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Journal articles on the topic 'T-cell mediated immunity'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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11

FUKAZAWA, Yoshimura. "Function of T cell subset in cell-mediated immunity." Nippon Saikingaku Zasshi 46, no. 4 (1991): 785–804. http://dx.doi.org/10.3412/jsb.46.785.

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12

van der Heyde, H. C., D. Huszar, C. Woodhouse, D. D. Manning, and W. P. Weidanz. "The resolution of acute malaria in a definitive model of B cell deficiency, the JHD mouse." Journal of Immunology 152, no. 9 (May 1, 1994): 4557–62. http://dx.doi.org/10.4049/jimmunol.152.9.4557.

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Abstract Because the role of cell-mediated immunity (CMI) in the resolution of blood-stage malaria remains unclear, we examined the question of whether mice completely lacking Ab-mediated immunity (AMI) but possessing some CMI can resolve experimental malaria previously reported not to require AMI for resolution. Severe combined immunodeficient mice reconstituted with enriched immune T cells (< 0.5% B220+ cells) suppressed acute Plasmodium chabaudi adami parasitemia, suggesting that T, but not B, cells are required to clear this form of malaria. In addition, JHD mice, which are a definitive model of B cell deficiency, were also shown to resolve P. chabaudi adami, Plasmodium vinckei petteri and Plasmodium chabaudi chabaudi malaria. These observations collectively establish that CMI alone can mediate the clearance of acute malaria caused by these subspecies of Plasmodium. Moreover, the protective cell-mediated immune response involved depends upon CD4+ T cells because JHD mice treated with anti-CD4 mAb do not resolve their infections. These results suggest that evaluation of immunization regimens to activate CD4+ T cell dependent cell mediated immunity against Plasmodium falciparum may be appropriate.

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13

Gattinoni, Luca, Anju Ranganathan, Deborah R. Surman, Douglas C. Palmer, Paul A. Antony, Marc R. Theoret, David M. Heimann, Steven A. Rosenberg, and Nicholas P. Restifo. "CTLA-4 dysregulation of self/tumor-reactive CD8+ T-cell function is CD4+ T-cell dependent." Blood 108, no. 12 (December 1, 2006): 3818–23. http://dx.doi.org/10.1182/blood-2006-07-034066.

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AbstractCytotoxic T lymphocyte–associated antigen 4 (CTLA-4) maintains peripheral tolerance by suppressing T-cell activation and proliferation but its precise role in vivo remains unclear. We sought to elucidate the impact of CTLA-4 expression on self/tumor-reactive CD8+ T cells by using the glycoprotein (gp) 100–specific T-cell receptor (TCR) transgenic mouse, pmel-1. pmel-1 CLTA-4–/– mice developed profound, accelerated autoimmune vitiligo. This enhanced autoimmunity was associated with a small but highly activated CD8+ T-cell population and large numbers of CD4+ T cells not expressing the transgenic TCR. Adoptive transfer of pmel-1 CLTA-4–/– CD8+ T cells did not mediate superior antitumor immunity in the settings of either large established tumors or tumor challenge, suggesting that the mere absence of CTLA-4–mediated inhibition on CD8+ T cells did not directly promote enhancement of their effector functions. Removal of CD4+ T cells by crossing the pmel-1 CLTA-4–/– mouse onto a Rag-1–/– background resulted in the complete abrogation of CD8+ T-cell activation and autoimmune manifestations. The effects of CD4+ CLTA-4–/– T cells were dependent on the absence of CTLA-4 on CD8+ T cells. These results indicated that CD8+ CLTA-4–/– T-cell–mediated autoimmunity and tumor immunity required CD4+ T cells in which the function was dysregulated by the absence of CTLA-4–mediated negative costimulation.

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14

Kumar, Sunil, Yideul Jeong, Muhammad Umer Ashraf, and Yong-Soo Bae. "Dendritic Cell-Mediated Th2 Immunity and Immune Disorders." International Journal of Molecular Sciences 20, no. 9 (May 1, 2019): 2159. http://dx.doi.org/10.3390/ijms20092159.

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Dendritic cells (DCs) are the professional antigen-presenting cells that recognize and present antigens to naïve T cells to induce antigen-specific adaptive immunity. Among the T-cell subsets, T helper type 2 (Th2) cells produce the humoral immune responses required for protection against helminthic disease by activating B cells. DCs induce a Th2 immune response at a certain immune environment. Basophil, eosinophil, mast cells, and type 2 innate lymphoid cells also induce Th2 immunity. However, in the case of DCs, controversy remains regarding which subsets of DCs induce Th2 immunity, which genes in DCs are directly or indirectly involved in inducing Th2 immunity, and the detailed mechanisms underlying induction, regulation, or maintenance of the DC-mediated Th2 immunity against allergic environments and parasite infection. A recent study has shown that a genetic defect in DCs causes an enhanced Th2 immunity leading to severe atopic dermatitis. We summarize the Th2 immune-inducing DC subsets, the genetic and environmental factors involved in DC-mediated Th2 immunity, and current therapeutic approaches for Th2-mediated immune disorders. This review is to provide an improved understanding of DC-mediated Th2 immunity and Th1/Th2 immune balancing, leading to control over their adverse consequences.

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15

Steinert, Elizabeth M., Karthik Vasan, and Navdeep S. Chandel. "Mitochondrial Metabolism Regulation of T Cell–Mediated Immunity." Annual Review of Immunology 39, no. 1 (April 26, 2021): 395–416. http://dx.doi.org/10.1146/annurev-immunol-101819-082015.

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Recent evidence supports the notion that mitochondrial metabolism is necessary for T cell activation, proliferation, and function. Mitochondrial metabolism supports T cell anabolism by providing key metabolites for macromolecule synthesis and generating metabolites for T cell function. In this review, we focus on how mitochondrial metabolism controls conventional and regulatory T cell fates and function.

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16

Awad, Wael, Geraldine Ler, Jeffrey Y. W. Mak, Jérôme Le Nours, James McCluskey, Alexandra J. Corbett, David P. Fairlie, and Jamie Rossjohn. "Molecular basis underpinning metabolite-mediated T-cell immunity." Acta Crystallographica Section A Foundations and Advances 77, a2 (August 14, 2021): C110. http://dx.doi.org/10.1107/s0108767321095702.

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17

Zeelenberg, Ingrid S., Wendy W. C. van Maren, Alexandre Boissonnas, Maaike A. Van Hout-Kuijer, Martijn H. M. G. M. Den Brok, Jori A. L. Wagenaars, Alie van der Schaaf, et al. "Antigen Localization Controls T Cell-Mediated Tumor Immunity." Journal of Immunology 187, no. 3 (June 24, 2011): 1281–88. http://dx.doi.org/10.4049/jimmunol.1003905.

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18

STEINMAN, RALPH M., SUMI KOIDE, MARGIT WITMER, MARY CROWLEY, NINA BHARDWAJ, PETER FREUDENTHAL, JAMES YOUNG, and KAYO INABA. "The Sensitization Phase of T-Cell-Mediated Immunity." Annals of the New York Academy of Sciences 546, no. 1 Molecular Bas (December 1988): 80–90. http://dx.doi.org/10.1111/j.1749-6632.1988.tb21622.x.

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19

Ivanovska, N., S. Philipov, and M. Hristova. "Influe of Berberine On T-Cell Mediated Immunity." Immunopharmacology and Immunotoxicology 21, no. 4 (January 1999): 771–86. http://dx.doi.org/10.3109/08923979909007141.

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20

Mayes, Kimberly, Suehyb G. Alkhatib, Kristen Peterson, Aiman Alhazmi, Carolyn Song, Vivian Chan, Tana Blevins, et al. "BPTF Depletion Enhances T-cell–Mediated Antitumor Immunity." Cancer Research 76, no. 21 (September 20, 2016): 6183–92. http://dx.doi.org/10.1158/0008-5472.can-15-3125.

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21

García-Ortiz, Almudena, and Juan M. Serrador. "Nitric Oxide Signaling in T Cell-Mediated Immunity." Trends in Molecular Medicine 24, no. 4 (April 2018): 412–27. http://dx.doi.org/10.1016/j.molmed.2018.02.002.

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22

PACHECO, R., T. GALLART, C. LLUIS, and R. FRANCO. "Role of glutamate on T-cell mediated immunity." Journal of Neuroimmunology 185, no. 1-2 (April 2007): 9–19. http://dx.doi.org/10.1016/j.jneuroim.2007.01.003.

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23

Stoltze, L., H. Rezaei, G. Jung, J. Grosclaude, P. Debey, H. Schild, and H. G. Rammensee. "CD4 + T cell-mediated immunity against prion proteins." Cellular and Molecular Life Sciences (CMLS) 60, no. 3 (March 1, 2003): 629–38. http://dx.doi.org/10.1007/s000180300054.

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24

Ogasawara, Kouetsu, and Lewis L. Lanier. "NKG2D in NK and T Cell-Mediated Immunity." Journal of Clinical Immunology 25, no. 6 (November 2005): 534–40. http://dx.doi.org/10.1007/s10875-005-8786-4.

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25

Bednarczuk, Tomasz, Yuji Hiromatsu, Yoichi Inoue, Kazuhiko Yamamoto, Jack R. Wall, and Janusz Nauman. "T-Cell–Mediated Immunity in Thyroid-Associated Ophthalmopathy." Thyroid 12, no. 3 (March 2002): 209–15. http://dx.doi.org/10.1089/105072502753600151.

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Quaranta, Valeria, and Michael C. Schmid. "Macrophage-Mediated Subversion of Anti-Tumour Immunity." Cells 8, no. 7 (July 19, 2019): 747. http://dx.doi.org/10.3390/cells8070747.

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Despite the incredible clinical benefits obtained by the use of immune checkpoint blockers (ICBs), resistance is still common for many types of cancer. Central for ICBs to work is activation and infiltration of cytotoxic CD8+ T cells following tumour-antigen recognition. However, it is now accepted that even in the case of immunogenic tumours, the effector functions of CD8+ T cells are highly compromised by the presence of an immunosuppressive tumour microenvironment (TME) at the tumour site. Tumour-associated macrophages (TAMs) are among the most abundant non-malignant stromal cell types within the TME and they are crucial drivers of tumour progression, metastasis and resistance to therapy. TAMs are able to regulate either directly or indirectly various aspects of tumour immunity, including T cell recruitment and functions. In this review we discuss the mechanisms by which TAMs subvert CD8+ T cell immune surveillance and how their targeting in combination with ICBs represents a very powerful therapeutic strategy.

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Wang, Jinghua, Brian Manick, Jun Li, Ming Bi, Vassilios Kalabokis, Anthony Person, and Guoping Wu. "CD300e Acts As A Ligand To Inhibit T Cell Immunity." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 54.16. http://dx.doi.org/10.4049/jimmunol.208.supp.54.16.

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Abstract CD300e has been reported as either an activating or inhibitory receptor and is involved in the tuning of immune responses. In this study, we demonstrate that CD300e acts as a ligand through an unknown receptor to inhibit T cell immunity. In PBMCs, CD300e protein is expressed on the cell surface of CD14+ monocytes, but not on T and B cells. CD300e-Fc fusion protein significantly reduced the expression of CD69 and CD25 on T cells, which suggest that CD300e inhibits the activation of T cells. Furthermore, CD300e-Fc fusion protein significantly inhibited TCR-mediated T cell proliferation and cytokine production including IL-2, IFN-gamma, IL-17, TNF-alpha, IL-8 and IP-10/CXCL10. Florescent conjugated CD300e-Fc fusion protein significantly bound to activated T cells and weakly to inactive T cells, suggesting that the putative CD300e counter-receptor is expressed on the cell surface of T cells, and the expression levels are upregulated upon T cell activation. CD300e-Fc fusion protein inhibited TCR-mediated p38 MAPK phosphorylation which indicates that CD300e negatively regulates T cell activation by impairing the p38 MAPK dependent antigen presentation. Moreover, our results support the notion that CD300e might be a new player in the regulation of the expansion of T cell-mediated responses. This CD300e novel T cell inhibitory pathway may provide a new strategy to modulate T cell-mediated immunity to treat immune-related diseases.

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van der Heyde, Henri C., and William P. Weidanz. "γδ T cells function in cell-mediated immunity to malaria." Nature Reviews Immunology 4, no. 8 (August 2004): 656. http://dx.doi.org/10.1038/nri1311-c1.

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29

Doherty, Peter C. "Cell Mediated Immunity in Virus Infections." Bioscience Reports 17, no. 4 (August 1, 1997): 367–87. http://dx.doi.org/10.1023/a:1027305300453.

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Parent, Michelle A., Kiera N. Berggren, Lawrence W. Kummer, Lindsey B. Wilhelm, Frank M. Szaba, Isis K. Mullarky, and Stephen T. Smiley. "Cell-Mediated Protection against Pulmonary Yersinia pestis Infection." Infection and Immunity 73, no. 11 (November 2005): 7304–10. http://dx.doi.org/10.1128/iai.73.11.7304-7310.2005.

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ABSTRACT Pulmonary infection with the bacterium Yersinia pestis causes pneumonic plague, an often-fatal disease for which no vaccine is presently available. Antibody-mediated humoral immunity can protect mice against pulmonary Y. pestis infection, an experimental model of pneumonic plague. Little is known about the protective efficacy of cellular immunity. We investigated the cellular immune response to Y. pestis in B-cell-deficient μMT mice, which lack the capacity to generate antibody responses. To effectively prime pulmonary cellular immunity, we intranasally vaccinated μMT mice with live replicating Y. pestis. Vaccination dramatically increased survival of μMT mice challenged intranasally with a lethal Y. pestis dose and significantly reduced bacterial growth in pulmonary, splenic, and hepatic tissues. Vaccination also increased numbers of pulmonary T cells, and administration of T-cell-depleting monoclonal antibodies at the time of challenge abrogated vaccine-induced survival. Moreover, the transfer of Y. pestis-primed T cells to naive μMT mice protected against lethal intranasal challenge. These findings establish that vaccine-primed cellular immunity can protect against pulmonary Y. pestis infection and suggest that vaccines promoting both humoral and cellular immunity will most effectively combat pneumonic plague.

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Mathur, A., and B. S. Michalowicz. "Cell-Mediated Immune System Regulation in Periodontal Diseases." Critical Reviews in Oral Biology & Medicine 8, no. 1 (January 1997): 76–89. http://dx.doi.org/10.1177/10454411970080010401.

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The adaptive immune system consists of humoral and cell-mediated immunity. T-lymphocytes are the key components of cell-mediated immunity. CD4+ helper T-lymphocytes facilitate B-cells to differentiate and produce specific antibodies, whereas CD8+ cytotoxic T-lymphocytes kill virally infected cells. Periodontal diseases have been associated with a variety of imbalances in the regulation of immune responses. Changes in the ratios of peripheral blood CD4+ and CD8+ T-lymphocytes, depressed proliferative responses of peripheral blood lymphocytes, and increased frequency of CD45RO+ memory T-lymphocytes in diseased tissues have been reported in individuals with various forms of periodontal disease. While some studies have shown an increased frequency of γδ+ T-cells in periodontal lesions, the role of γδ+ T-cells in periodontal disease remains controversial. The ability of putative periodontopathic bacteria selectively to stimulate certain V(3-expressing T-cells is intriguing and could determine whether a CD4+ Th I or a CD4+ Th2 cell response is elicited. The prominence of a particular subset of helper T-cells within the periodontal lesion could be a reflection of the stage and activity of the disease, or the types of bacteria present. Regardless, longitudinal studies of the involvement of T-cell subsets and cytokines in periodontal disease are clearly needed.

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Butler, Noah S., Nathan W. Schmidt, and John T. Harty. "Novel role for TNF-alpha in memory CD8 T cell-mediated protection against liver stage Plasmodium berghei infection (129.27)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 129.27. http://dx.doi.org/10.4049/jimmunol.182.supp.129.27.

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Abstract Malaria results in >1,000,000 deaths per year worldwide. Although no licensed vaccine yet exists, much effort is currently focused on subunit vaccines that elicit CD8 T cell responses directed against liver stage antigens. Multiple T cell effector molecules play a role in anti-microbial immunity mediated by memory CD8 T cells including IFN-gamma, perforin, TRAIL, FasL and TNF-alpha. However, it is not known which effector pathways are required for memory CD8 T cell-mediated immunity to liver stage Plasmodium infection. Here, we used a novel immunization strategy to generate memory CD8 T cells in the wild type and gene-deficient BALB/c mouse model of Plasmodium berghei sporozoite infection to examine the role of these T cell effector molecules in resistance to the liver stage infection. In contrast to previous work examining protection mediated by TCR transgenic effector CD8 T cells, our studies reveal that endogenous memory CD8 T cell-mediated protection is in part IFN-gamma-dependent. Importantly, we also show that neutralization of TNF-alpha in immunized mice markedly reduces memory CD8 T cell-mediated protection. Thus, our studies identify both IFN-gamma and TNF-alpha as important components of the non-cytolytic pathways that underlie memory CD8 T cell-mediated immunity against liver stage Plasmodium infection. Supported by grants from the NIH (to JTH) and an NRSA fellowship (T32AI007260-23 to NSB).

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Djaoud, Zakia, and Peter Parham. "HLAs, TCRs, and KIRs, a Triumvirate of Human Cell-Mediated Immunity." Annual Review of Biochemistry 89, no. 1 (June 20, 2020): 717–39. http://dx.doi.org/10.1146/annurev-biochem-011520-102754.

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In all human cells, human leukocyte antigen (HLA) class I glycoproteins assemble with a peptide and take it to the cell surface for surveillance by lymphocytes. These include natural killer (NK) cells and γδ T cells of innate immunity and αβ T cells of adaptive immunity. In healthy cells, the presented peptides derive from human proteins, to which lymphocytes are tolerant. In pathogen-infected cells, HLA class I expression is perturbed. Reduced HLA class I expression is detected by KIR and CD94:NKG2A receptors of NK cells. Almost any change in peptide presentation can be detected by αβ CD8+ T cells. In responding to extracellular pathogens, HLA class II glycoproteins, expressed by specialized antigen-presenting cells, present peptides to αβ CD4+ T cells. In comparison to the families of major histocompatibility complex (MHC) class I, MHC class II and αβ T cell receptors, the antigenic specificity of the γδ T cell receptors is incompletely understood.

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Mathurin, Keisha S., Gregory W. Martens, Hardy Kornfeld, and Raymond M. Welsh. "CD4 T-Cell-Mediated Heterologous Immunity between Mycobacteria and Poxviruses." Journal of Virology 83, no. 8 (February 4, 2009): 3528–39. http://dx.doi.org/10.1128/jvi.02393-08.

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ABSTRACT The bacillus Calmette-Guerin (BCG) strain of Mycobacterium bovis is used in many parts of the world as a vaccine against Mycobacterium tuberculosis. Some epidemiological evidence has suggested that BCG immunization may have unpredicted effects on resistance to other pathogens. We show here in a mouse model that BCG immunization followed by antibiotic treatment to clear the host of the pathogen rendered three strains of mice partially resistant to infection with vaccinia virus (VV) but not to lymphocytic choriomeningitis virus (LCMV). VV-challenged BCG-immune mice developed a striking splenomegaly and elevated CD4 and CD8 T-cell responses by 6 days postinfection (p.i.). However, resistance to VV infection could be seen as early as 1 to 2 days p.i. and was lost after antibody depletion of CD4 T-cell populations. BCG- but not LCMV-immune memory phenotype CD4 T cells preferentially produced gamma interferon (IFN-γ) in vivo after VV challenge. In contrast, LCMV-immune CD8 T cells preferentially produced IFN-γ in vivo in response to VV infection. In BCG-immune mice the resistance to VV infection and VV-induced CD4 T-cell IFN-γ production were ablated by cyclosporine A, which inhibits signaling through the T-cell receptor. This study therefore demonstrates CD4 T-cell-mediated heterologous immunity between a bacterium and virus. Further, it poses the question of whether BCG immunization of humans alters resistance to unrelated pathogens.

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Ura, Takehiro, Masaki Takeuchi, Tatsukata Kawagoe, Nobuhisa Mizuki, Kenji Okuda, and Masaru Shimada. "Current Vaccine Platforms in Enhancing T-Cell Response." Vaccines 10, no. 8 (August 21, 2022): 1367. http://dx.doi.org/10.3390/vaccines10081367.

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The induction of T cell-mediated immunity is crucial in vaccine development. The most effective vaccine is likely to employ both cellular and humoral immune responses. The efficacy of a vaccine depends on T cells activated by antigen-presenting cells. T cells also play a critical role in the duration and cross-reactivity of vaccines. Moreover, pre-existing T-cell immunity is associated with a decreased severity of infectious diseases. Many technical and delivery platforms have been designed to induce T cell-mediated vaccine immunity. The immunogenicity of vaccines is enhanced by controlling the kinetics and targeted delivery. Viral vectors are attractive tools that enable the intracellular expression of foreign antigens and induce robust immunity. However, it is necessary to select an appropriate viral vector considering the existing anti-vector immunity that impairs vaccine efficacy. mRNA vaccines have the advantage of rapid and low-cost manufacturing and have been approved for clinical use as COVID-19 vaccines for the first time. mRNA modification and nanomaterial encapsulation can help address mRNA instability and translation efficacy. This review summarizes the T cell responses of vaccines against various infectious diseases based on vaccine technologies and delivery platforms and discusses the future directions of these cutting-edge platforms.

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Haile, Samuel, Sonia Dalal, Virginia Clements, Koji Tamada, and Suzanne Ostrand-Rosenberg. "Soluble CD80 restores T cell activation and overcomes tumor cell Programmed Death Ligand-1-mediated suppression (P2041)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 53.21. http://dx.doi.org/10.4049/jimmunol.190.supp.53.21.

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Abstract Many tumor cells escape anti-tumor immunity through their expression of Programmed Death Ligand 1 (PDL1 or B7-H1), which interacts with T cell-expressed PD1 and results in T cell apoptosis. We previously reported that transfection of human tumor cells with a membrane-bound form of the costimulatory molecule CD80 prevented PD1 binding and restored T cell activation. We now report that membrane-bound CD80 similarly reduces PDL1-PD1-mediated suppression by mouse tumor cells, and that a fusion protein consisting of the extracellular domains of CD80 fused to an Fc domain of IgG1 overcomes PDL1-mediated suppression by human tumor cells. T cell activation experiments assessing costimulation indicate that the soluble CD80 fusion protein mediates its effects by binding to PDL1 and inhibiting PDL1-PD1 interactions. Comparison of the CD80 fusion protein to antibodies specific for PD1 or PDL1 demonstrate that soluble CD80 treatment is more effective in restoring T cell activation than treatment with mAb to either PD1 or PDL1. These studies identify soluble CD80 as an alternative and potentially more efficacious therapeutic agent for overcoming PDL1-induced immune suppression and facilitating tumor-specific immunity.

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Sugata, Kenji, Yorifumi Satou, Jun-ichirou Yasunaga, Hideki Hara, Kouichi Ohshima, Atae Utsunomiya, Masao Mitsuyama, and Masao Matsuoka. "HTLV-1 bZIP factor impairs cell-mediated immunity by suppressing production of Th1 cytokines." Blood 119, no. 2 (January 12, 2012): 434–44. http://dx.doi.org/10.1182/blood-2011-05-357459.

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Adult T-cell leukemia (ATL) patients and human T-cell leukemia virus-1 (HTLV-1) infected individuals succumb to opportunistic infections. Cell mediated immunity is impaired, yet the mechanism of this impairment has remained elusive. The HTLV-1 basic leucine zipper factor (HBZ) gene is encoded in the minus strand of the viral DNA and is constitutively expressed in infected cells and ATL cells. To test the hypothesis that HBZ contributes to HTLV-1–associated immunodeficiency, we challenged transgenic mice that express the HBZ gene in CD4 T cells (HBZ-Tg mice) with herpes simplex virus type 2 or Listeria monocytogenes, and evaluated cellular immunity to these pathogens. HBZ-Tg mice were more vulnerable to both infections than non-Tg mice. The acquired immune response phase was specifically suppressed, indicating that cellular immunity was impaired in HBZ-Tg mice. In particular, production of IFN-γ by CD4 T cells was suppressed in HBZ-Tg mice. HBZ suppressed transcription from the IFN-γ gene promoter in a CD4 T cell–intrinsic manner by inhibiting nuclear factor of activated T cells and the activator protein 1 signaling pathway. This study shows that HBZ inhibits CD4 T-cell responses by directly interfering with the host cell-signaling pathway, resulting in impaired cell-mediated immunity in vivo.

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38

Wang, Jing, and Yang-Xin Fu. "The Role of LIGHT in T Cell-Mediated Immunity." Immunologic Research 30, no. 2 (2004): 201–14. http://dx.doi.org/10.1385/ir:30:2:201.

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39

Stevens, R. H., D. A. Cole, P. A. Lindholm, and H. F. Cheng. "Identification of environmental carcinogens utilizing T-cell mediated immunity." Medical Hypotheses 19, no. 3 (March 1986): 267–85. http://dx.doi.org/10.1016/0306-9877(86)90074-5.

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Sakata, Daiji, Chengcan Yao, and Shuh Narumiya. "Emerging roles of prostanoids in T cell-mediated immunity." IUBMB Life 62, no. 8 (July 21, 2010): 591–96. http://dx.doi.org/10.1002/iub.356.

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41

Bulfone-Paus, Silvia, Erietta Stelekati, Rajia Bahri, Orietta D'Orlando, and Zane Orinska. "Mast cell-mediated antigen presentation regulates CD8 T cell effector functions (33.15)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 33.15. http://dx.doi.org/10.4049/jimmunol.182.supp.33.15.

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Abstract Mast cells (MCs) - long-living cells at sites of host-environment interphase, are important players of the innate immunity and central regulatory cells in adaptive immunity. We have previously described that MCs can detect viral infections and that TLR3-activated MCs contribute to antiviral host defence. MCs can regulate CD8 T cell- dependent autoimmune responses and CD8 T cell chemotaxis. Using three model antigens, we demonstrate that MCs induce antigen-specific CD8 T cell activation and proliferation. This requires direct cell contact and MHC class I-dependent antigen cross-presentation by MCs and induces the secretion of IL-2, IFN-γ and MIP-1α by CD8 T cells. Furthermore, MCs regulate antigen-specific CD8 T cell cytotoxicity by increasing granzyme B expression and promoting CD8 T cell degranulation. MCs also upregulate their expression of costimulatory molecules, and release the T cell proliferation inducer osteopontin upon direct contact. In vivo, adoptive transfer of antigen-pulsed MCs induces MHC class I-dependent, antigen-specific CD8 T cell proliferation. Furthermore, we characterised the bidirectional crosstalk between MCs and CD8 T cells and identified a new pathway of MC activation induced by MC interaction with CD8 T cells. Specifically, a number of genes coding for proteins involved in the IFN-mediated antiviral response are upregulated upon MC-CD8 T cell interaction.

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Thiel, Andreas, Marco Frentsch, Joanna Listopad, Regina Stark, Alberto Sada Japp, Nadine Matzmohr, Sarah Meier, Ichiro Taniuchi, and Thomas Blankenstein. "CD40L+ CD8+ T-Cell Dependent Antitumor Immunity." Blood 124, no. 21 (December 6, 2014): 5818. http://dx.doi.org/10.1182/blood.v124.21.5818.5818.

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Abstract CD40 is frequently expressed on malignant cells of different origin. Due to the observed antitumorigenic effects induced after CD40 engagement it represents an attractive target for immunotherapies. We demonstrate here that CD40L expressing tumor-specific CD8+ T-cell population can act as potent physiological CD40 agonist against CD40 expressing tumor cells. We demonstrate that in the course of cancer cell rejection high frequencies of tumor-specific CD40L+ CD8+ T cells are induced. Strikingly, in contrast to wild-type (wt), CD40L deficient CD8+ T cells were unable to prevent tumor formation in lymphopenic as well as in fully immunocompetent hosts. Apparently, in our setting CD40L expressed by CD8+ T cells is essential for cancer cell rejection. CD40L-mediated rejection does not depend on interaction with CD40+ host cells such as antigen-presenting cells but on CD40 expression by cancer cells. Our findings disclose CD40L expression by CD8+ T cells as a new antitumor effector function that should be implemented in future adoptive T-cell therapies against cancer. Disclosures No relevant conflicts of interest to declare.

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Noble, Alistair, Lydia Durant, Lesley Hoyles, Anne L. Mccartney, Ripple Man, Jonathan Segal, Samuel P. Costello, et al. "Deficient Resident Memory T Cell and CD8 T Cell Response to Commensals in Inflammatory Bowel Disease." Journal of Crohn's and Colitis 14, no. 4 (October 26, 2019): 525–37. http://dx.doi.org/10.1093/ecco-jcc/jjz175.

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Abstract Background and Aims The intestinal microbiota is closely associated with resident memory lymphocytes in mucosal tissue. We sought to understand how acquired cellular and humoral immunity to the microbiota differ in health versus inflammatory bowel disease [IBD]. Methods Resident memory T cells [Trm] in colonic biopsies and local antibody responses to intraepithelial microbes were analysed. Systemic antigen-specific immune T and B cell memory to a panel of commensal microbes was assessed. Results Systemically, healthy blood showed CD4 and occasional CD8 memory T cell responses to selected intestinal bacteria, but few memory B cell responses. In IBD, CD8 memory T cell responses decreased although B cell responses and circulating plasmablasts increased. Possibly secondary to loss of systemic CD8 T cell responses in IBD, dramatically reduced numbers of mucosal CD8+ Trm and γδ T cells were observed. IgA responses to intraepithelial bacteria were increased. Colonic Trm expressed CD39 and CD73 ectonucleotidases, characteristic of regulatory T cells. Cytokines/factors required for Trm differentiation were identified, and in vitro-generated Trm expressed regulatory T cell function via CD39. Cognate interaction between T cells and dendritic cells induced T-bet expression in dendritic cells, a key mechanism in regulating cell-mediated mucosal responses. Conclusions A previously unrecognised imbalance exists between cellular and humoral immunity to the microbiota in IBD, with loss of mucosal T cell-mediated barrier immunity and uncontrolled antibody responses. Regulatory function of Trm may explain their association with intestinal health. Promoting Trm and their interaction with dendritic cells, rather than immunosuppression, may reinforce tissue immunity, improve barrier function, and prevent B cell dysfunction in microbiota-associated disease and IBD aetiology.

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Popova, N. N., and V. G. Savchenko. "Reconstitution of T-cell-mediated immunity in patients after allogeneic stem cell transplantation." Russian journal of hematology and transfusiology 65, no. 1 (March 11, 2020): 24–38. http://dx.doi.org/10.35754/0234-5730-2020-65-1-24-38.

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Background. The timely reconstitution of the donor-derived immune system is a key factor in the prevention of such post-transplant complications as graft versus host disease, relapse or secondary tumours and various infections. These complications affect the long-term survival of patients after allogeneic stem cell transplantation.Aim — to describe the main stages of T Cell–mediated immune recovery in patients after allogeneic stem cell transplantation.General ﬁndings. T-cell–mediated immunity is responsible for anti-infective and anti-tumour immune response. The early post-transplant period is characterized by the thymus-independent pathway of T-cell recovery largely involving proliferation of mature donor T cells, which were transplanted to the patient together with hematopoietic stem cells. To a lesser extent, this recovery pathway is realized through the expansion of host naïve and memory T cells, which survived after conditioning. Thymus-dependent reconstitution involves generation of de novo naïve T cells and subsequent formation of a pool of memory T-cells providing the main immunological effects — graft versus tumour and graft versus host reactions. A better understanding of the T-cell immune reconstitution process is important for selecting optimized pre-transplant conditioning regimens and patient-speciﬁc immunosuppressive therapy approaches, thus reducing the risks of post-transplant complications and improving the long-term survival of patients after allogeneic stem cell transplantation.

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Endsley, Janice J., Alison Hogg, Lis Shell, Martin McAlauy, Charles Capinos Scherer, Tracey Coffey, Chris Howard, Brian Nonnecke, W. Ray Waters, and D. Mark Estes. "Biomarkers of CD4+ CTL cell mediated immunity to tuberculosis (43.51)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S46. http://dx.doi.org/10.4049/jimmunol.178.supp.43.51.

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Abstract The immune responses mediated by interactions between T-lymphocyte subsets and mycobacteria-infected macrophages are critical for control of tuberculosis . In these studies, the bovine model was used to characterize the cytolytic and mycobactericidal CD4+ T cell response induced by BCG vaccination. Antigenic stimulation of CD4+ T-cells from BCG vaccinated cattle induced expression of perforin and IFNgamma in cells expressing a CD45RA−, CD45RO+, and CD62L+ cell surface phenotype. Antigen specific enhancement of granulysin, IFNgamma, perforin, IL-4, IL-13, and IL-21 mRNA expression was detected and not detected for IL-2, IL-6, IL-10, IL-15, TNFα, FasL, and CD40L. Following antigenic stimulation, CD4+ T cells from BCG vaccinated animals contributed to reduction of intracellular BCG in infected macrophages. These results demonstrate that vaccination with BCG induces a subpopulation of mycobacteria-specific CD4+ T cells that are characterized by the expression of a cell-surface memory phenotype, enhanced expression of mycobactericidal molecules, and anti-mycobacterial activity against intracellular M. bovis. This work was supported by the NIAID Fellowship for Training in Emerging and Re-emerging Infectious Disease and the Sealy Center for Vaccine Development, UTMB, the Texas-United Kingdom Collaborative Research Initiative, and the Institute for Animal Health by DEFRA and the BBSRC, UK.

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46

Mirenda, Vincenzo, Sarah J. Jarmin, Rachel David, Julian Dyson, Diane Scott, Yan Gu, Robert I. Lechler, Klaus Okkenhaug, and Federica M. Marelli-Berg. "Physiologic and aberrant regulation of memory T-cell trafficking by the costimulatory molecule CD28." Blood 109, no. 7 (November 21, 2006): 2968–77. http://dx.doi.org/10.1182/blood-2006-10-050724.

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Abstract Productive T-cell immunity requires both the activation and the migration of specific T cells to the antigenic tissue. The costimulatory molecule CD28 plays an essential role in the initiation of T-cell–mediated immunity. We investigated the possibility that CD28 may also regulate migration of primed T cells to target tissue. In vitro, CD28-mediated signals enhanced T-cell transendothelial migration, integrin clustering, and integrin-mediated migration. In vivo, T cells bearing a mutation in the CD28 cytoplasmic domain, which abrogates PI3K activation, displayed normal clonal expansion but defective localization to antigenic sites following antigenic rechallenge. Importantly, antibody-mediated CD28 stimulation led to unregulated memory T-cell migration to extra-lymphoid tissue, which occurred independently of T-cell receptor (TCR)–derived signals and homing-receptor expression. Finally, we provide evidence that CD28- and CTLA-4–mediated signals exert opposite effects on T-cell trafficking in vivo. These findings highlight a novel physiologic function of CD28 that has crucial implications for the therapeutic manipulation of this and other costimulatory molecules.

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Esen, Emel, Ismail Sergin, Rajiv Jesudason, Patricia Himmels, Joshua D. Webster, Hua Zhang, Min Xu, et al. "MAP4K4 negatively regulates CD8 T cell–mediated antitumor and antiviral immunity." Science Immunology 5, no. 45 (March 27, 2020): eaay2245. http://dx.doi.org/10.1126/sciimmunol.aay2245.

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During cytotoxic T cell activation, lymphocyte function-associated antigen–1 (LFA-1) engages its ligands on antigen-presenting cells (APCs) or target cells to enhance T cell priming or lytic activity. Inhibiting LFA-1 dampens T cell–dependent symptoms in inflammation, autoimmune diseases, and graft-versus-host disease. However, the therapeutic potential of augmenting LFA-1 function is less explored. Here, we show that genetic deletion or inhibition of mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) enhances LFA-1 activation on CD8 T cells and improves their adherence to APCs or LFA-1 ligand. In addition, loss of Map4k4 increases CD8 T cell priming, which culminates in enhanced antigen-dependent activation, proliferation, cytokine production, and cytotoxic activity, resulting in impaired tumor growth and improved response to viral infection. LFA-1 inhibition reverses these phenotypes. The ERM (ezrin, radixin, and moesin) proteins reportedly regulate T cell–APC conjugation, but the molecular regulator and effector of ERM proteins in T cells have not been defined. In this study, we demonstrate that the ERM proteins serve as mediators between MAP4K4 and LFA-1. Last, systematic analyses of many organs revealed that inducible whole-body deletion of Map4k4 in adult animals is tolerated under homeostatic conditions. Our results uncover MAP4K4 as a potential target to augment antitumor and antiviral immunity.

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Kumamoto, Yosuke, Melissa Linehan, Jason S. Weinstein, Brian J. Laidlaw, Joseph E. Craft, and Akiko Iwasaki. "CD301b+ Dermal Dendritic Cells Drive T Helper 2 Cell-Mediated Immunity." Immunity 39, no. 4 (October 2013): 733–43. http://dx.doi.org/10.1016/j.immuni.2013.08.029.

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O'Leary, Jacqueline G., Mahmoud Goodarzi, Danielle L. Drayton, and Ulrich H. von Andrian. "T cell– and B cell–independent adaptive immunity mediated by natural killer cells." Nature Immunology 7, no. 5 (April 16, 2006): 507–16. http://dx.doi.org/10.1038/ni1332.

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50

Griffith, Thomas S., Stephanie A. Condotta, Lorraine T. Tygrett, Deepa Rai, Jessica A. Yang, Kathryn A. Pape, Katherine A. Murphy, Javier Cabrera-Perez, Thomas J. Waldschmidt, and Vladimir P. Badovinac. "Sepsis compromises primary B cell-mediated responses." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 195.15. http://dx.doi.org/10.4049/jimmunol.196.supp.195.15.

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Abstract Sepsis is the leading cause of death in non-coronary ICU’s, and one hallmark of sepsis patients is sustained immune suppression. Septic patients exhibit compromised innate and adaptive immunity, making them highly susceptible to secondary infections. Using the cecal ligation and puncture (CLP) model of sepsis, we recently showed the recovery of CD4 T cells from CLP-induced lymphopenia is accompanied by alterations in the composition and function of the Ag-specific CD4 T cell repertoire. These data led us to hypothesize that CD4 T cell-dependent B cell responses would also be impaired after CLP. Using the same CLP model, we immunized sham (control) and CLP mice with PE-conjugated 2W1S56 peptide 30 d after surgery, and then we quantitated the number of 2W1S-specific CD4 T cells and PE-specific B cells 7 d later. Compared to sham mice, CLP-treated mice immunized with PE-2W1S56 had a sustained reduction in number of 2W1S-specific Tfh CD4 T cells and naïve/memory PE-specific B cells after CLP. Next, we immunized sham and CLP mice with TNP-KLH plus either CpG or alum early (2 d) or late (30 d) after surgery to induce Th1 or Th2 Ab responses, respectively. We observed compromised production of anti-TNP Ab in mice immunized with either TNP-KLH/CpG or alum early (2 d) after CLP. Importantly, Ab production remained reduced in mice immunized with TNP-KLH/alum late (30 d) after CLP. Together, our data show CLP-induced sepsis impacts humoral immunity by affecting the number and function of Ag-specific B cells and CD4 Tfh cells. Moreover, these data suggest potential for defects in humoral immunity to newly introduced Ag (e.g., vaccines) in sepsis survivors long after the septic event has resolved.

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