Relevant bibliographies by topics / TIM3

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'TIM3'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "TIM3"

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Gong, Zhiliang, Daniel Kerr, Gregory T. Tietjen, James Michael Henderson, Adrienne M. Luoma, Wei Bu, Kathleen D. Cao, et al. "Mechanism of TIM1, TIM3, and TIM4 Binding to Lipid Membranes." Biophysical Journal 110, no. 3 (February 2016): 592a. http://dx.doi.org/10.1016/j.bpj.2015.11.3159.

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Alderton, Gemma K. "TIM3 suppresses antitumour DCs." Nature Reviews Cancer 12, no. 9 (August 24, 2012): 584. http://dx.doi.org/10.1038/nrc3349.

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Buckland, Jenny. "Tim3 – tolerance's little helper!" Nature Reviews Immunology 3, no. 11 (November 2003): 844. http://dx.doi.org/10.1038/nri1235.

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Alderton, Gemma K. "TIM3 suppresses antitumour DCs." Nature Reviews Immunology 12, no. 9 (August 24, 2012): 621. http://dx.doi.org/10.1038/nri3288.

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Jayaraman, Pushpa, Isabel Sada-Ovalle, Sarah Beladi, Ana C. Anderson, Valerie Dardalhon, Chie Hotta, Vijay K. Kuchroo, and Samuel M. Behar. "Tim3 binding to galectin-9 stimulates antimicrobial immunity." Journal of Experimental Medicine 207, no. 11 (October 11, 2010): 2343–54. http://dx.doi.org/10.1084/jem.20100687.

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T cell immunoglobulin and mucin domain 3 (Tim3) is a negative regulatory molecule that inhibits effector TH1-type responses. Such inhibitory signals prevent unintended tissue inflammation, but can be detrimental if they lead to premature T cell exhaustion. Although the role of Tim3 in autoimmunity has been extensively studied, whether Tim3 regulates antimicrobial immunity has not been explored. Here, we show that Tim3 expressed on TH1 cells interacts with its ligand, galectin-9 (Gal9), which is expressed by Mycobacterium tuberculosis–infected macrophages to restrict intracellular bacterial growth. Tim3–Gal9 interaction leads to macrophage activation and stimulates bactericidal activity by inducing caspase-1–dependent IL-1β secretion. We propose that the TH1 cell surface molecule Tim3 has evolved to inhibit growth of intracellular pathogens via its ligand Gal9, which in turn inhibits expansion of effector TH1 cells to prevent further tissue inflammation.
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Fu, Rong, Shaoxue Ding, Chunyan Liu, Bingnan Liu, Hui Liu, Liu Zhaoyun, Tong Chen, Tian Zhang, Zonghong Shao, and Ting Wang. "The Role of Decreased TIM-3 Expression of Natural Killer Cells in the Immune Pathogenesis of Severe Aplastic Anemia." Blood 134, Supplement_1 (November 13, 2019): 3747. http://dx.doi.org/10.1182/blood-2019-127769.

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In this study, we intend to detect the expression of TIM3 on peripheral blood NK cells in SAA patients to reveal the further immune pathogenesis of SAA. Furthermore, we tried to further elucidate the changes of functions of TIM3+ NK and TIM3-NK cells in SAA by measuring the functional molecules and cytotoxic activity of TIM3+ NK and TIM3-NK cells. Finally, we observed the therapeutic effects of TIM3 blocker, TIM3+ NK infusion and TIM3-NK infusion on SAA mice model. 1.The TIM3 expression on NK cells in SAA untreated patients was significantly lower than that in SAA remission patients (P<0.05) and normal controls (P<0.01). 2. TIM3-NK cells expressed higher NKG2D and Granzyme B than TIM3+ NK cells in untreated SAA patients. The expression of NKG2A, CD158a and CD158b on TIM3-NK cells were lower than TIM3+ NK cells. 3. The expression of CD80 and CD86 were significantly decreased after being incubated with TIM3-NK and TIM3+NK cells in SAA, especially mDC+ TIM3-NK group, significantly lower than mDC+TIM3+NK group(P<0.01). 4. The apoptosis rate (AR) of K562 cells were significantly increased after being incubated with TIM3-NK and TIM3+ NK cells in SAA, especially K562+TIM3-NK group, significantly higher than K562+TIM3+NK groups(P<0.01). 5. There was no significant difference in the level of AKT of receptor post-signal pathway protein between TIM3-NK and TIM3+ NK cells in patients with SAA, but the level of P-AKT in TIM3-NK cells is higher than TIM3+ NK cells. 6. AA mice model was established. The TIM3 expression on peripheral blood NK cells in SAA mice was significantly lower than that in TBI mice (P<0.05) and normal controls (P<0.05). TIM3-NK cells expressed higher NKG2D than TIM3+ NK cells (P<0.05). The level of P-AKT and PI3K in TIM3-NK cells is higher than TIM3+NK cells. 7. On the 17th day of model establishment, the weight, hemogram and bone marrow cells count of AA mice were significantly lower than that of NC group (p<0.05).The weight, hemogram and bone marrow cells count of CsA treatment group, TIM3+ NK cell infusion treatment group, TIM3-NK cell infusion treatment group, CsA combined with TIM3-NK cell infusion treatment group, CsA combined with TIM3 blocker treatment group has some improvement, TIM3 blocker alone treatment of AA mice slightly increased, the effect is not significant(P>0.05), and combined with CsA has no significant synergistic effect. The therapeutic effect of TIM3-NK cell infusion group was better than that of TIM3+ NK cell infusion group. The therapeutic effect of CsA combined with TIM3-NK cell infusion group was more significant than that of CsA alone group. TIM3-NK cell infusion therapy may have some synergistic effect with CSA. Conclusions 1. In this study, we found that untreated patients with SAA had lower TIM3 expression on NK cells compared with normal controls, andwere correlated with the severity of pancytopenia of SAA. 2. We further confirmed that the expression of activation molecules on TIM3-NK cells was increased and the killing function was enhanced compared with TIM3+NK cells. In addition, TIM3-NK cells have enhanced inhibition of mDCs and K562 cells and play an immunomodulatory role in SAA. Therefore, TIM3 exerts its inhibitory effect on NK cells and participates in the immune pathogenesis of SAA. Low expression of TIM3 contributes to the enhancement of NK cell function, which in turn inhibits the immune activation state of SAA and improves the disease level. 3. The expression of TIM3 on NK cells of AA mice decreased, and the activity of TIM3-NK cells was stronger than that of TIM3+ NK cells, which was consistent with the decrease of TIM3 on NK cells of SAA patients and the strong activity of TIM3-NK cells. After TIM3-NK cell reinfusion, the general condition, blood cell count and bone marrow cell count of SAA mice were improved, and the combined treatment of CsA was more effective. It may further clarify the immune pathogenesis of SAA and provide a new treatment target to improve the efficacy of SAA treatment. Disclosures No relevant conflicts of interest to declare.
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Koguchi, Ken, David E. Anderson, Li Yang, Kevin C. O'Connor, Vijay K. Kuchroo, and David A. Hafler. "Dysregulated T cell expression of TIM3 in multiple sclerosis." Journal of Experimental Medicine 203, no. 6 (June 5, 2006): 1413–18. http://dx.doi.org/10.1084/jem.20060210.

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T cell immunoglobulin- and mucin domain–containing molecule (TIM)3 is a T helper cell (Th)1–associated cell surface molecule that regulates Th1 responses and promotes tolerance in mice, but its expression and function in human T cells is unknown. We generated 104 T cell clones from the cerebrospinal fluid (CSF) of six patients with multiple sclerosis (MS) (n = 72) and four control subjects (n = 32) and assessed their cytokine profiles and expression levels of TIM3 and related molecules. MS CSF clones secreted higher amounts of interferon (IFN)-γ than did those from control subjects, but paradoxically expressed lower levels of TIM3 and T-bet. Interleukin 12–mediated polarization of CSF clones induced substantially higher amounts of IFN-γ secretion but lower levels of TIM3 in MS clones relative to control clones, demonstrating that TIM3 expression is dysregulated in MS CSF clones. Reduced levels of TIM3 on MS CSF clones correlated with resistance to tolerance induced by costimulatory blockade. Finally, reduction of TIM3 on ex vivo CD4+ T cells using small interfering (si)RNA enhanced proliferation and IFN-γ secretion, directly demonstrating that TIM3 expression on human T cells regulates proliferation and IFN-γ secretion. Failure to up-regulate T cell expression of TIM3 in inflammatory sites may represent a novel, intrinsic defect that contributes to the pathogenesis of MS and other human autoimmune diseases.
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Roussel, Mikaël, Kieu-Suong Le, Clémence Granier, Francisco Llamas Gutierrez, Etienne Foucher, Simon Le Gallou, Céline Pangault, et al. "Functional characterization of PD1+TIM3+ tumor-infiltrating T cells in DLBCL and effects of PD1 or TIM3 blockade." Blood Advances 5, no. 7 (March 31, 2021): 1816–29. http://dx.doi.org/10.1182/bloodadvances.2020003080.

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Abstract In diffuse large B-cell lymphoma (DLBCL), tumor-infiltrating T lymphocytes (TILs) are involved in therapeutic responses. However, tumor-specific TILs can be dysfunctional, with impaired effector functions. Various mechanisms are involved in this exhaustion, and the increased expression of programmed cell death receptor 1 (PD1) and TIM3 on dysfunctional cells suggests their involvement. However, conflicting data have been published regarding their expression or coexpression in DLBCL. We evaluated the presence and phenotype of CD4+ and CD8+ TILs in freshly collected tumor tissues in DLBCL and compared the results with those in follicular lymphoma, classical Hodgkin lymphoma, and nonmalignant reactive lymphadenopathy. We found that TILs expressing both PD1 and TIM3 were expanded in DLBCL, particularly in the activated B cell–like subgroup. Isolated PD1+TIM3+ TILs exhibited a transcriptomic signature related to T-cell exhaustion associated with a reduction in cytokine production, both compromising the antitumor immune response. However, these cells expressed high levels of cytotoxic molecules. In line with this, stimulated PD1+TIM3+ TILs from DLBCL patients exhibited reduced proliferation and impaired secretion of interferon-γ, but these functions were restored by the blockade of PD1 or TIM3. In summary, the PD1+TIM3+ TIL population is expanded and exhausted in DLBCL but can be reinvigorated with appropriate therapies.
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Josuttis, Manfred. "1 Tim3, 16 24.12.2007 Christvesper." Göttinger Predigtmeditationen 62, no. 1 (October 2007): 42–47. http://dx.doi.org/10.13109/gpre.2007.62.1.42.

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Leavy, Olive. "TIM3: dual role in immunity." Nature Reviews Immunology 8, no. 1 (January 2008): 4. http://dx.doi.org/10.1038/nri2239.

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Dissertations / Theses on the topic "TIM3"

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Barlow, J. L. "Investigation of the immunomodulatory roles of Tim1 and Tim3 in the lung." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596370.

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To specifically investigate the necessity for Tim1 and Tim3 during an ovalbumin- (OVA) induced, type 2-mediated allergic lung model, havcr1-/- and havcr2-/- mice were backcrossed to the BALB/c background over six generations. The allergic lung response was assessed using unrestrained whole body plethysmography to test lung function and, by analysing, cellular infiltration into the bronchoalveolar lavage (BAL), mucus production in the lung, eosinophilia, the cytokine and proliferative response of OVA-restimulated lymph node cells, and OVA-specific serum immunoglobulin production. The data demonstrate that whilst Tim3 is expressed in the lung by CD4+CD25+, and CD11c+ cells, it is not essential for any aspect of the allergic lung response tested. Tim1 was also expressed in the lung following an OVA-induced type 2 immune response, but only on CD19+B cells. Whilst Tim1 was not essential for many aspects of the allergic lung response which were tested, OVA treated havcr1-/- mice did show a statistically significant deficit in blood and BAL eosinophils. To further understand the role of Tim3 in the naïve immune response, in vitro, a Tim3-human IgG1 fusion protein (Tim3Ig) was generated. Similarly, as Tim5 is not expressed in naïve tissue, a Tim5-human IgG1 fusion protein (Tim5Ig) was also generated as a control. Flow cytometric analysis using Tim3Ig led to the detection of an unknown binding partner for Tim3Ig on CD19/B220+ B cells, but not on CD3+ T cells. The interaction of Tim3Ig with B cells led to a Toll4- and FcgRII receptor-independent increase in proliferation and upregulation of the lymphocyte activation marker CD69, in a naive, as well as in an anti-IgM stimulated B cell population. These data demonstrate the identification of a novel function for Tim3 in the regulation of B cell proliferation and activation.
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Zhang, Shengtao. "Klonierung, Expression und initiale Charakterisierung vom humanen TIM3." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972570357.

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Jacques, Miye K. "Role of Tim3 in Mediating T Cell Exhaustion During Chronic Mycobacterium Tuberculosis Infection." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/912.

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Mycobacterium tuberculosis infection is one of the leading causes of mortality worldwide. One third of the population is estimated to be infected, however only 5-10% of those individuals can transmit the disease. While T cell immunity initially limits mycobacterium growth, it is unclear why T cell immunity fails to sterilize the infection and prevent subsequent recrudescence. One hypothesis is T cell exhaustion is mediating the failure of T cell immunity late during infection. Here we show the development of T cell exhaustion during chronic infection, and that the inhibitory receptor T cell-immunoglobulin and mucin domain containing 3 (TIM3) mediates the development of T cell exhaustion. TIM3 accumulates on the surface of T cells throughout the course of infection and there is a subsequent decrease in effector cytokine production, such as IL-2, TNFα, and IFNγ. Furthermore, antibody blockade of TIM3 restores T cell function and improves bacterial control. Our results show that TIM3 is mediating T cell exhaustion during chronic TB infection and leading to suboptimal bacterial control.
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Jacques, Miye K. "Role of Tim3 in Mediating T Cell Exhaustion During Chronic Mycobacterium Tuberculosis Infection." eScholarship@UMMS, 2007. http://escholarship.umassmed.edu/gsbs_diss/912.

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Mycobacterium tuberculosis infection is one of the leading causes of mortality worldwide. One third of the population is estimated to be infected, however only 5-10% of those individuals can transmit the disease. While T cell immunity initially limits mycobacterium growth, it is unclear why T cell immunity fails to sterilize the infection and prevent subsequent recrudescence. One hypothesis is T cell exhaustion is mediating the failure of T cell immunity late during infection. Here we show the development of T cell exhaustion during chronic infection, and that the inhibitory receptor T cell-immunoglobulin and mucin domain containing 3 (TIM3) mediates the development of T cell exhaustion. TIM3 accumulates on the surface of T cells throughout the course of infection and there is a subsequent decrease in effector cytokine production, such as IL-2, TNFα, and IFNγ. Furthermore, antibody blockade of TIM3 restores T cell function and improves bacterial control. Our results show that TIM3 is mediating T cell exhaustion during chronic TB infection and leading to suboptimal bacterial control.
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Zhang, Shengtao [Verfasser], K. [Gutachter] Erb, O. [Gutachter] Liesenfeld, and T. [Gutachter] Kamradt. "Klonierung, Expression und initiale Charakterisierung vom humanen TIM3 / Shengtao Zhang ; Gutachter: K. Erb, O. Liesenfeld, T. Kamradt." Berlin : Humboldt-Universität zu Berlin, 2004. http://d-nb.info/1207664405/34.

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Stein, Julia [Verfasser], and Marion [Akademischer Betreuer] Subklewe. "Bispezifische Antikörper in der Immuntherapie der Akuten Myeloischen Leukämie: Charakterisierung eines TIM3/CD3-Konstrukts in Hinblick auf Resistenzmechanismen / Julia Stein ; Betreuer: Marion Subklewe." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://nbn-resolving.de/urn:nbn:de:bvb:19-283412.

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Takeuchi, Yasuhide. "Frequent germline mutations of HAVCR2 in sporadic subcutaneous panniculitis-like T-cell lymphoma." Kyoto University, 2020. http://hdl.handle.net/2433/253177.

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Joelsons, Gabriel. "Avaliação molecular das disfunções subclínicas do enxerto renal : quantificação gênica de perforina, TIM3, FOXP3, TGF-β, CTGF e CD138 no sangue periférico de pacientes com função estável que realizaram biópsia protocolar no terceiro mês após o transplante renal." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2014. http://hdl.handle.net/10183/106762.

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Introdução: A sobrevivência em curto prazo dos transplantes renais tem melhorado notavelmente nas últimas duas décadas. No entanto, a sobrevivência em longo prazo de enxertos e pacientes ainda são muito inferiores ao desejado e a maioria dos enxertos são perdidos por falecimento dos receptores e deterioração crônica da função do enxerto. Acredita-se que a maior parte das lesões que resultam em encurtamento da sobrevida do enxerto se iniciam logo após o transplante e muitas vezes são subclínicas. O desenvolvimento de biomarcadores não invasivos para identificar com precisão as lesões sub-clínicas, sem a necessidade de biópsias de protocolo, seria um grande passo para a prática clínica de transplantes de órgãos, uma vez que permitiria o reconhecimento precoce de eventos de agressões ao enxerto e poderia levar a adequadas ações terapêuticas potencialmente propiciando sobrevida mais prolongada dos aloenxertos. Objetivos: O objetivo do presente estudo foi avaliar o potencial diagnóstico de agressões sub-clínicas da análise molecular não-invasiva da expressão gênica de leucócitos do sangue periférico em receptores de transplante renal com função estável em curto prazo. Métodos: Cento e trinta e seis pacientes renais com função estável do enxerto foram arrolados no estudo e realizaram biópsia protocolar no 3º mês póstransplante. Foram coletadas amostras de sangue periférico concomitantemente para realizarmos a quantificação da expressão gênica de perforina, TIM3, FOXP3, TGF-B, CTGF e CD138 através da metodologia de PCR em tempo real. Resultados: Trinta e nove pacientes foram diagnosticados com rejeição aguda (28,7%), sendo 33 destes com alterações borderline, 5 com rejeição aguda Banff IA e um paciente com rejeição Banff IB, vinte pacientes apresentaram fibrose intersticial e atrofia tubular (14,7%), sete apresentaram necrose tubular aguda (5,1%), três infecções pelo vírus do polioma (2,2%) e um caso de nefrotoxicidade aguda por inibidores da calcineurina (0,8%). A mensuração da expressão gênica foi realizada através de qPCR e os pacientes com disfunção do enxerto apresentaram expressões diminuídas de perforina, TIM3, FOXP3 e TGF-β em relação aos pacientes com rejeição aguda e histologia normal do enxerto. Outras análises demonstraram que a perforina, TIM3 e FOXP3 também são capazes de excluir o diagnóstico de rejeição aguda, com valores preditivos negativos (VPN) de 83%, 83% e 79,6%, respectivamente. Em uma análise combinada dos 3 genes associados o VPN para rejeição aguda foi de 86.4%. A avaliação do RNA mensageiro dos genes TGF-B e CTGF mostrou que eles estão hiperexpressos nos enxertos com fibrose intersticial e atrofia tubular. Conclusões: Existe uma elevada incidência de agressões sub-clínicas dos enxertos renais que podem ser detectadas por biópsias protocolares. A mensuração do RNA mensageiro, em amostras do sangue periférico, mostrou ser uma ferramenta de potencial utilidade em identificar essas agressões de forma não-invasiva.
Background: Short term survival of kidney transplants has improved remarkably over the last two decades. However, long term survival of grafts and patients are still much lower than desired and most of the grafts are lost by recipients’ death and chronic graft function deterioration. It is believed that most of the injuries that result in graft shortening survival are initiated early after transplantation and many times are subclinical. The development of noninvasive biomarkers to accurately identify sub-clinical injuries, without the need of protocol biopsies, would be a major step forward in the practice of clinical organ transplantation since it would allow the early recognition of graft insulting events and lead to proper therapeutic actions potentially leading to more prolonged allograft survivals Objective: The aim of the present study was to evaluate the diagnosis potential of the non-invasive molecular analyzes of peripheral blood leukocytes gene expression in stable kidney recipients in the short-term. Methods: One hundred and thirty-six patients were enrolled in this study and underwent protocol biopsies at 3 months after grafting. Peripheral blood samples were collected concomitantly for the gene expression quantitation of perforin, TIM3, FOXP3, TGF-B, CTGF and CD138 through qPCR methodology. Results: Thirty-nine patients were diagnosed as acute rejection (28.7%), being 33 with borderline histological changes, 5 Banff IA acute rejection and 1 patient with Banff IB acute rejection, twenty patients had interstitial fibrosis and tubular atrophy (14.7%), seven had acute tubular necrosis (5.1%), three had poliomavirus infection (2.2%) and one patient had calcineurin inhibitor toxicity (0.8%). Gene expression was measured through qPCR and patients with graft dysfunction presented lower expressions of perforin, TIM3, FOXP3 and TGF-β than patients with acute rejection and normal graft histology. Other analyzes showed that perforin, TIM3 and FOXP3 are also able to rule out acute rejection, with negative predictive values (NPV) of 83%, 83% and 79.6% respectively. In a combined analysis of the 3 genes associated the NPV was 86.4%. CTGF and TGF-B mRNA were overexpressed in grafts with interstitial fibrosis and tubular atrophy. Conclusions: An elevated incidence of sub-clinical injuries can be detected by protocol biopsies of stable grafts. The evaluation of mRNA in the peripheral blood has shown to be a potentially useful tool to uncover these injuries noninvasively.
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Adam, Alexander. "Tim8 und Tim9, neue Komponenten der TIM22 Präproteintranslokase in Mitochondrien." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-31385.

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Feld, Timo [Verfasser]. "Response time analyses of adaptive variable-rate-tasks / Timo Feld." Ulm : Universität Ulm, 2020. http://d-nb.info/1203716273/34.

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Books on the topic "TIM3"

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Ferin, Giovanna. Tim MacMillan: The man who captured time. London: LCP, 2002.

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Spațiu fără timp: Arhitectura ortodoxă contemporană = Space without time : contemporary Orthodox architecture. București: Igloo Media, 2013.

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Time after time. Dublin: Poolbeg, 2008.

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Time before time. Bloomington, IN: AuthorHouse, 2011.

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Appel, Allen. Time after time. New York: Dell, 1987.

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Stockenberg, Antoinette. Time after time. New York: St. Martin's Paperbacks, 1995.

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Time after time. Sanbornville, N.H: Large Print Book Co., 2004.

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Hooper, Kay. Time after time. Toronto: Bantam Books, 1986.

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Time after time. New York, N.Y: Dell, 1995.

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Kemp, Penny. Time less time. London, Ont: Pendas Productions, 2001.

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Book chapters on the topic "TIM3"

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Hazzan, Orit, and Yael Dubinsky. "Time Time Time." In Agile Software Engineering, 1–22. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84800-198-5_4.

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Damour, Thibault. "Time and Relativity." In Time, 1–17. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0359-5_1.

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Villani, Cédric. "(Ir)reversibility and Entropy." In Time, 19–79. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0359-5_2.

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Villani, Cédric. "(Ir)réversibilité et entropie." In Time, 81–143. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0359-5_3.

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Jarzynski, Christopher. "Equalities and Inequalities: Irreversibility and the Second Law of Thermodynamics at the Nanoscale." In Time, 145–72. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0359-5_4.

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Salomon, Christophe. "Time Measurement in the XXIst Century." In Time, 173–86. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0359-5_5.

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Price, Huw. "Time’s Arrow and Eddington’s Challenge." In Time, 187–215. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0359-5_6.

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REICHENBACH, HANS. "The Tenses of Verbs." In Time, edited by Jan Christoph Meister and Wilhelm Schernus, 1–12. Berlin, Boston: DE GRUYTER, 2011. http://dx.doi.org/10.1515/9783110227185.1.

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Jaszczolt, Kasia M., and Louis De Saussure. "Introduction: time, temporality, and tense." In Time, 1–11. Oxford University Press, 2013. http://dx.doi.org/10.1093/acprof:oso/9780199589876.003.0001.

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Asher, Nicholas. "Temporal modification." In Time, 15–36. Oxford University Press, 2013. http://dx.doi.org/10.1093/acprof:oso/9780199589876.003.0002.

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Conference papers on the topic "TIM3"

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Smith, Courtney M., Alice Li, Nithya Krishnamurthy, and Mark A. Lemmon. "Abstract PO032: TIM3 regulation by phosphatidylserine." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po032.

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Gray, J. Dixon, Irina Krapf, Heyue Zhou, and Gunnar Kaufmann. "Abstract 3214: A fully human anti-TIM3 antibody with co-stimulatory activity." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3214.

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Fromm, George, Suresh de Silva, Kellsey Johannes, Arpita Patel, Josiah C. Hornblower, and Taylor H. Schreiber. "Abstract 5559: Agonist-redirected checkpoint (ARC), TIM3-Fc-OX40L, for cancer immunotherapy." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5559.

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Wong, Jamie, Ryan Phennicie, Igor Feldman, Sriram Sathyanarayanan, Don Shaffer, Mohammad Zafari, Steve Sazinsky, Kenneth Crook, and Debbie Law. "Abstract 586: Discovery of a novel TIM3 binding partner and a key role for TIM3 on macrophages: Identification of specific antibodies capable of converting immune-suppressive macrophages to immune-enhancing." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-586.

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Edmunds, G., C. Wuelfing, and DJ Morgan. "PO-400 Dual targeting of TIM3 and adenosine produces synergistic improvement in anti-tumour immunity." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.912.

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Zheng, Lei, Xuesong Huang, Wenyi Ouyang, Gang Chen, Annie Xiaoyu An, Xin Dong, Jay Liu, Jean Pierre Wery, Qian Shi, and Davy Xuesong Ouyang. "Abstract A203: Generation of human TIM3 knock-in mice for preclinical efficacy assessment of therapeutic antibodies." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a203.

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Sasikumar, Pottayil, N. S. Sudarshan, Nagaraj Gowda, D. S. Samiulla, Raghuveer Ramachandra, T. Chandrasekhar, Sreenivas Adurthi, et al. "Abstract 4861: Oral immune checkpoint antagonists targeting PD-L1/VISTA or PD-L1/Tim3 for cancer therapy." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4861.

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Lindsted, Trine, Monika Gad, Michael V. Grandal, Camilla Frölich, Vikram K. Bhatia, Torben Gjetting, Johan Lantto, et al. "Abstract 5629: Preclinical characterization of Sym023 a human anti-TIM3 antibody with a novel mechanism of action." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5629.

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Moon, Edmund K., Raghuveer Ranganathan, Xiaojun Liu, Raluca Verona, Linda Snyder, Carl H. June, Yangbing Zhao, and Steven M. Albelda. "Abstract 4706: TCR engineered adoptive T-cell therapy for lung cancer is augmented by combined PD1 and TIM3 antibody blockade." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4706.

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Fueyo, Juan, Candelaria Gomez-Manzano, Pamela Villalobos, Jaime Rodriguez-Canales, Barbara Mino, Ignacio Wistuba, Kenneth Hess, et al. "Abstract LB-235: Delta-24-RGD oncolytic adenovirus treatment downmodulates the key regulator of T-cell exhaustion TIM3 in malignant gliomas." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-235.

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Reports on the topic "TIM3"

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M'Raihi, D., S. Machani, M. Pei, and J. Rydell. TOTP: Time-Based One-Time Password Algorithm. RFC Editor, May 2011. http://dx.doi.org/10.17487/rfc6238.

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Hamermesh, Daniel. The Timing of Work Time Over Time. Cambridge, MA: National Bureau of Economic Research, December 1996. http://dx.doi.org/10.3386/w5855.

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Khwaja, Ahmed, Dan Silverman, and Frank Sloan. Time Preference, Time Discounting, and Smoking Decisions. Cambridge, MA: National Bureau of Economic Research, October 2006. http://dx.doi.org/10.3386/w12615.

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Mills, D. L. Internet Time Synchronization: The Network Time Protocol. RFC Editor, October 1989. http://dx.doi.org/10.17487/rfc1129.

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Taylor, Chasity, and Sponsor Lalon Alexander. Time Trapped. Ames: Iowa State University, Digital Repository, February 2013. http://dx.doi.org/10.31274/itaa_proceedings-180814-605.

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Kesselman, Carl, and Marry Hall. Combining Interprocedural Compile-Time and Run-Time Parallelization. Fort Belvoir, VA: Defense Technical Information Center, May 1999. http://dx.doi.org/10.21236/ada363906.

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Franke, D., D. Sibold, K. Teichel, M. Dansarie, and R. Sundblad. Network Time Security for the Network Time Protocol. RFC Editor, September 2020. http://dx.doi.org/10.17487/rfc8915.

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Matsakis, Demetrios. Time Transfer Methodologies for International Atomic Time (TAI). Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada464011.

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Bastian, Jacob, and Lance Lochner. The EITC and Maternal Time Use: More Time Working and Less Time with Kids? Cambridge, MA: National Bureau of Economic Research, August 2020. http://dx.doi.org/10.3386/w27717.

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Campos, Sergio V., and Edmund M. Clarke. Real-Time Symbolic Model Checking for Discrete Time Models. Fort Belvoir, VA: Defense Technical Information Center, May 1994. http://dx.doi.org/10.21236/ada282878.

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