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Gotowe bibliografie tematyczne / Molecular immunology

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Gotowa bibliografia na temat „Molecular immunology”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 29 lipca 2024

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Artykuły w czasopismach na temat "Molecular immunology"

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Parham, P. "Molecular immunology". Immunology Today 10, nr 4 (kwiecień 1989): 141–42. http://dx.doi.org/10.1016/0167-5699(89)90251-x.

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Born, Willi. "Molecular immunology". Cell 55, nr 5 (grudzień 1988): 745–46. http://dx.doi.org/10.1016/0092-8674(88)90130-4.

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Nezlin, Roald. "Molecular immunology". Molecular Immunology 26, nr 10 (październik 1989): 1011–12. http://dx.doi.org/10.1016/0161-5890(89)90121-1.

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Schroeder, Harry W. "Molecular immunology of self reactivity (immunology series/55)". Immunology Today 13, nr 10 (styczeń 1992): 423–24. http://dx.doi.org/10.1016/0167-5699(92)90099-s.

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Mautner, Beatrice, i David Huang. "Molecular biology and immunology". Seminars in Oncology Nursing 19, nr 3 (sierpień 2003): 154–61. http://dx.doi.org/10.1016/s0749-2081(03)00043-3.

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Turner, M. W. "Introduction to molecular immunology". Journal of Immunological Methods 79, nr 1 (maj 1985): 170–71. http://dx.doi.org/10.1016/0022-1759(85)90407-7.

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Li, Chenghua, i Ming Guo. "Frontiers in molecular immunology". Frontiers in Molecular Immunology 1, nr 1 (7.11.2018): 1–2. http://dx.doi.org/10.25082/fmi.2018.01.001.

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Denman, A. M. "Cellular and Molecular Immunology". Postgraduate Medical Journal 68, nr 798 (1.04.1992): 305. http://dx.doi.org/10.1136/pgmj.68.798.305.

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Chang, Nan-Shan. "Laboratory of Molecular Immunology". Guthrie Journal 63, nr 2 (kwiecień 1994): 59–60. http://dx.doi.org/10.3138/guthrie.63.2.059.

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Chang, Nan-Shan. "Laboratory of Molecular Immunology". Guthrie Journal 71, nr 2 (kwiecień 2002): 60–61. http://dx.doi.org/10.3138/guthrie.71.2.060.

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Rozprawy doktorskie na temat "Molecular immunology"

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Johansson, Alina. "Molecular mechanisms behind TRIM28expression". Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-252834.

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All-Ericsson, Charlotta. "Uveal melanoma : cytogenetics, molecular biology and tumor immunology /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-278-7.

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Eckert, Rachael. "Molecular Mechanisms of Neutrophil Migration". NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-10312007-134315/.

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This work is an investigative look behind the mechanisms of neutrophil migration. Each of three chapters involves exploration into a different signaling pathway important for migration downstream of chemoattractant stimulation through inhibition of a kinase or disruption of the function of an effector and examination of the effects on migration, adhesion, and actin reorganization in primary human or equine neutrophils. Chapter II examines the requirement for the signaling molecule p38 Mitogen Activated Kinase (MAPK) in equine neutrophil chemotaxis through use of the p38 specific inhibitor SB203580. SB203580 reduced LTB4- and PAF-induced migration and disrupted the ability of cells to polarize, but did not affect b2 integrin-dependent adhesion or surface b2 integrin expression. Chapter III is a comprehensive inquiry into the regulation of the phosphorylation of serine 157 of the cytoskeletal protein Vasodilator-stimulated Phosphoprotein (VASP). The rapid and transient phosphorylation of VASP serine 157 corresponded with F-actin levels in chemoattractant-stimulated human neutrophils. fMLF-induced serine 157 phosphorylation was abolished by pretreatment with the PKA inhibitor H89 and the adenylyl cyclase inhibitor SQ22536. In contrast, fMLF-induced serine 157 phosphorylation was unaffected by PKC inhibitors, PKG inhibitors, and the CamKII inhibitor KN-62. Inhibition of adhesion did not alter fMLF-induced VASP phosphorylation or dephosphorylation. This study demonstrated that chemoattractant stimulation of human neutrophils induces a rapid and transient PKA-dependent and adhesion-independent VASP serine 157 phosphorylation. Chapter IV probed into the function of the actin binding protein and PKC substrate Myristoylated Alanine-Rich C-kinase Substrate (MARCKS) through utilization of a cell permeant peptide derived from the MARCKS myristoylated aminoterminus (MANS peptide). Treatment of isolated human neutrophils with 50 μM MANS, but not a scrambled control peptide, significantly inhibited their migration and adhesion in response to fMLF, IL8, or LTB4. MANS significantly reduced F-actin content in neutrophils 30s after fMLF-induced polymerization, but did not alter the ability of cells to polarize, spread, or upregulate surface b2 integrin expression. These data provided evidence that MARCKS, via its myristoylated aminoterminus, is a key regulator of neutrophil migration and adhesion.

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Wijewardana, Thula Gaurie. "Molecular immunology of bovine isolates of Pasteurella multocida type A". Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/24424.

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Chou, Richard M. "Use of Phage Display Libraries to Select For B-cell Receptor-specific Peptides of Chronic Lymphocytic Leukemia Cells". Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1346584096.

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Duarte, Nádia. "Molecular and cellular mechanisms contributing to the pathogenesis of autoimmune diabetes". Doctoral thesis, Umeå universitet, Medicinsk biovetenskap, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-601.

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Type 1 diabetes is an autoimmune disorder determined both by genetic and environmental factors. The Non-obese diabetic (NOD) mouse is one of the best animal models of this disease. It spontaneously develops diabetes through a process resembling the human pathogenesis. The strong association of NOD Type 1 diabetes to the MHC region and the existence of other diabetes susceptibility loci are also in parallel with the human disease. The identity of the genetic factors and biological function mediated by these loci remain, however, largely unknown. Like in other autoimmune diseases, defects in tolerance mechanisms are thought to be at the origin of type 1 diabetes. Accordingly, defects in both central and peripheral tolerance mechanisms have been reported in the NOD mouse model. Using a subphenotype approach that aimed to dissect the disease into more simple phenotypes, we have addressed this issue. In paper I, we analyzed resistance to dexamethasone-induced apoptosis in NOD immature thymocytes previously mapped to the Idd6 locus. Using a set of congenic mice carrying B6-derived Idd6 regions on a NOD background and vice-versa we could restrict the Idd6 locus to an 8cM region on the telomeric end of chromosome 6 and the control of apoptosis resistance to a 3cM region within this area. In paper II, further analysis of diabetes incidence in these congenic mice separated the genes controlling these two traits, excluding the region controlling the resistance to apoptosis as directly mediating susceptibility to diabetes. These results also allowed us to further restrict the Idd6 locus to a 3Mb region. Expression analysis of genes in this chromosomal region highlighted the Lrmp/Jaw1 gene as a prime candidate for Idd6. Lrmp encodes an endoplasmatic reticulum resident protein. Papers III and IV relate to peripheral tolerance mechanisms. Several T cell populations with regulatory functions have been implicated in type 1 diabetes. In paper III, we analyzed NOD transgenic mice carrying a diverse CD1d-restricted TCR αVa3.2b9), named 24abNOD mice. The number of nonclassical NKT cells was found to be increased in these mice and almost complete protection from diabetes was observed. These results indicate a role for nonclassical NKT cells in the regulation of autoimmune diabetes. In paper IV, we studied the effects of introducing the diverse CD1d-restricted TCR (Va3.2b9) in immunodeficient NOD Rag-/- mice (24abNODRag-/- mice). This resulted in a surprising phenotype with inflammation of the ears and augmented presence of mast cells as well as spleenomegaly and hepatomegaly associated with extended fibrosis and increased numbers of mast cells and eosinophils in the tissues. These observations supported the notion that NKT cells constitute an “intermediary” cell type, not only able to elicit the innate immune system to mount an inflammatory response, but also able to interact with the adaptive immune system affecting the action of effector T cells in an autoimmune situation. In this context the 24abNODRag-/- mice provide an appropriate animal model for studying the interaction of NKT cells with both innate and adaptive components of the immune systemα.

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Basak, Sanjukta. "Studies of Hepatitis C virus immunology : translation and replication". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97903.

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Hepatitis C virus (HCV) has become a worldwide problem. Roughly 3% of world population are estimated to be infected with the virus, producing high rates of progressive liver disease, leading to cirrhosis and hepatocellular carcinoma. The present therapy, a combined administration of pegylated interferon-alpha (IFN) and ribavirin is costly and only successful in 50% of patients infected with HCV. It is also associated with serious side effects. Thus, there is an urgent need for better tolerated and more effective treatment modalities. A therapeutic vaccine may be the solution.
Recent efforts to produce efficient vaccines require not only the identification of potential viral antigens but also vaccine adjuvants or enhancers of immunity. Dendritic cells (DC) are being considered one such adjuvant for the activation of CD4+ and CD8+ T-cells. As potent antigen presenting cells, they are capable of capturing antigens, processing them into peptides, and presenting them on products of the MHC to T cells. For such reasons, peptide loading of antigens onto DCs to enhance T cell responses is becoming of increasing interest. Using cell penetrating peptides, or motifs capable of transporting cargo freely across cell membranes, we have developed a peptide based delivery system suitable for the transport of all HCV proteins into immature DCs. In our studies we demonstrated that 3.1% of immature DCs internalized the reporter cargo, eGFP. This system was then optimized to 53.81 % in target HeLa cells.
Another area of recent focus is the regulation of HCV translation and replication. Positive stranded viruses such as HCV use the genomic RNA as a common template for translation as well as for RNA replication, both proceeding in inverse directions. Thus, specific regulatory mechanisms must be in place in order to coordinate these two antagonistic processes. In this study, we investigated the role of HCV Core protein as a translational inhibitor and enhancer of replication. Using several transient and stable in vivo reporter assays, we showed that Core expression inhibited HCV IRES-mediated translation in trans, in a dose-dependent manner. Furthermore, HCV Core protein is able to dramatically inhibit HCV translation in the Huh7 replicon system, more so than the bicistronic reporter systems tested and subsequently increase total levels of replicon RNA by 1.5 log fold and thus, affect replication. We believe that Core may indeed be the sought regulator of translation and replication.

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Emani, Sirisha. "MOLECULAR CHARACTERIZATION OF T REGULATORY CELLS IN FIV-INFECTION". NCSU, 2006. http://www.lib.ncsu.edu/theses/available/etd-01192006-105756/.

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Naturally occurring CD4+CD25+ T regulatory cells (Treg) play important roles in maintaining immunologic self-tolerance in addition to controlling the magnitude of anti-microbial immune responses. However, the capacity of these CD4+CD25+ Treg cells to control immune responses both in vivo and in vitro is not well established. CD4+CD25+ Treg cell-mediated suppression can control autoimmune diseases; transplantation tolerance and graft verses host disease and, in contrast hinder tumor immunity and immunity to infectious agents. As Treg cells have been reported to be involved in several diseases, this study focused on molecular characteristics that enables them to maintain anergy and also resistance to programmed cell death along with the effect of FIV-infection on regulation of the above phenotypic characteristics. Our results show that feline CD4+CD25+ Treg cells are phenotypically and functionally anergic as indicated by elevated levels of the cyclin dependent kinase inhibitors, CdkI¡¦s, (p21cip1,p16ink4, and p27kip1) , and resistance to mitogen-induced proliferation compared to their counter parts CD4+CD25- T cells. Importantly, CdkI¡¦s are constitutively over-expressed only in FIV-infected cats. As expected Treg cells from FIV-infected cats that over-expressed CdkI¡¦s expressed low levels of the cyclins (mainly cyclins D) and phosphorylated retinoblastoma protein (pRb) that are responsible for cell cycle progression. We investigated the role of TGF?Ò signaling and found that TGF?Ò1 plus ConA stimulation was able to convert CD4+CD25- T cells to CD4+CD25+ T cells with functional and phenotypic characteristics including upregulation of CdkI¡¦s and bcl-2. The differential expression of CdkI¡¦s and bcl-2 between the two CD4+ T cell subsets may be linked to TGF?Ò-Smad pathway. Consistent with upregulation of CdkI¡¦s and bcl-2, we found that although natural and TGF?Ò1 converted CD4+CD25+ Treg cells are anergic, they are more resistant to activation induced cell death compared to CD4+CD25- T cells functionally which correlated with increased bcl-2 to bax ratio in Treg cells. Thus, the molecular characterization of this unique population of Treg cells may be essential for understanding their role and function for developing effective therapeutics and vaccination especially against chronic infections such as Acquired Immune Deficiency Syndrome (AIDS).

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Schauenburg, Andrea J. A. "Molecular mechanisms underlying pMHC-II recognition". Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/96291/.

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The immune system is a complex network of cells and molecules working together with the purpose of fending off potentially harmful pathogens. CD4+ T cells take key roles within this network by orchestrating a multitude of its players. They recognise pathogen or self-derived peptides (p) bound to molecules of the major histocompatibility class II (MHC-II) through their T cell receptor (TCR). Cytokines secreted in response to recognition aid antibody production and cytotoxic T cell activity, both critical for anti-viral immunity. In this thesis, TCR/pMHC-II interactions were investigated using a range of functional and molecular approaches in order to gain valuable insight into the mechanisms underlying successful antigen recognition. To aid these investigations, a versatile, insect cell based expression system for HLA-DR1 was successfully implemented to generate soluble protein for use in multimer stainings and biophysical assays. Two HLA-DR1 restricted peptides encoded within influenza heamagglutinin (HA) were confirmed as being highly conserved making them ideal targets for vaccine development and allowing identification of influenza specific CD4+ T cells. Furthermore, the various roles of peptide flanking residues (PFR) were investigated using two experimental models. In a HA derived peptide, C-terminal PFR proved essential for peptide binding stability to HLA-DR1 and in consequence, CD4+ T cell activation. Clonotyping of CD4+ T cells grown against peptides of varying PFR lengths showed that TCR gene selection was heavily influenced by PFR. A HIV gag24 derived peptide displaying an unusual secondary structure within its N-terminal PFR gave further insight into how seemingly small modifications to PFR can have wide reaching impact on CD4+ T cell activation. Both studies highlighted the need for more in depths investigations into this emerging field and the wide reaching impacts of this inherent feature of MHC-II restricted peptides. Overall, the results in this thesis added novel insight into the mechanisms underlying TCR/pMHC-II interactions.

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Huang, Bei. "Molecular interaction of the CD4 and MHC class II molecules : mapping the contact sites on CD4". Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42056.

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T cells expressing CD4 recognize antigens presented by class II following the contact of CD4 with non-polymorphic regions of class II. CD4 enhances T cell activation by acting as an adhesion molecule (co-ligand function), or by bringing the CD4 associated p56$ sp{lck}$ to the vicinity of the TCR (co-receptor function).
To dissect the molecular interactions which lead to CD4 function(s), wild-type (WT) and mutant CD4 molecules were expressed in the CD4-dependent 3DT52.5.8 T cell hybridomas. Results showed that multiple sites on CD4 encompassing the CDR1, the CDR3 regions of D1 and the FG loop of D2 are involved in class II interaction. The opposite face containing the CDR2 region also plays a role, either as another class II binding site, or the TCR docking site, or in another function of CD4. Co-receptor function requires a much larger site on CD4, compared to co-ligand function. A stretch of 15 amino acids which links D2 and D3 of CD4 appears to be very important for maintaining CD4 conformation, or to provide CD4 the flexibility required for its interaction with other cell surface molecules, including class II, the TCR, etc.
Crystallographic and functional studies have suggested that CD4 may dimerize, although biochemical evidence is lacking. To investigate the CD4 dimerization issue both human and mouse CD4 WT were co-expressed in 3DT52.5.8 cells. Surprisingly this led to a severe disruption of CD4 functions, although it has been shown that both human and mouse CD4 molecules are capable of interacting with human class II efficiently. As expected, co-expression of h-CD4 WT with class II-interaction-deficient CD4 mutants within the CDR1, CDR3 and the FG loop did not rescue CD4 functions. However, co-expression of CD4 WT with mutants from the CDR2 region resulted in an enhanced response. This result suggests that CDR2 mutants do not dimerize with WT molecule, therefore cannot behave as a dominant negative mutant, which is not the case for class II-interaction-deficient mutants from the CDR1, CDR3 and FG loop. Based on these results we suggest a model whereby dimerization involves, at least in part the CDR2 region. Final confirmation of this model awaits further structural data.

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Książki na temat "Molecular immunology"

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Carlberg, Carsten, i Eunike Velleuer. Molecular Immunology. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04025-2.

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D, Hames B., i Glover David M, red. Molecular immunology. Wyd. 2. London: IRL, 1995.

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D, Hames B., i Glover David M, red. Molecular immunology. Wyd. 2. Oxford: IRL Press at Oxford University Press, 1996.

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D, Hames B., i Glover David M, red. Molecular immunology. Oxford: IRL Press, 1988.

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H, Lichtman Andrew, i Pober Jordon S, red. Cellular and molecular immunology. Wyd. 2. Philadelphia: W.B. Saunders, 1994.

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H, Lichtman Andrew, i Pillai Shiv, red. Cellular and molecular immunology. Wyd. 6. Philadelphia: Saunders/Elsevier, 2010.

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H, Lichtman Andrew, i Pober Jordan S, red. Cellular and molecular immunology. Wyd. 3. Philadelphia: Saunders, 1997.

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H, Lichtman Andrew, red. Cellular and molecular immunology. Wyd. 5. Philadelphia, PA: Saunders, 2005.

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H, Lichtman Andrew, i Pober Jordan S, red. Cellular and molecular immunology. Philadelphia: Saunders, 1991.

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H, Lichtman Andrew, i Pillai Shiv, red. Cellular and molecular immunology. Wyd. 6. Philadelphia: Saunders Elsevier, 2007.

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Części książek na temat "Molecular immunology"

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Modrow, Susanne, Dietrich Falke, Uwe Truyen i Hermann Schätzl. "Immunology". W Molecular Virology, 69–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-20718-1_7.

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Carlberg, Carsten, i Eunike Velleuer. "Cancer Immunology". W Molecular Immunology, 197–213. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04025-2_11.

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Carlberg, Carsten, Eunike Velleuer i Ferdinand Molnár. "Cancer Immunology". W Molecular Medicine, 519–34. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-27133-5_33.

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Giese, Matthias. "Basic Vaccine Immunology". W Molecular Vaccines, 23–58. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1419-3_2.

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Carlberg, Carsten, i Eunike Velleuer. "Tolerance and Transplantation Immunology". W Molecular Immunology, 155–69. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04025-2_9.

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Giese, Matthias. "Pediatric Immunology". W Introduction to Molecular Vaccinology, 97–110. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25832-4_4.

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Giese, Matthias. "Elderly Immunology". W Introduction to Molecular Vaccinology, 111–21. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25832-4_5.

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Adlung, Lorenz. "Immunology". W Cell and Molecular Biology for Non-Biologists, 89–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65357-9_8.

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Ygberg, Sofia, i Anna Nilsson. "Pediatric Immunology and Vaccinology". W Molecular Vaccines, 85–98. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1419-3_4.

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Carlberg, Carsten, Eunike Velleuer i Ferdinand Molnár. "Tolerance and Transplantation Immunology". W Molecular Medicine, 365–80. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-27133-5_22.

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Streszczenia konferencji na temat "Molecular immunology"

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Galich, N. E., i M. V. Filatov. "Laser fluorescence fluctuation excesses in molecular immunology experiments". W SPIE Proceedings, redaktorzy Alexander I. Melker i Teodor Breczko. SPIE, 2006. http://dx.doi.org/10.1117/12.726756.

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Waxman, Stephen G. "901 SYMPOSIUM: Molecular biology and immunology of pain". W LUPUS 21ST CENTURY 2022 CONFERENCE, Abstracts of Sixth Scientific Meeting of North American and European Lupus Community, Tucson, AZ, USA – September 20–23, 2022. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-lupus21century.52.

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"Study on the Molecular Immunology Control between Type I and II Schizophrenics". W 2017 International Conference on Materials Science and Biological Engineering. Francis Academic Press, 2017. http://dx.doi.org/10.25236/icmsbe.2017.15.

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Castro, Alonso, i Brooks Shera. "Electrophoresis of Single Fluorescent Molecules". W Laser Applications to Chemical Analysis. Washington, D.C.: Optica Publishing Group, 1994. http://dx.doi.org/10.1364/laca.1994.thd.3.

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The fast, efficient detection and separation of minute quantities of biologically important molecules plays a central role in a variety of fields, such as molecular biology, biotechnology, immunology, medical diagnostics, and forensic analysis. It has proven difficult to identify and separate biomolecules at such low concentrations by existing means. Thus, it is of importance to develop methods that are able to probe such low concentrations with adequate sensitivity, resolution and ease. Here, we describe a new method for detecting and identifying individual fluorescent molecules in solution. The technique involves the measurement of electrophoretic velocities of individual molecules in a mixture, and identification by comparison with the electrophoretic velocity known to be characteristic of a particular molecular species. The application of the method to the detection and size identification of DNA restriction fragments in solution at the single molecule level has been demonstrated. In a similar experiment, the electrophoretic velocities of single molecules of the protein phycoerythrin was determined. Although we have focused on the detection and identification of biologically important molecules, the technique has the potential to find applications in organic and inorganic chemical analysis.

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Heiniö, Camilla, Riikka Havunen, Mikko Siurala i Akseli Hemminki. "Abstract A30: Molecular insight into pathogen-associated molecular pattern signaling during TNFa and IL2 armed oncolytic adenovirus treatments". W 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-a30.

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Collins, Natalie B., Robert Manguso, Hans Pope i W. Nicholas Haining. "Abstract A16: Defining molecular mechanisms of resistance to tumor immunity". W Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-a16.

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Sheffer, Michal, Emily Lowry, Nicky Beelen, Minasri Borah, Suha Naffar-Abu Amara, Chris C. Mader, Jennifer Roth i in. "Abstract PO041: Landscape of molecular events regulating tumor cell responses to natural killer cells". W 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-po041.

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Park, Saem, Anna Brooks, Chun-Jen Chen i Rod Dunbar. "Abstract B101: Molecular characteristics of tumor-associated macrophages in human melanoma metastases". W Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b101.

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Schietinger, Andrea. "Abstract IA14: Molecular programs defining tumor-specific T-cell dysfunction and reprogrammability". W Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-ia14.

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Schreiber, Robert D. "Abstract IA2: The molecular basis of tumor immunogenicity." W Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-ia2.

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Raporty organizacyjne na temat "Molecular immunology"

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Yusim, Karina, Bette Tina Korber, Christian Brander, Dan Barouch, Rob de Boer, Barton F. Haynes, Richard Koup, John P. Moore, Bruce D. Walker i David Watkins. HIV Molecular Immunology 2015. Office of Scientific and Technical Information (OSTI), kwiecień 2016. http://dx.doi.org/10.2172/1248095.

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Yusim, Karina, Bette Tina Marie Korber, Dan Barouch, Richard Koup, Rob de Boer, John P. Moore, Christian Brander, Barton F. Haynes i Bruce D. Walker. HIV Molecular Immunology 2014. Office of Scientific and Technical Information (OSTI), luty 2015. http://dx.doi.org/10.2172/1169681.

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Kaiser, Ivan I. Rattlesnake Neurotoxin Structure, Mechanism of Action, Immunology and Molecular Biology. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 1990. http://dx.doi.org/10.21236/ada228003.

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Kurman, Robert J., i Ie-Ming Shih. Pathogenesis of Ovarian Serous Carcinoma as the Basis for Immunologic Directed Diagnosis and Treatment. Project 1 - Molecular Characterization of Ovarian Serous Tumors Developing Along Different Pathways. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2003. http://dx.doi.org/10.21236/ada420920.

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