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Relevant bibliographies by topics / Immunology; Molecular dynamics

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Academic literature on the topic 'Immunology; Molecular dynamics'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "Immunology; Molecular dynamics"

1

Stavrakoudis, Athanassios. "Conformational Flexibility in Designing Peptides for Immunology: The Molecular Dynamics Approach." Current Computer Aided-Drug Design 6, no. 3 (September 1, 2010): 207–22. http://dx.doi.org/10.2174/157340910791760073.

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Kortkhonjia, Ekaterine, Relly Brandman, Joe Zhongxiang Zhou, Vincent A. Voelz, Ilya Chorny, Bruce Kabakoff, Thomas W. Patapoff, Ken A. Dill, and Trevor E. Swartz. "Probing antibody internal dynamics with fluorescence anisotropy and molecular dynamics simulations." mAbs 5, no. 2 (March 2013): 306–22. http://dx.doi.org/10.4161/mabs.23651.

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Grossman, Zvi, Charles L. Greenblatt, and Irun R. Cohen. "Parasite immunology and lymphocyte population dynamics." Journal of Theoretical Biology 121, no. 2 (July 1986): 129–39. http://dx.doi.org/10.1016/s0022-5193(86)80088-1.

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4

Mallik, Buddhadeb, and Dimitrios Morikis. "Applications of Molecular Dynamics Simulations in Immunology: A Useful Computational Method in Aiding Vaccine Design." Current Proteomics 3, no. 4 (December 1, 2006): 259–70. http://dx.doi.org/10.2174/157016406780655568.

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5

Lopes, António M., and José A. Tenreiro Machado. "Symmetry in Complex Systems." Symmetry 12, no. 6 (June 8, 2020): 982. http://dx.doi.org/10.3390/sym12060982.

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Complex systems with symmetry arise in many fields, at various length scales, including financial markets, social, transportation, telecommunication and power grid networks, world and country economies, ecosystems, molecular dynamics, immunology, living organisms, computational systems, and celestial and continuum mechanics [...]

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Dongmo Foumthuim, Cedrix J., Alessandra Corazza, Rodolfo Berni, Gennaro Esposito, and Federico Fogolari. "Dynamics and Thermodynamics of Transthyretin Association from Molecular Dynamics Simulations." BioMed Research International 2018 (June 5, 2018): 1–14. http://dx.doi.org/10.1155/2018/7480749.

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Molecular dynamics simulations are used in this work to probe the structural stability and the dynamics of engineered mutants of transthyretin (TTR), i.e., the double mutant F87M/L110M (MT-TTR) and the triple mutant F87M/L110M/S117E (3M-TTR), in relation to wild-type. Free energy analysis from end-point simulations and statistical effective energy functions are used to analyze trajectories, revealing that mutations do not have major impact on protein structure but rather on protein association, shifting the equilibria towards dissociated species. The result is confirmed by the analysis of 3M-TTR which shows dissociation within the first 10 ns of the simulation, indicating that contacts are lost at the dimer-dimer interface, whereas dimers (formed by monomers which pair to form two extended β-sheets) appear fairly stable. Overall the simulations provide a detailed view of the dynamics and thermodynamics of wild-type and mutant transthyretins and a rationale of the observed effects.

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Mills, David M., and John C. Cambier. "B lymphocyte activation during cognate interactions with CD4+ T lymphocytes: molecular dynamics and immunologic consequences." Seminars in Immunology 15, no. 6 (December 2003): 325–29. http://dx.doi.org/10.1016/j.smim.2003.09.004.

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Klinke, David J., and Qing Wang. "Understanding Immunology via Engineering Design: The Role of Mathematical Prototyping." Computational and Mathematical Methods in Medicine 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/676015.

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A major challenge in immunology is how to translate data into knowledge given the inherent complexity and dynamics of human physiology. Both the physiology and engineering communities have rich histories in applying computational approaches to translate data obtained from complex systems into knowledge of system behavior. However, there are some differences in how disciplines approach problems. By referring to mathematical models as mathematical prototypes, we aim to highlight aspects related to the process (i.e., prototyping) rather than the product (i.e., the model). The objective of this paper is to review how two related engineering concepts, specifically prototyping and “fitness for use,” can be applied to overcome the pressing challenge in translating data into improved knowledge of basic immunology that can be used to improve therapies for disease. These concepts are illustrated using two immunology-related examples. The prototypes presented focus on the beta cell mass at the onset of type 1 diabetes and the dynamics of dendritic cells in the lung. This paper is intended to illustrate some of the nuances associated with applying mathematical modeling to improve understanding of the dynamics of disease progression in humans.

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Yamashita, Takefumi. "Toward rational antibody design: recent advancements in molecular dynamics simulations." International Immunology 30, no. 4 (January 28, 2018): 133–40. http://dx.doi.org/10.1093/intimm/dxx077.

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Loeffler, Dirk, and Timm Schroeder. "Understanding cell fate control by continuous single-cell quantification." Blood 133, no. 13 (March 28, 2019): 1406–14. http://dx.doi.org/10.1182/blood-2018-09-835397.

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Abstract Cells and the molecular processes underlying their behavior are highly dynamic. Understanding these dynamic biological processes requires noninvasive continuous quantitative single-cell observations, instead of population-based average or single-cell snapshot analysis. Ideally, single-cell dynamics are measured long-term in vivo; however, despite progress in recent years, technical limitations still prevent such studies. On the other hand, in vitro studies have proven to be useful for answering long-standing questions. Although technically still demanding, long-term single-cell imaging and tracking in vitro have become valuable tools to elucidate dynamic molecular processes and mechanisms, especially in rare and heterogeneous populations. Here, we review how continuous quantitative single-cell imaging of hematopoietic cells has been used to solve decades-long controversies. Because aberrant cell fate decisions are at the heart of tissue degeneration and disease, we argue that studying their molecular dynamics using quantitative single-cell imaging will also improve our understanding of these processes and lead to new strategies for therapies.

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Dissertations / Theses on the topic "Immunology; Molecular dynamics"

1

Smith, Michael J. "Molecular modelling of MHC/peptide complexes." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297304.

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Janani, Ramesh. "B cell development and death in mouse bone marrow : effect of a bcl-2 transgene and Iprgld mutations on in vivo dynamics and localisation of precursor B cells." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=34647.

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The possible roles of the anti-apoptotic protein, Bcl-2, and pro-apoptotic Fas receptor-ligand interactions in cell death decisions during the development of B lymphocytes in mouse bone marrow and their maturation in the spleen have been evaluated in gene-modified and mutant mice.
In Emu-bcl-2 transgenic mice, the population dynamics and tissue organisation of phenotypically defined precursor B cells, have been evaluated by immunofluorescence labeling, mitotic arrest, BrdU uptake, flow cytometry and in vivo radioimmunolabeling combined with light and electron microscope radioautography. In bone marrow of Emu-bcl-2 mice, the number and production rate of proliferating precursor B cells were increased. Immature B lymphocytes also increased in number, accumulating extravascularly around the central venous sinus, and the total rate of production of these rapidly-renewed IgM + B cells was increased. Phenotypically mature B lymphocytes and B lymphocytes having a slow turnover rate greatly increased in number. Many mature B cells were located within the lumen of venous sinusoids and in perisinusoidal locations. In the spleen, the usual population of rapidly-renewed IgM + B cells was undetectable. In contrast, both slowly renewing B cells and a further stable population of very long-lived B cells were greatly increased in numbers but had unchanged longevity. The rates of apoptosis among B cell subsets in short term bone marrow cultures from bcl-2 transgenic mice were reduced, while bcl-2/scid mice accumulated many B220+mu- pro-B cells in bone marrow. The results indicate that overexpression of bcl-2 inhibits apoptosis during B cell development in bone marrow and promotes survival of newly-formed B cells in the spleen and their entry into a long-lived recirculating B cell pool.
In Ipr and gld mutant mice lacking functional Fas and Fas ligand, respectively, pre-B cells were increased in number and production rate in bone marrow, while in spleen, in addition to an increase in number of mature B cells, a population of B220+mu - cells was expanded. Thus, Fas ligation may contribute to B cell death in bone marrow.
The findings suggest that Bcl-2 and Fas can help to regulate the developmental stage-specific apoptosis of B cells designed to prevent the persistence of nonfunctional, preneoplastic or autoreactive cells.

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3

Nadas, Janos Istvan. "Computational Structure Activity Relationship Studies on the CD1d/Glycolipid/TCR Complex using AMBER and AUTODOCK." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1251145085.

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4

Ozen, Aysegul. "Structure and Dynamics of Viral Substrate Recognition and Drug Resistance: A Dissertation." eScholarship@UMMS, 2005. http://escholarship.umassmed.edu/gsbs_diss/677.

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Drug resistance is a major problem in quickly evolving diseases, including the human immunodeficiency (HIV) and hepatitis C viral (HCV) infections. The viral proteases (HIV protease and HCV NS3/4A protease) are primary drug targets. At the molecular level, drug resistance reflects a subtle change in the balance of molecular recognition; the drug resistant protease variants are no longer effectively inhibited by the competitive drug molecules but can process the natural substrates with enough efficiency for viral survival. Therefore, the inhibitors that better mimic the natural substrate binding features should result in more robust inhibitors with flat drug resistance profiles. The native substrates adopt a consensus volume when bound to the enzyme, the substrate envelope. The most severe resistance mutations occur at protease residues that are contacted by the inhibitors outside the substrate envelope. To guide the design of robust inhibitors, we investigate the shared and varied properties of substrates with the protein dynamics taken into account to define the dynamic substrate envelope of both viral proteases. The NS3/4A dynamic substrate envelope is compared with inhibitors to detect the structural and dynamic basis of resistance mutation patterns. Comparative analyses of substrates and inhibitors result in a solid list of structural and dynamic features of substrates that are not shared by inhibitors. This study can help guiding the development of novel inhibitors by paying attention to the subtle differences between the binding properties of substrates versus inhibitors.

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Ozen, Aysegul. "Structure and Dynamics of Viral Substrate Recognition and Drug Resistance: A Dissertation." eScholarship@UMMS, 2013. https://escholarship.umassmed.edu/gsbs_diss/677.

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Drug resistance is a major problem in quickly evolving diseases, including the human immunodeficiency (HIV) and hepatitis C viral (HCV) infections. The viral proteases (HIV protease and HCV NS3/4A protease) are primary drug targets. At the molecular level, drug resistance reflects a subtle change in the balance of molecular recognition; the drug resistant protease variants are no longer effectively inhibited by the competitive drug molecules but can process the natural substrates with enough efficiency for viral survival. Therefore, the inhibitors that better mimic the natural substrate binding features should result in more robust inhibitors with flat drug resistance profiles. The native substrates adopt a consensus volume when bound to the enzyme, the substrate envelope. The most severe resistance mutations occur at protease residues that are contacted by the inhibitors outside the substrate envelope. To guide the design of robust inhibitors, we investigate the shared and varied properties of substrates with the protein dynamics taken into account to define the dynamic substrate envelope of both viral proteases. The NS3/4A dynamic substrate envelope is compared with inhibitors to detect the structural and dynamic basis of resistance mutation patterns. Comparative analyses of substrates and inhibitors result in a solid list of structural and dynamic features of substrates that are not shared by inhibitors. This study can help guiding the development of novel inhibitors by paying attention to the subtle differences between the binding properties of substrates versus inhibitors.

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Morris, Matthew. "Molecular mechanisms responsible for the dynamic modulation of macrophage responses to varying dosages of lipopolysaccharide." Diss., Virginia Tech, 2014. http://hdl.handle.net/10919/64253.

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The innate immune system depends for its effectiveness on the function of specialized pattern recognition receptors which enable it to target pathogens for destruction on the basis of conserved molecular patterns such as flagellin or lipopolysaccharide (LPS). Specifically, LPS is recognized by the Toll-like receptor 4 (TLR4), activating a signaling pathway which triggers the production of both pro- and anti-inflammatory mediators. Very low doses of LPS, however, preferentially induce pro-inflammatory cytokines, which can lead to persistent low-grade inflammation, a contributing factor in a host of chronic diseases. The mild pro-inflammatory skewing induced by super-low-dose LPS also potentiates the inflammatory response to later challenge with a higher dose of LPS in a phenomenon known as the "Shwartzman reaction" or "endotoxin priming". We investigated the mechanisms involved in pro-inflammatory skewing by super-low-dose LPS in THP-1 cells and found it to be governed by a regulatory circuit of competitive inhibition between glycogen synthase kinase 3 (GSK3) and Akt, which promote the activity of the transcription factors FoxO1 and CREB, respectively. Super-low-dose LPS mildly activated FoxO1 and pro-inflammatory gene transcription without inducing anti-inflammatory genes or activating CREB, and this pro-inflammatory skewing could be abolished by inhibition of GSK3 or direct activation of CREB. We then examined the dynamics of the LPS response at various different dosages in murine bone-marrow-derived macrophages (BMDM). The pro-inflammatory cytokine IL-12 was most strongly induced by intermediate LPS dosages, with very low or high doses inducing less robust IL-12 production. Knockout of the inhibitory TLR4 pathway molecules Lyn or IRAK-M resulted in sustained induction of IL-12 by high doses of LPS. By activating CREB, we were able to reduce inflammation in WT BMDM, and saw that this corresponded with increased phosphorylation of CREB. Overall, we are confident that this subnetwork is an important switch regulating the resolution of inflammation in response to TLR4 stimulation. Furthermore, we propose that endotoxin priming is an example of the generalized capacity of all signaling networks to recall prior states, and that an appreciation for the history and context of exposure to stimuli is critical for the understanding of signaling behavior.
Ph. D.

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7

Bailey, Alistair. "Relating the structure, function and dynamics of the MHC Class I antigen presenting molecule." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/376359/.

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8

Posgai, Monica Therese. "Energetic and dynamic characterization of the IgA1:FcαRI interaction reveals long-range conformational changes in IgA1 upon receptor binding." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1354043317.

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9

Bashour, Keenan. "Spatial Dynamics and the Mechanoresponse in CD4+ T Cell Activation." Thesis, 2013. https://doi.org/10.7916/D80864PP.

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The activation of naïve CD4+ T cells by antigen presenting cells is a critical step in the response of the immune system to foreign pathogens and in its acclimation to host tissues. Activation of naïve T cells proceeds through TCR engagement and is further augmented by CD28 costimulation: ensuring T cell survival and conferring numerous functional capabilities. The work in this dissertation highlights the spatial and temporal dynamics that regulate the initial coupling of CD28 with TCR signaling and also dissects the mechanical properties conferred by downstream effectors that are required to relay CD28 costimulation. A reaction-diffusion model that describes the spatial regulation of costimulation in activating human T cells is developed. The Src kinase Lck, though predominantly cytosolic, is an ideal candidate for the coupling of the TCR and CD28 pathways. Membrane associations bring Lck in contact with these receptors, where mediation of its active state by kinase activity and regulation of its spatial dynamics dictate its capacity to integrate early TCR and CD28 signaling. This developed reaction-diffusion model focusing on Lck is then extrapolated to mouse cells that do not share similar sensitivity to segregation of TCR and CD28 triggering: indicating that while Lck is essential for costimulation, it does not confer spatial sensitivity in activating mouse T cells. A comparison of human and mouse cells demonstrate underlying differences in the diffusivity of Lck across the membrane and the enrichment of the cytoskeleton at the interface. The role of the cytoskeleton in generating TCR-driven contractile forces is then investigated through use of micropillar arrays. This approach also enables the quantification of forces generated by T cells during cellular activation. The impact of CD28 costimulation on TCR-driven force generation is assessed and noted to increase cellular forces by 80% beyond what is induced through TCR triggering. By manipulating the presentation of CD28 activation, CD28 is determined to be a mechanoresponsive receptor that is not directly responsible for mechanosensitivty. Rather, CD28 mediates a change in cellular forces through PI3 kinase, whose inhibition normalizes force generation in T cells activated by TCR and those costimulated with TCR and CD28. Downstream of PI3 kinase, PDK1 is identified as being essential in both TCR and CD28 costimulatory force generation; inhibition of PDK1 fully abrogates cellular forces. Lastly, we qualitatively characterize T cell activation on micropillar arrays, where their complex topology reveals a multiphasic behavior during activation. Whereas T cells activated on planar surfaces are relatively stationary, T cells activated on micropillars slowly migrate towards the base of the array. Forces exerted during this migration are substantially greater than those previously measured, and the slow migration leads to the characterization of multiple phases and the relocalization of key cellular proteins.

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10

"The dynamics of Plasmodium falciparum variation in western Kenya." Tulane University, 1996.

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In an area of intense transmission, a malaria vaccine could reduce infection due to the parasite types represented in the vaccine, but have no detectable effect on the overall frequency of infection if there were multiple parasite types and immunization did not protect against heterologous parasites. These studies were performed to determine whether immunization with SPf66 decreased infection with parasites containing the 11 amino acid peptide from merozoite surface protein-1 (MSP-1) present in SPf66, or increased infection due to heterologous parasites containing alternate (heterologous) MSP-1 sequences. Based on this 11 amino acid peptide (YSLFQ KEKMVL) from MSP-1 in SPf66, 3 forward primers (S,Q,V) were designed to amplify the MSP-1 sequence present in SPf66, and 3 additional forward primers (G,H,I) to amplify the alternative MSP-1 sequence (YGLFHKEKMIL). This strategy was validated by PCR amplification and dideoxy sequencing with 14 cloned laboratory isolates, which demonstrated that each of the 6 forward primers amplified one MSP-1 sequence or the other, but not both. This technique was then used to examine filter paper blots from an SPf66 vaccine study of 85 subjects in Saradidi, KENYA. In that study, the prevalence of infection with YSLFQKEKMVL or YGLFHKEKMIL type parasites was unaffected by immunization with SPf66 (based on amplification with the S and G primers $\rm\lbrack p\ge 0.12$ as analyzed by chi-square), the Q and H primers $\rm\lbrack p\ge 0.13\rbrack ,$ or the V and I primers $\rm\lbrack p\ge 0.18\rbrack ).$ These results suggest that SPf66 does not exert a selective effect in vivo. Because the Block 1 sequence in SPf66 is typical for the MAD20 and RO33 allotypes of MSP-1 (YSLFQKEKMVL), immunization with SPf66 should select for the alternative K1 allotype in Block 1 of MSP-1 (YGLFHKEKMIL), and may by linkage also select for K1 (increase the frequency of K1) in the adjacent Block 2 of MSP-1. To test this hypothesis we typed parasites by PCR using MSP-1 allele-specific primers flanking Block 2 to distinguish K1, MAD20 and RO33 parasites. The results of these studies indicate that there were no significant differences in the frequencies of these Block 2 allotypes among persons who received SPf66 im, SPf66 sc or the placebo (hepatitis B vaccine im) $\rm (p\ge 0.17).$ These findings suggest that immunization with SPf66 also does not exert a selective effect on Block 2 of MSP-1 in vivo. As a control we used PCR to amplify the polymorphic Block 3 region of MSP-2. Because MSP-2 is on a different chromosome from MSP-1, there should be no linkage between selection for Block 2 MSP-1 allotypes after immunization with SPf66 and the frequencies of different Block 3 MSP-2 types. We found no significant differences among 10 MSP-2 genotypes between SPf66 im and placebo, or between SPf66 sc and placebo $\rm (p\ge 0.1$ by Fisher's exact test). We found a significant difference between genotype 548/559 for SPf66 im and placebo or between SPf66 sc and placebo, prior to immunization with SPf66 (p = 0.05 and 0.03 respectively). Because these samples were collected before immunization with SPf66, the effect could not be due to immunization with SPf66. These studies have developed a molecular method to indirectly assess vaccine efficacy
acase@tulane.edu

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Books on the topic "Immunology; Molecular dynamics"

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J, Wood Kathryn, ed. Principles of cellular and molecular immunology. Oxford: Oxford University Press, 1993.

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Book chapters on the topic "Immunology; Molecular dynamics"

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Carrasco, Yolanda R. "Molecular and Cellular Dynamics at the Early Stages of Antigen Encounter: The B-Cell Immunological Synapse." In Current Topics in Microbiology and Immunology, 51–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03858-7_3.

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Eliseev, A. V., and J. M. Lehn. "Dynamic Combinatorial Chemistry: Evolutionary Formation and Screening of Molecular Libraries." In Current Topics in Microbiology and Immunology, 159–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60142-2_9.

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Hruby, Victor J., and Terry O. Matsunaga. "Applications of Synthetic Peptides." In Synthetic Peptides. Oxford University Press, 2002. http://dx.doi.org/10.1093/oso/9780195132618.003.0008.

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The tremendous advances in the development of methods for the design and synthesis of peptides. pseudo-peptides and related compounds, as well as the corresponding advances in our understanding of peptide and protein structure, conformation, topography, and dynamics provides unique opportunities to apply designed synthetic peptides for an enormous variety of problems in chemistry, biology, and medicine. In addition, if these advances can be coupled to the advances in molecular biology and the human genome project, on the one hand, and asymmetric synthesis and catalysis, on the other, it should be possible to provide hitherto unavailable, indeed unthinkable, approaches to diverse areas of drug design, behavioral neuroscience, molecular immunology, chemotherapy, and a wide variety of other uses. Already it is clear that peptide therapy has enormous potential in such diverse areas as growth control, blood pressure management, neurotransmission, hormone action, satiety, addiction, pain, digestion, reproduction, and so forth. Nature has “discovered” that it can control nearly all biological processes by various kinds of molecular recognition, and that peptides and proteins are uniquely suited for this control because of their enormous potential for diversity and their unique physico-chemical properties. This finding may, perhaps, be most readily understood if one recognizes that, considering only the 20 normal eukaryotic amino acids, the number of unique chemical entities for a pentapeptide is 3,200,000 (205), for a hexapeptide it is 64,000,000 (206), and so on. Considered from this perspective, perhaps it is not unexpected that Nature has “discovered” that peptides and proteins can do it all, from providing structure and motion, to catalysis, to information transduction, to growth and maturation, and so on. The ability of the immune system in higher animals, including humans, to recognize literally millions of foreign materials made by Nature as well as humans, and to get rid of them as part of its survival strategy, is just one example that illustrates the potential of peptide-based drugs, therapeutics, and modulators of biological function. Despite the enormous potential of peptides and small proteins for these areas, surprisingly little advantage has been taken of the potential of these molecules as drugs and tools for use in basic and clinical research.

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Monnot, Gwennaëlle C., and Pedro Romero. "Immunotherapy and tumour resistance to immune-mediated control and elimination." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr, 423–37. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0029.

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The field of tumour immunology has gradually reached a consensus that the immune system and tumours sustain a rich set of dynamic interactions starting early during carcinogenesis. Incipient tumours may be eliminated by the immune system via adaptive immune responses mediated mainly by cytotoxic CD8 T lymphocytes, which recognize short antigenic peptides presented by polymorphic major histocompatibility complex (MHC) class I molecules. Advanced tumours, however, are generally highly resistant to the main effectors of the immune system. Moreover, the molecular and cellular composition of the tumour microenvironment is strongly immunosuppressive. Recent research efforts have focused on the dissection of the mechanisms operating at the tumour sites, which neutralize antitumour immunity in both experimental models and directly in cancer patients. All along this basic research, translational scientists have tried to harness the immune system to design novel therapeutic modalities that have collectively been coined as cancer immunotherapy. The overall goal has been to increase the numbers of tumour antigen-specific T cells in cancer patients via either vaccination or adoptive transfer of large numbers of immune cells. It is safe to state that cancer immunotherapy will provide a revolution in the treatment of cancer and the future may bear the prospect of effective tumour control in many cancer types, and that immunotherapy will be one of the main components of effective therapeutic options.

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Conference papers on the topic "Immunology; Molecular dynamics"

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Alexandrov, Vitaly, and Konstantin Klyukin. "Abstract A98: Molecular dynamics study of pH-dependent interactions between immune checkpoint receptor PD-1 and PD-L1." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a98.

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