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Relevant bibliographies by topics / T-cell mediated immunity

Academic literature on the topic 'T-cell mediated immunity'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "T-cell mediated immunity"

1

Chakravarti, Bulbul, and George N. Abraham. "Aging and T-cell-mediated immunity." Mechanisms of Ageing and Development 108, no. 3 (May 1999): 183–206. http://dx.doi.org/10.1016/s0047-6374(99)00009-3.

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Pribila, Jonathan T., Angie C. Quale, Kristen L. Mueller, and Yoji Shimizu. "Integrins and T Cell–Mediated Immunity." Annual Review of Immunology 22, no. 1 (April 2004): 157–80. http://dx.doi.org/10.1146/annurev.immunol.22.012703.104649.

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Kurup, Samarchith P., Noah S. Butler, and John T. Harty. "T cell-mediated immunity to malaria." Nature Reviews Immunology 19, no. 7 (April 2, 2019): 457–71. http://dx.doi.org/10.1038/s41577-019-0158-z.

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Ouyang, Kelsey, David X. Zheng, and George W. Agak. "T-Cell Mediated Immunity in Merkel Cell Carcinoma." Cancers 14, no. 24 (December 9, 2022): 6058. http://dx.doi.org/10.3390/cancers14246058.

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Merkel cell carcinoma (MCC) is a rare and frequently lethal skin cancer with neuroendocrine characteristics. MCC can originate from either the presence of MCC polyomavirus (MCPyV) DNA or chronic ultraviolet (UV) exposure that can cause DNA mutations. MCC is predominant in sun-exposed regions of the body and can metastasize to regional lymph nodes, liver, lungs, bone, and brain. Older, light-skinned individuals with a history of significant sun exposure are at the highest risk. Previous studies have shown that tumors containing a high number of tumor-infiltrating T-cells have favorable survival, even in the absence of MCPyV DNA, suggesting that MCPyV infection enhances T-cell infiltration. However, other factors may also play a role in the host antitumor response. Herein, we review the impact of tumor infiltrating lymphocytes (TILs), mainly the CD4+, CD8+, and regulatory T-cell (Tregs) responses on the course of MCC, including their role in initiating MCPyV-specific immune responses. Furthermore, potential research avenues related to T-cell biology in MCC, as well as relevant immunotherapies are discussed.

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Stenger, Steffen, and Robert L. Modlin. "T cell mediated immunity to Mycobacterium tuberculosis." Current Opinion in Microbiology 2, no. 1 (February 1999): 89–93. http://dx.doi.org/10.1016/s1369-5274(99)80015-0.

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SCHMID, D. "T cell-mediated immunity to quinolones*1." Journal of Allergy and Clinical Immunology 113, no. 2 (February 2004): S72. http://dx.doi.org/10.1016/j.jaci.2003.12.234.

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Hellström, Karl Erik, Lieping Chen, and I. Hellström. "Costimulation of T-cell-mediated tumor immunity." Cancer Chemotherapy and Pharmacology 38, no. 7 (1996): S40. http://dx.doi.org/10.1007/s002800051036.

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Askonas, B. A., and P. M. Taylor. "T cell mediated immunity in virus infection." Immunology Letters 16, no. 3-4 (December 1987): 337–40. http://dx.doi.org/10.1016/0165-2478(87)90167-2.

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White, Douglas W., Adam MacNeil, Dirk H. Busch, Ingrid M. Pilip, Eric G. Pamer, and John T. Harty. "Perforin-Deficient CD8+ T Cells: In Vivo Priming and Antigen-Specific Immunity Against Listeria monocytogenes." Journal of Immunology 162, no. 2 (January 15, 1999): 980–88. http://dx.doi.org/10.4049/jimmunol.162.2.980.

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Abstract CD8+ T cells require perforin to mediate immunity against some, but not all, intracellular pathogens. Previous studies with H-2b MHC perforin gene knockout (PO) mice revealed both perforin-dependent and perforin-independent pathways of CD8+ T cell-mediated immunity to Listeria monocytogenes (LM). In this study, we address two previously unresolved issues regarding the requirement for perforin in antilisterial immunity: 1) Is CD8+ T cell-mediated, perforin-independent immunity specific for a single Ag or generalizable to multiple Ags? 2) Is there a deficiency in the priming of the CD8+ T cell compartment of PO mice following an immunizing challenge with LM? We used H-2d MHC PO mice to generate CD8+ T cell lines individually specific for three known Ags expressed by a recombinant strain of virulent LM. Adoptive transfer experiments into BALB/c host mice revealed that immunity can be mediated by PO CD8+ T cells specific for all Ags examined, indicating that perforin-independent immunity is not limited to CD8+ T cells that recognize listeriolysin O. Analysis of epitope-specific CD8+ T cell expansion by MHC class I tetramer staining and ELISPOT revealed no deficiency in either the primary or secondary response to LM infection in PO mice. These results demonstrate that the perforin-independent pathway of antilisterial resistance mediated by CD8+ T cells is generalizable to multiple epitopes. Furthermore, the results show that reduced antilisterial resistance observed with polyclonal PO CD8+ T cells is a consequence of a deficiency in effector function and not a result of suboptimal CD8+ T cell priming.

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White, Douglas W., and John T. Harty. "Perforin-Deficient CD8+ T Cells Provide Immunity to Listeria monocytogenes by a Mechanism That Is Independent of CD95 and IFN-γ but Requires TNF-α." Journal of Immunology 160, no. 2 (January 15, 1998): 898–905. http://dx.doi.org/10.4049/jimmunol.160.2.898.

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Abstract CD8+ T cells are effective mediators of immunity against Listeria monocytogenes, but the mechanisms by which they provide antilisterial immunity are poorly understood. CD8+ T cells efficiently lyse target cells in vitro by at least two independent pathways. To test the hypothesis that CD8+ T cell-mediated immunity to L. monocytogenes is dependent on perforin or CD95 (Fas, Apo-1), we used C57Bl/6 (B6) and perforin-deficient (PO) mice to generate CD8+ T cell lines specific for the L. monocytogenes-encoded Ag listeriolysin O (LLO). Both lines specifically produce IFN-γ and TNF-α, and mediate target cell lysis in vitro. Cytolysis mediated by the PO-derived CD8+ T cell line is delayed relative to the B6-derived line and is completely inhibited by anti-CD95 Abs. In vivo, PO-derived CD8+ T cells provide specific antilisterial immunity in B6 hosts, CD95-deficient hosts, and IFN-γ-depleted hosts. However, PO-derived CD8+ T cells fail to provide antilisterial immunity in hosts depleted of TNF-α. These results indicate that single Ag-specific CD8+ T cells derived from PO mice can mediate antilisterial immunity by a mechanism that is independent of CD95 or IFN-γ, but requires TNF-α.

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Dissertations / Theses on the topic "T-cell mediated immunity"

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Abdulahad, Wayel Habib. "T-cell mediated immunity in Wegener's granulomatosis." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn/.

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Lindencrona, Jan Alvar. "Enhancing T cell mediated immunity in DNA vaccination /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-710-x.

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Lee, Laurel Yong-Hwa. "T cell mediated immunity to influenza in humans." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670049.

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Liew, F. Y. "Cell mediated-immunity against infectious diseases." Thesis, Canberra, ACT : The Australian National University, 1990. http://hdl.handle.net/1885/142999.

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Hu, Yong. "Altered T Cell-Mediated Immunity and Infectious Factors in Autism." DigitalCommons@USU, 2000. https://digitalcommons.usu.edu/etd/6846.

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Three major questions were addressed in this dissertation: 1)Do immune abnormalities associated with autism primarily alter CD4+ T cell-mediated or humoral immune responses? 2) Are specific T cell clones expanded in autism? 3) Which, if any, infectious agents play a role in autism? CD4+ T cell-mediated (Th1) or humoral (Th2) immune responses can be distinguished on the basis of the cytokines expressed. CD4+ T-cells secrete interleukin type 2 (IL-2) and interferon-γ, whereas a Th2 response is associated with secretion of interleukin type 4(IL-4). mRNA extracted from peripheral blood mononuclear nuclear cells (PBMC) showed significantly increased levels of IL-2 and interferon-γ expression in 24 autistic subjects relative to 19 normal controls. IL-4 mRNA was undetectable in the same group of autistic subjects. These results indicate that a CD4+ T cell-mediated immune response is associated with autism. The expression of V-β chain mRNA was used as a marker or particular T cell clone expression. The expression of V-β 13 was significantly elevated in the study group of 11 autistic subjects, but not in 9 normal subjects. This suggests that T cell-mediated autoimmunity is a factor in the disease. Two types of human leukocyte antigens (HLA) alleles, DR4 and DR1, are associated with autism. The association between V-β 13 expressing T cell clones and autism was shown even more strongly in the subgroups expressing HLA DR4 or DR1. This result suggests a link between antigen presentation by HLA DR4 or DR1 and expansion of V-β 13 T cell clones. The potential involvement of pathogens suspected to trigger autism was investigated by examining T cell proliferation responses to peptide epitopes. As a group, the 24 autistic subjects did not show a decreased response to peptides derived from rubella virus, influenza A virus, herpes simplex virus type 1, cytomegalovirus, and Clostridium tetani. Another model of autism postulates that autism is induced by pathogens that possess epitopes identical to the hypervariable region 3 (HVR-3) of the HLA DR4 or DR1 alleles. Two antigens derived from the Escherichia coli dna J protein and the Epstein-Barr virus glycoprotein 110 peptides that contain sequences identical to the HVR-3 of the DR4 and DR1 alleles were examined for their ability to induce T cell proliferation in autistic and normal subjects. No effect of the DR4 or DR1 alleles on the response to these two antigens was detected. Therefore, both types of results do not support the model of immune tolerance in autism. However, average T cell proliferative activity was significantly lower in the same autistic subjects. This confirms many prior reports that reduced T-cell responses may shape susceptibility to autism. Further understanding of how immune abnormalities and infectious agents lead to autism should guide development of preventative and therapeutic strategies for this disease. (152 pages)

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Ling, Khoon Lin. "Investigations into T cell mediated tumour immunity in the colon." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422657.

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Borysiewicz, L. K. "Cell mediated immunity to human cytomegalovirus infection (cytotoxic T cell and natural killer cell mediated lysis of human cytomegalovirus infected cells)." Thesis, Imperial College London, 1986. http://hdl.handle.net/10044/1/37949.

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Haßel, Silvana Katharina [Verfasser]. "Aptamers for targeted activation of T cell-mediated immunity / Silvana Katharina Haßel." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/1162953004/34.

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Klemetti, Paula. "T-cell mediated immunity in the pathogenesis of insulin-dependent diabetes mellitus." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/klemetti/.

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Agrawal, T. "Epithelial ErbB2 regulation of thymus homeostasis and age-associated T cell mediated immunity." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10048131/.

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The molecular mechanisms governing the functional and structural decline of thymus with age, causing thymic immunosenescence, are incompletely identified. Using a bitransgenic mouse model, Dr Giangreco discovered that the over-expression of receptor tyrosine kinase ErbB2 causes reversible thymic atrophy. The over-expression of epithelial ErbB2 upon doxycycline administration in bitransgenic mice led to decreased thymus size and cellularity, loss of cortical-medullary boundary and abnormal T cell differentiation, bearing similarity to age-dependent thymic involution. This thesis set out to investigate this observation in more detail. I demonstrated that the observed atrophy in bitransgenic thymuses was because of thymus-specific ErbB2 expression, by employing foetal thymic organ cultures. In addition, I showed that over-expression of epithelial ErbB2 disrupted the thymic epithelial cells distribution. Also, an increase in Sca1+Cd49f+ epithelial cells with stem cell potential was noted, explaining why the thymic atrophy in bitransgenic mice was reversible. Exploration of the potential mechanistic pathways found that the thymic atrophy phenotype of K14-NICDER mice, in which epithelial Notch is activated upon tamoxifen administration, resembled the bitransgenic mouse thymic atrophy phenotype. However, mechanistic studies failed to establish ErbB2 acting upstream of Notch, and require further investigation. Administration of Lapatinib, an ErbB2 inhibitor improved the thymic organization and function in aged mice. Lapatinib treatment of aged mice also enhanced vaccine responses to Prevenar 13, a Streptococcus pneumoniae glycoconjugate vaccine, and increased the efficacy of vaccination to protect against subsequent pneumonia challenge. However my results showed that ErbB2 inhibition does not reverse thymic atrophy in scurfy mice, which have truncated Foxp3 protein, and an autoimmune phenotype. In conclusion, this study highlights the importance of ErbB2 in maintaining thymus homeostasis and thymus mediated immunity, and proposes a novel ErbB2 inhibition therapy for rejuvenating an aged thymus, to counter the associated immunosenescence and thereby improve vaccine responses.

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Books on the topic "T-cell mediated immunity"

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1943-, Watson James D., and Marbrook John, eds. Recognition and regulation in cell-mediated immunity. New York, N.Y: M. Dekker, 1985.

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Eljaafari, Assia, and Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.

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PODACK, E. ED. Cytotoxic Effector Mechanisms (Current Topics in Microbiology & Immunology). Springer, 1989.

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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.

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Dambuza, Ivy M., Jeanette Wagener, Gordon D. Brown, and Neil A. R. Gow. Immunology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0009.

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Advances in modern medicine, such as organ transplantations and the appearance of HIV (human immunodeficiency virus), have significantly increased the patient cohort at risk of developing chronic superficial and life-threatening invasive fungal infections. To tackle this major healthcare problem, there is an urgent need to understand immunity against fungal infections for the purposes of vaccine design or immune-mediated interventions. In this chapter, we give an overview of the components of the innate and adaptive immune system and how they contribute to host defence against fungi. The various cell types contributing to fungal recognition and the subsequent stimulation of phagocytosis, the activation of inflammatory and B- and T-cell responses, and fungal clearance are discussed using the major fungal pathogens as model systems.

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Baldridge, Jory R. T cells which mediate protective immunity to Listeria Monocytogenes are H-2K restricted and distinct from the T cells mediating DTH. 1989.

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Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.

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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.

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Book chapters on the topic "T-cell mediated immunity"

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Weinberg, Adriana, and Myron J. Levin. "VZV T Cell-Mediated Immunity." In Current Topics in Microbiology and Immunology, 341–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_31.

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Broere, Femke, and Willem van Eden. "T Cell Subsets and T Cell-Mediated Immunity." In Nijkamp and Parnham's Principles of Immunopharmacology, 23–35. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-10811-3_3.

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Weringer, Elora J., and Ronald P. Gladue. "T cell-mediated diseases of immunity." In In Vivo Models of Inflammation, 237–63. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-7775-6_10.

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Khanna, Nina, and Claudia Stuehler. "T-Cell-Mediated Cross-Protective Immunity." In Methods in Molecular Biology, 295–312. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7104-6_20.

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Broere, Femke, Sergei G. Apasov, Michail V. Sitkovsky, and Willem van Eden. "A2 T cell subsets and T cell-mediated immunity." In Principles of Immunopharmacology, 15–27. Basel: Birkhäuser Basel, 2011. http://dx.doi.org/10.1007/978-3-0346-0136-8_2.

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Tatsumi, Tomohide, Amy Wesa, James H. Finke, Ronald M. Bukowski, and Walter J. Storkus. "CD4+ T-Cell-Mediated Immunity to Cancer." In Cancer Immunotherapy at the Crossroads, 67–86. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-743-7_4.

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Liew, F. Y. "Regulation of Cell-Mediated Immunity in Leishmaniasis." In T-Cell Paradigms in Parasitic and Bacterial Infections, 53–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74983-4_4.

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Lang, Pierre Olivier. "T Cell-Mediated Immunity in the Immunosenescence Process." In Immunology of Aging, 161–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-39495-9_10.

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Benedict, Chris A., Ramon Arens, Andrea Loewendorf, and Edith M. Janssen. "Modulation of T-Cell Mediated Immunity by Cytomegalovirus." In Control of Innate and Adaptive Immune Responses during Infectious Diseases, 121–39. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0484-2_7.

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Bergmann, Cornelia C., Norman W. Marten, David R. Hinton, Beatriz Parra, and Stephen A. Stohlman. "CD8 T Cell Mediated Immunity to Neurotropic MHV Infection." In Advances in Experimental Medicine and Biology, 299–308. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_46.

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Conference papers on the topic "T-cell mediated immunity"

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Piasecki, Julia, Jim Rottman, Tiep Le, Rafael Ponce, and Courtney Beers. "Abstract 4287: Talimogene laherparepvec activates systemic T-cell-mediated anti-tumor immunity." 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.am2015-4287.

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Park, Jang Hyun, and Heung Kyu Lee. "Abstract PO013: The mechanism of γδ T cell-mediated antitumor immunity in Glioblasotma multiforme." 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-po013.

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Park, Jang Hyun, and Heung Kyu Lee. "Abstract A22: A mechanism of γδ T cell-mediated antitumor immunity against brain cancer." In Abstracts: AACR Special Conference on the Microbiome, Viruses, and Cancer; February 21-24, 2020; Orlando, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.mvc2020-a22.

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Barsoum, Ivraym B., Chelsea A. Smallwood, D. Robert Siemens, and Charles H. Graham. "Abstract 447: Hypoxia induces tumor cell escape from T cell-mediated immunity via up-regulation of B7-H1." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-447.

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Khan, Samia Q., Mohd H. Faridi, Shehryar J. Khaliqdina, Antonio J. Barbosa, Judith A. Varner, and Vineet Gupta. "Abstract B03: Integrin agonists reduce infiltration of tumor-associated macrophages to promote T-cell mediated anti-tumor immunity." In 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-b03.

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Nakagawa, Satoshi, Satoshi Serada, Satoko Matsuzaki, Yutaka Ueda, Kiyoshi Yoshino, Minoru Fujimoto, Tadashi Kimura, and Tetsuji Naka. "Abstract 4911: SOCS-1 inhibits tumor growth by enhancing T cell mediated antitumor immunity related to PD-L1." 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.am2016-4911.

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Lamb, McKenna, Yao Wei, Xiaoxin Ren, Rachel O'Connor, Austin Dulak, Matthew Rausch, Jamie Strand, et al. "489 NPX267, a first-in-class monoclonal antibody targeting KIR3DL3, blocks HHLA2-mediated immunosuppression and potentiates T and NK cell-mediated antitumor immunity." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0489.

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Weber, Amy M., Hao Liu, Krithika N. Kodumudi, Amod A. Sarnaik, and Shari Pilon-Thomas. "Abstract 4978: T cell mediated immunity after combination therapy with intralesional PV-10 and co-inhibitory blockade in a melanoma model." 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.am2016-4978.

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Duperret, Elizabeth K., Alfredo Perales-Puchalt, Regina Stoltz, G. H. Hiranjith, Nitin Mandloi, James Barlow, Amitabha Chaudhuri, Niranjan Y. Sardesai, and David B. Weiner. "Abstract B67: Synthetic DNA multi-neoantigen vaccine drives predominately MHC class I CD8+ T cell-mediated effector immunity impacting tumor challenge." 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-b67.

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Lester, Daniel K., Matt Mercurio, Pasquale Innamorato, Kodumudi Krithika, Williamson Danial, Watson Gregory, Pilon-Thomas Shari, et al. "Abstract B24: Using L-fucose to render melanomas immune hot: Roles of melanoma HLA-DRB1 and CD4+T cell-mediated antitumor immunity." In 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-b24.

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Reports on the topic "T-cell mediated immunity"

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Lillehoj, Hyun, Dan Heller, and Mark Jenkins. Cellular and molecular identification of Eimeria Acervulina Merozoite Antigens eliciting protective immunity. United States Department of Agriculture, November 1992. http://dx.doi.org/10.32747/1992.7561056.bard.

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Coccidiosis, ubiquitous diseases of poultry, seriously impair the growth and feed utilization of livestock and poultry. Coccidiosis causes over $600 million annual losses world-wide and no vaccine is currently available. The goal of this study was to investigate the cellular and molecular mechanisms controlling protective immune responses to coccidia parasites in order to develop immunological control strategy against coccidiosis. The major findings of this study were: 1) cell-mediated immunity plays a major role in protection against coccidiosis, 2) when different genetic lines showing different levels of disease susceptibility were compared, higher T-cell response was seen in the strains of chickens showing higher disease resistance, 3) early interferon secretion was observed in more coccidia-resistant chicken strains, 4) both sporozoite and merozoite antigens were able to induce interferon production, and 5) chicken monoclonal antibodies which detect immunogenic coccidia proteins have been developed. This study provided a good background work for future studies toward the development of recombinant coccidial vaccine. Availability of chicken monoclonal antibodies which detect immunogenic coccidia proteins will enhance our ability to identify potential coccidial vaccine antigens.

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Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska, and Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, March 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.

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