-term memory deficits (P<0.05). TUNEL assay results showed that NI-FS increased the count of hippocampal apoptotic neurons in Cornu Ammonis 1 (CA1), Cornu Ammonis 3 (CA3) and dentate gyrus (DG) subfields (P<0.001, P<0.001 and P<0.001). Also, NI increased the count of hippocampal TUNEL positive cells in CA3 and DG subfields (P<0.05 and P<0.01). In addition, FS increased the count of hippocampal apoptotic neurons in DG subfield (P<0.05). Conclusion: The present results showed that NS exerted apoptotic effect and induced memory deficits in the hippocampus of rat neonate.

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Yokochi, T., Y. Kato, T. Sugiyama, et al. "Lipopolysaccharide induces apoptotic cell death of B memory cells and regulates B cell memory in antigen-nonspecific manner." FEMS Immunology & Medical Microbiology 15, no. 1 (1996): 1–8. http://dx.doi.org/10.1111/j.1574-695x.1996.tb00351.x.

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Gisbergen, Klaas P. J. M., Kyra D. Zens, and Christian Münz. "T‐cell memory in tissues." European Journal of Immunology 51, no. 6 (2021): 1310–24. http://dx.doi.org/10.1002/eji.202049062.

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Jameson, Stephen C. "T Cell Memory: without Prompting." Journal of Immunology 190, no. 9 (2013): 4443–44. http://dx.doi.org/10.4049/jimmunol.1300671.

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Miloshevsky, Alexander, Niketh Nair, Neena Imam, and Yehuda Braiman. "High-Tc Superconducting Memory Cell." Journal of Superconductivity and Novel Magnetism 35, no. 2 (2021): 373–82. http://dx.doi.org/10.1007/s10948-021-06069-5.

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Todryk, Stephen M. "T Cell Memory to Vaccination." Vaccines 6, no. 4 (2018): 84. http://dx.doi.org/10.3390/vaccines6040084.

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Most immune responses associated with vaccination are controlled by specific T cells of a CD4+ helper phenotype which mediate the generation of effector antibodies, cytotoxic T lymphocytes (CTLs), or the activation of innate immune effector cells. A rapidly growing understanding of the generation, maintenance, activity, and measurement of such T cells is leading to vaccination strategies with greater efficacy and potentially greater microbial coverage.

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Stone, N. J., and H. Ahmed. "Silicon single electron memory cell." Applied Physics Letters 73, no. 15 (1998): 2134–36. http://dx.doi.org/10.1063/1.122401.

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Fuchs, Ephraim. "Clues to B–cell memory." Nature Medicine 2, no. 7 (1996): 743–44. http://dx.doi.org/10.1038/nm0796-743.

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O'Connor, K. J. "The twin-port memory cell." IEEE Journal of Solid-State Circuits 22, no. 5 (1987): 712–20. http://dx.doi.org/10.1109/jssc.1987.1052804.

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Heidt, Sebastiaan, and Frans HJ Claas. "Preventing Memory B Cell Formation." Transplantation 100, no. 8 (2016): 1605–6. http://dx.doi.org/10.1097/tp.0000000000001254.

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Hosokawa, Tomohide, Akira Aoike, Masamichi Hosono, Shigehiro Motoi, and Keiichi Kawai. "Studies on B-Cell Memory." Microbiology and Immunology 33, no. 11 (1989): 941–49. http://dx.doi.org/10.1111/j.1348-0421.1989.tb00981.x.

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Reed, M. A., J. Chen, A. M. Rawlett, D. W. Price, and J. M. Tour. "Molecular random access memory cell." Applied Physics Letters 78, no. 23 (2001): 3735–37. http://dx.doi.org/10.1063/1.1377042.

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Tuma, Rabiya S. "Signaling memory from cell shape." Journal of Cell Biology 170, no. 7 (2005): 1015. http://dx.doi.org/10.1083/jcb1707iti4.

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Sun, Joseph C., and Lewis L. Lanier. "Versatility in NK cell memory." Immunology & Cell Biology 89, no. 3 (2010): 327–29. http://dx.doi.org/10.1038/icb.2010.162.

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Selin, Liisa K., Meei Y. Lin, Kristy A. Kraemer, et al. "Attrition of T Cell Memory." Immunity 11, no. 6 (1999): 733–42. http://dx.doi.org/10.1016/s1074-7613(00)80147-8.

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Aksan, Isil. "Transcriptional memory during cell division." Trends in Biochemical Sciences 27, no. 5 (2002): 228–29. http://dx.doi.org/10.1016/s0968-0004(02)02121-7.

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Journal articles on the topic 'Memory Cell'

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