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Journal articles on the topic 'T cell transfer'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Chapman, Paul B. "Programming T cells for adoptive T cell transfer therapy." Pigment Cell & Melanoma Research 23, no. 2 (February 1, 2010): 155–56. http://dx.doi.org/10.1111/j.1755-148x.2010.00681.x.

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2

Sharma, Preeti, and David M. Kranz. "T Cell Receptors for Gene Transfer in Adoptive T Cell Therapy." Critical Reviews in Immunology 39, no. 2 (2019): 105–22. http://dx.doi.org/10.1615/critrevimmunol.2019030788.

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3

Berger, Carolina, Michael C. Jensen, and Stanley R. Riddell. "Establishing T Cell Memory by Adoptive Transfer of T Cell Clones." Blood 108, no. 11 (November 16, 2006): 866. http://dx.doi.org/10.1182/blood.v108.11.866.866.

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Abstract Adoptive transfer of T cells has been employed to reconstitute T cell immunity to viruses such as cytomegalovirus (CMV) in immunodeficient allogeneic stem cell transplant (SCT) patients and is being investigated to treat malignancies. In the allogeneic SCT setting, the T cells are derived from the donor and need to be isolated as clones or highly pure populations to avoid graft-versus-host disease. CD8+ T cells can be divided into defined subsets including CD62L− effector memory (TEM) and central memory T cells (TCM) expressing the CD62L lymph node homing molecule. Both TCM and TEM can give rise to cytolytic effector T cells (TE) after antigen stimulation and can be expanded in vitro for immunotherapy. However, the potential of T cells derived from either the TEM or TCM subset to persist in vivo has not been investigated. We used a macaque model to determine whether reconstitution of T cell memory to CMV by adoptive transfer of CD8+ T cell clones depended on their origin from either the CD62L+ TCM or CD62L− TEM subset. T cell clones were retrovirally transduced to express the macaque CD19 or CD20 surface marker to allow tracking of T cells in vivo. Clones derived from both TCM and TEM had similar avidity and proliferative capacity in vitro, and had a TE phenotype (CD62L−CCR7−CD28−CD127−, granzyme B+). TCM and TEM-derived T cell clones were transferred to macaques at doses of 3–6×108/kg and were both detected in the blood one day after transfer at 1.2–2.7% (low dose) to 20–25% (high dose) of CD8+ T cells. However, the frequency of TEM-derived T cells was undetectable after 3–5 days, and the cells were not present in lymph node or bone marrow obtained at day 14. By contrast, TCM-derived clones persisted in peripheral blood, migrated to tissue sites, and were detectable long-term at significant levels. A distinguishing feature of TCM-derived cells was their responsiveness to homeostatic cytokines. Only TCM-derived clones were rescued from apoptotic cell death by low-dose IL15 for >30 days in vitro and this correlated with higher levels of IL15Rα, IL2Rβ, and IL2Rγ, and of Bcl-xL and Bcl-2, which promote cell survival. To determine if the inability of TEM-derived clones to survive in vitro correlated with an increased susceptibility of cell death in vivo, we measured the proportion of infused cells that were positive for propidium iodide (PI) and Annexin V during the short period of in vivo persistence. One day after transfer, 41–45% of TEM-derived T cells were Annexin V+/PI+, analyzed directly in the blood or after 24 hours of culture. By contrast, only a minor fraction of an adoptively transferred TCM-derived T cell clone was Annexin V+/PI+ and the infused cells survived in vivo. A subset of the persisting T cells reacquired TCM marker (CD62L+CCR7+CD127+CD28+) in vivo and regained functional properties of TCM (direct lytic activity; rapid proliferation to antigen). These T cells produced IFN-γ and TNF-α after peptide stimulation, and studies are in progress to assess their in vivo response to antigen by delivery of T cells expressing CMV proteins. Our studies in a large animal model show for the first time that CD8+ TE derived from TCM but not TEM can persist long-term, occupy memory T cell niches, and restore TCM subsets of CMV-specific immunity. Thus, taking advantage of the genetic programming of cells that have become TCM might yield T cells with greater therapeutic activity and could be targeted for human studies of T cell therapy for both viral and malignant disease.

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4

Itzhaki, Orit, Daphna Levy, Dragoslav Zikich, Avraham J. Treves, Gal Markel, Jacob Schachter, and Michal J. Besser. "Adoptive T-cell transfer in melanoma." Immunotherapy 5, no. 1 (January 2013): 79–90. http://dx.doi.org/10.2217/imt.12.143.

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5

Kessels, Helmut W. H. G., Monika C. Wolkers, and Ton N. M. Schumacher. "Adoptive transfer of T-cell immunity." Trends in Immunology 23, no. 5 (May 2002): 264–69. http://dx.doi.org/10.1016/s1471-4906(02)02219-6.

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6

Conrad, Heinke, Peter Meyerhuber, Barbara Kast, Julia Mueller, Christian Peschel, Wolfgang Uckert, and Helga Bernhard. "Redirection of human T lymphocytes towards HER2 by T cell receptor gene transfer for adoptive T cell transfer (41.6)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 41.6. http://dx.doi.org/10.4049/jimmunol.182.supp.41.6.

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Abstract The clinical goal of our studies is the adoptive transfer of primary T cells transduced with a HER2-specific T cell receptor (TCR) for patients with HER2-overexpressing breast cancer. HLA-A2-, CD8 T cells were stimulated with allogeneic HLA-A2+ dendritic cells (DC) pulsed with the peptide HER2369-377. HER2369-377-reactive T cells were screened, cloned and further tested in functional assays. The TCR from the HER2-reactive CTL clone KU1 was cloned into a retrovirus. Primary T lymphocytes were transduced with this construct and functionally compared with the parental CTL clone KU1. The TCR-transduced primary T cells recognized the peptide HER2369-377 exogenously loaded onto T2 cells or endogenously expressed by tumor cells and transfectants. Similar to the parental CTL clone KU1, the transgenic T cells were not only able to recognize HER2369-377, but also the corresponding peptides from HER3 and HER4. Following TCR optimization (codon optimization, murinization), the TCR-transduced T cells displayed an enhanced tumor cell recognition. In conclusion, the fine specificity of a HER2-reactive TCR is conserved following transduction into primary T lymphocytes. These results facilitate the design of HER2-directed immunotherapies based on TCR-transduced T cells. The observed cross-recognition especially with HER3 may be beneficial as HER2 and HER3 overexpressing tumors are particularly aggressive. DFG

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7

Katsura, Y., T. Kina, T. Amagai, T. Tsubata, K. Hirayoshi, Y. Takaoki, T. Sado, and S. I. Nishikawa. "Limiting dilution analysis of the stem cells for T cell lineage." Journal of Immunology 137, no. 8 (October 15, 1986): 2434–39. http://dx.doi.org/10.4049/jimmunol.137.8.2434.

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Abstract Stem cell activities of bone marrow, spleen, thymus, and fetal liver cells for T cell lineage were studied comparatively by transferring the cells from these organs through i.v. or intrathymus (i.t.) route into right leg- and tail-shielded (L-T-shielded) and 900 R-irradiated recipient mice, which were able to survive without supplying hemopoietic stem cells. Cells from B10.Thy-1.1 (H-2b, Thy-1.1) mice were serially diluted and were transferred into L-T-shielded and irradiated C57BL/6 (H-2b, Thy-1.2) mice, and 21 days later the thymus cells of recipient mice were assayed for Thy-1.1+ cells by flow cytofluorometry. The percentage of recipient mice possessing donor-type T cells was plotted against the number of cells transferred, and the stem cell activity in each cell source was expressed as the 50% positive value, the number of donor cells required for generating donor-type T cells in the thymuses of 50% of recipient mice. In i.v. transfer experiments, the activity of bone marrow cells was similar to that of fetal liver cells, and about 100 times and nearly 1000 times higher than those of spleen cells and thymus cells, respectively. In i.t. transfer experiments, the number of cells required for generating donor-type T cells was much lower than that in i.v. transfer experiments, although the ratio in 50% positive values between i.v. and i.t. transfers differed among cell sources. In i.t. transfers, the 50% positive value of bone marrow cells was five times, 400 times, and 500 times higher than that of fetal liver cells, spleen cells, and thymus cells, respectively. Our previous finding that stem cells are enriched in the spleens of mice which were whole body-irradiated and marrow-reconstituted 7 days earlier was confirmed also by the present limiting dilution assay carried out in i.v. as well as i.t. transfers.

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8

Heemskerk, Mirjam H. M., Manja Hoogeboom, Renate Hagedoorn, Michel G. D. Kester, Roel Willemze, and J. H. Frederik Falkenburg. "Reprogramming of Virus-specific T Cells into Leukemia-reactive T Cells Using T Cell Receptor Gene Transfer." Journal of Experimental Medicine 199, no. 7 (March 29, 2004): 885–94. http://dx.doi.org/10.1084/jem.20031110.

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T cells directed against minor histocompatibility antigens (mHags) might be responsible for eradication of hematological malignancies after allogeneic stem cell transplantation. We investigated whether transfer of T cell receptors (TCRs) directed against mHags, exclusively expressed on hematopoietic cells, could redirect virus-specific T cells toward antileukemic reactivity, without the loss of their original specificity. Generation of T cells with dual specificity may lead to survival of these TCR-transferred T cells for prolonged periods of time in vivo due to transactivation of the endogenous TCR of the tumor-reactive T cells by the latent presence of viral antigens. Furthermore, TCR transfer into restricted T cell populations, which are nonself reactive, will minimize the risk of autoimmunity. We demonstrate that cytomegalovirus (CMV)-specific T cells can be efficiently reprogrammed into leukemia-reactive T cells by transfer of TCRs directed against the mHag HA-2. HA-2-TCR–transferred CMV-specific T cells derived from human histocompatibility leukocyte antigen (HLA)-A2+ or HLA-A2− individuals exerted potent antileukemic as well as CMV reactivity, without signs of anti–HLA-A2 alloreactivity. The dual specificity of these mHag-specific, TCR-redirected virus-specific T cells opens new possibilities for the treatment of hematological malignancies of HLA-A2+ HA-2–expressing patients transplanted with HLA-A2–matched or –mismatched donors.

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9

Koste, L., T. Beissert, H. Hoff, L. Pretsch, Ö. Türeci, and U. Sahin. "T-cell receptor transfer into human T cells with ecotropic retroviral vectors." Gene Therapy 21, no. 5 (April 3, 2014): 533–38. http://dx.doi.org/10.1038/gt.2014.25.

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10

Vanham, Guido, Lieve Penne, Heidi Allemeersch, Luc Kestens, Betty Willems, Guido van der Groen, Kuan-Teh Jeang, Zahra Toossi, and Elizabeth Rich. "Modeling HIV transfer between dendritic cells and T cells: importance of HIV phenotype, dendritic cell– T cell contact and T-cell activation." AIDS 14, no. 15 (October 2000): 2299–311. http://dx.doi.org/10.1097/00002030-200010200-00011.

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11

Rabinowitz, Ruth, Russell Pokroy, Yongmao Yu, and Michael Schlesinger. "Activated Human T-Cells Bestow T-Cell Antigens to Non-T-Cells by Intercellular Antigen Transfer." Human Immunology 59, no. 6 (June 1998): 331–42. http://dx.doi.org/10.1016/s0198-8859(98)00029-9.

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12

Isser, Ariel, and Jonathan P. Schneck. "High-affinity T cell receptors for adoptive cell transfer." Journal of Clinical Investigation 129, no. 1 (December 10, 2018): 69–71. http://dx.doi.org/10.1172/jci125471.

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13

Han, Fei, Emilia R. Dellacecca, Levi W. Barse, Cormac Cosgrove, Steven W. Henning, Christian M. Ankney, Dinesh Jaishankar, et al. "Adoptive T-Cell Transfer to Treat Lymphangioleiomyomatosis." American Journal of Respiratory Cell and Molecular Biology 62, no. 6 (June 2020): 793–804. http://dx.doi.org/10.1165/rcmb.2019-0117oc.

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14

Tey, Siok‐Keen, Catherine M. Bollard, and Helen E. Heslop. "Adoptive T‐cell transfer in cancer immunotherapy." Immunology & Cell Biology 84, no. 3 (June 2006): 281–89. http://dx.doi.org/10.1111/j.1440-1711.2006.01441.x.

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15

Alderton, Gemma K. "Promising results from autologous T cell transfer." Nature Reviews Cancer 14, no. 4 (March 24, 2014): 215. http://dx.doi.org/10.1038/nrc3716.

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16

Jensen, Michael C. "Engineering GVL Through T Cell Gene Transfer." Biology of Blood and Marrow Transplantation 14, no. 1 (January 2008): 5. http://dx.doi.org/10.1016/j.bbmt.2007.10.011.

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17

Theil, A., C. Wilhelm, M. Kuhn, A. Petzold, S. Tuve, U. Oelschlägel, A. Dahl, M. Bornhäuser, E. Bonifacio, and A. Eugster. "T cell receptor repertoires after adoptive transfer of expanded allogeneic regulatory T cells." Clinical & Experimental Immunology 187, no. 2 (November 27, 2016): 316–24. http://dx.doi.org/10.1111/cei.12887.

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18

Brusko, Todd M., Richard C. Koya, Shirley Zhu, Michael R. Lee, Amy L. Putnam, Stephanie A. McClymont, Michael I. Nishimura, et al. "Human Antigen-Specific Regulatory T Cells Generated by T Cell Receptor Gene Transfer." PLoS ONE 5, no. 7 (July 22, 2010): e11726. http://dx.doi.org/10.1371/journal.pone.0011726.

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19

Baumann, Tobias, Andreas Dunkel, Christian Schmid, Sabine Schmitt, Michael Hiltensperger, Kerstin Lohr, Vibor Laketa, et al. "Regulatory myeloid cells paralyze T cells through cell–cell transfer of the metabolite methylglyoxal." Nature Immunology 21, no. 5 (April 23, 2020): 555–66. http://dx.doi.org/10.1038/s41590-020-0666-9.

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20

Zakrzewski, Johannes L., Adam A. Kochman, Sydney X. Lu, Theis H. Terwey, Theo D. Kim, Vanessa M. Hubbard, Stephanie J. Muriglan, et al. "Adoptive transfer of T-cell precursors enhances T-cell reconstitution after allogeneic hematopoietic stem cell transplantation." Nature Medicine 12, no. 9 (August 27, 2006): 1039–47. http://dx.doi.org/10.1038/nm1463.

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21

Cheng, Jie, Guanghua Chen, Hui Lv, Liangjing XU, Huiwen LIU, Tianping Chen, Lijun Qu, et al. "CD4-Targeted T Cells Rapidly Induce Remissions in Mice with T Cell Lymphoma." BioMed Research International 2021 (March 27, 2021): 1–6. http://dx.doi.org/10.1155/2021/6614784.

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Objective. To explore the immune cell therapy for T cell lymphoma, we developed CD4-specific chimeric antigen receptor- (CAR-) engineered T cells (CD4CART), and the cytotoxic effects of CD4CART cells were determined in vitro and in vivo. Methods. CD4CART cells were obtained by transduction of lentiviral vector encoding a single-chain antibody fragment (scFv) specific for CD4 antigen, costimulatory factor CD28 fragment, and intracellular signal transduction domain of CD3 fragments. Control T cells were obtained by transduction of reporter lentiviral vector. The cytotoxicity, tumor growth, and survival rate of mice with T cell lymphoma were analyzed after adoptive T cell transfer in vivo. Results. CD4CART cells had potent cytotoxic activity against CD4+ T1301 tumor T cells in a concentration-dependent manner. In addition, adoptive CD4CART cell transfer significantly suppressed tumor growth and improved animal survival with T cell lymphoma, compared to the mice who received control T cells and PBS. Conclusion. CD4CART cells have potent cytotoxic effects on T cell lymphoma. The study provided an experimental basis for CD4CART-mediated therapy of T cell lymphoma.

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22

Houot, Roch, Liora Michal Schultz, Aurélien Marabelle, and Holbrook Kohrt. "T-cell–based Immunotherapy: Adoptive Cell Transfer and Checkpoint Inhibition." Cancer Immunology Research 3, no. 10 (October 2015): 1115–22. http://dx.doi.org/10.1158/2326-6066.cir-15-0190.

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23

Veatch, Joshua, Kelly Paulson, Yuta Asano, Lauren Martin, Bo Lee, Evan Thomas Hall, Shailender Bhatia, Paul Nghiem, and Aude Chapuis. "Merkel polyoma virus specific T-cell receptor transgenic T-cell therapy in PD-1 inhibitor refractory Merkel cell carcinoma." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): 9549. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.9549.

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9549 Background: Merkel cell carcinoma is an aggressive neuroendocrine tumor of skin origin with most cases caused by the Merkel polyoma virus (MCPyV). While many patients benefit from PD-1/PD-L1 axis blockade, most patients do not respond or develop resistance. We sought to ask whether adoptive transfer of autologous T cells transduced with MCPyV specific T cells could lead to clinical responses in PD-1 inhibitor refractory patients. Methods: Five MCPyV positive, HLA-A02 patients with PD-1 inhibitor refractory metastatic Merkel cell carcinoma were treated with adoptive transfer of CD62L+ CD8+ and CD4+ autologous T cells transduced with a T cell receptor (TCR) targeting an HLA-A0201 restricted MCPyV epitope. Two different strategies were used to facilitate T cell expansion: In 3 patients, single fraction radiation was administered to a subset of lesions prior to T cell transfer. In 2 patients, lymphodepleting chemotherapy with cyclophosphamide and fludarabine was administered prior to T cell transfer. Anti PD-1/PD-L1 therapy was given 14 days after T cell infusion. Transgenic T cells were visualized in tumor biopsies by multiplex immunohistochemistry. Results: 5 patients were treated, with 4 patients receiving 100 million tetramer positive CD8+ T cells and one patient receiving 500 million cells. 3 patients received second infusions with between 300 million and 900 million tetramer positive cells. No dose limiting toxicities or cytokine release syndrome were observed. T cell persistence was lower in the 2 patients treated with lymphodepleting chemotherapy relative to the 3 patients treated with single fraction radiation. Transgenic T cells persisted at tumor sites greater than 1 month following transfer. 4 patients experienced progressive disease, and a single patient had a mixed response and greater than 1 year disease free interval following local therapy of an isolated site of progression. The responding patient was the only patient with class I MHC staining on tumor cells prior to treatment, and the site of local progression in that patient showed the presence of TCR transgenic T cells but loss of class I MHC expression. Conclusions: MCPyV specific transgenic T cells are safe, traffic to tumor sites, and can result in a clinical response, but their clinical activity may be limited by down-regulation of class I MHC expression on tumors. A future trial will address strategies to increase class I MHC expression on Merkel tumors. Clinical trial information: NCT03747484.

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24

Feuchtinger, Tobias, Celine Richard, Rupert Handgretinger, Christiane Braun, Michael Schumm, and Peter Lang. "Hexon Specific T-Cells for Adoptive T-Cell Transfer as a Treatment of Adenovirus Infection after Allogeneic Stem Cell Transplantation." Blood 108, no. 11 (November 16, 2006): 2853. http://dx.doi.org/10.1182/blood.v108.11.2853.2853.

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Abstract Adenovirus infection (ADV) after allogeneic hematopoietic stem cell transplantation (HSCT) is an emerging pathogen causing relevant morbidity and mortality, with preponderance in children. Since a sufficient host T-cell response has been shown essential to clear the virus, diagnostic procedures for detection of virus-specific T-cells have recently developed to asses the specific cellular immune response. Furthermore adoptive immunotherapy is a new treatment option for patients with absent specific T-cell response and present systemic adenoviral infection. The possibility of an adoptive T-cell transfer depends on the availability of GMP compatible protocols and reagents. The adenoviral hexon protein was shown a immunodominant T-cell target within the viral capsid. In the present study we investigate the presence of Hexon-specific T-cell responses in HSCT donors, i.e. the availability of donors for an adoptive T-cell transfer. Secondly, the emergence of Hexon-specific T-cells in recipients post HSCT was analyzed. Thirdly, a protocol was established under GMP-conditions for adoptive T-cell immunotherapy through isolation of IFN-γ secreting T-cells after ex-vivo stimulation with the adenoviral Hexon protein. This procedure resulted in a mixed population of CD4 and CD8 positive T-cells with an effector memory phenotype and Th1 cytokine pattern (n=8). Isolated Hexon-specific T-cells show a strong expansion potential in vitro as well as specific cytotoxic activity. The availability of a donor was evaluated in 76 HSCT donors. Only 17.1% of donors had no ADV-specific T-cell response and 72.4% of donors were eligible for an adoptive T-cell transfer using the presented approach. The Hexon protein was responsible for almost the complete response to ADV, since no significant difference was seen against ADV lysate and the Hexon protein. In 76% HSCT recipients Hexon directed T-cell responses were evaluated and were shown to be responsible for clearance of the viral infection. In conclusion feasibility of an adoptive T-cell transfer for the treatment of ADV infection post HSCT is shown in accordance to current GMP regulations.

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25

Kieback, E., J. Charo, D. Sommermeyer, T. Blankenstein, and W. Uckert. "A safeguard eliminates T cell receptor gene-modified autoreactive T cells after adoptive transfer." Proceedings of the National Academy of Sciences 105, no. 2 (January 8, 2008): 623–28. http://dx.doi.org/10.1073/pnas.0710198105.

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26

Jamieson, B. D., and R. Ahmed. "T cell memory. Long-term persistence of virus-specific cytotoxic T cells." Journal of Experimental Medicine 169, no. 6 (June 1, 1989): 1993–2005. http://dx.doi.org/10.1084/jem.169.6.1993.

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This study documents that virus-specific CTL can persist indefinitely in vivo. This was accomplished by transferring Thy-1.1 T cells into Thy-1.2 recipient mice to specifically identify the donor T cell population and to characterize its antigenic specificity and function by using a virus-specific CTL assay. Thy-1.1+ T cells from mice previously immunized with lymphocytic choriomeningitis virus (LCMV) were transferred into Thy-1.2 mice persistently infected with LCMV. The transferred LCMV-specific CTL (Thy-1.1+ CD8+) eliminate virus from the chronically infected carriers and persist in the recipient mice in small numbers, comprising only a minor fraction of the total T cells. Upon re-exposure to virus, these long-lived "resting" CD8+ T cells proliferate in vivo to become the predominant cell population. These donor CD8+ T cells can be recovered up to a year post-transfer and still retain antigenic specificity and biological function. They kill LCMV infected H-2-matched cells in vitro and can eliminate virus upon transfer into a second infected host. In addition, these long-lived CD8+ T cells appear not to be dependent on help from CD4+ T cells, since depletion of CD4+ T cells has minimal or no effect on their biological properties (proliferation, CTL response, viral clearance). These donor CTL also exhibit an immunodominance over the host-derived LCMV-specific CTL response. When both host and donor T cells are present, the donor CTL response is dominant over the potential CTL response of the cured carrier host. Taken together, these results suggest that virus-specific CTL can persist for the life span of the host as memory cells.

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27

Nguyen, Vu H., Sumana Shashidhar, Daisy S. Chang, Lena Ho, Neeraja Kambham, Michael Bachmann, Janice M. Brown, and Robert S. Negrin. "The impact of regulatory T cells on T-cell immunity following hematopoietic cell transplantation." Blood 111, no. 2 (January 15, 2008): 945–53. http://dx.doi.org/10.1182/blood-2007-07-103895.

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Regulatory T cells (Tregs) prevent graft-versus-host disease (GvHD) by inhibiting the proliferation and function of conventional T cells (Tcons). However, the impact of Tregs on T-cell development and immunity following hematopoietic cell transplantation (HCT) is unknown. Using a murine GvHD model induced by Tcons, we demonstrate that adoptive transfer of Tregs leads to (1) abrogration of GvHD, (2) preservation of thymic and peripheral lymph node architecture, and (3) an accelerated donor lymphoid reconstitution of a diverse TCR-Vβ repertoire. The resultant enhanced lymphoid reconstitution in Treg recipients protects them from lethal cytomegalovirus (MCMV) infection. By contrast, mice that receive Tcons alone have disrupted lymphoid organs from GvHD and remain lymphopenic with a restricted TCR-Vβ repertoire and rapid death on MCMV challenge. Lymphocytes from previously infected Treg recipients generate secondary response specific to MCMV, indicating long-term protective immunity with transferred Tregs. Thymectomy significantly reduces survival after MCMV challenge in Treg recipients compared with euthymic controls. Our results indicate that Tregs enhance immune reconstitution by preventing GvHD-induced damage of the thymic and secondary lymphoid microenvironment. These findings provide new insights into the role of Tregs in affording protection to lymphoid stromal elements important for T-cell immunity.

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Romero, Diana. "T cell transfer after allo-HSCT in AML." Nature Reviews Clinical Oncology 16, no. 9 (July 9, 2019): 528. http://dx.doi.org/10.1038/s41571-019-0251-z.

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29

Maus, Marcela V. "Tumour tamed by transfer of one T cell." Nature 558, no. 7709 (May 30, 2018): 193–95. http://dx.doi.org/10.1038/d41586-018-05251-5.

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30

EPSTEIN, W., M. OKAMOTO, H. SUYA, and K. FUKUYAMA. "T-cell independent transfer of organized granuloma formation." Immunology Letters 14, no. 1 (November 17, 1986): 59–63. http://dx.doi.org/10.1016/0165-2478(86)90021-0.

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31

Moss, Paul A. H. "Redirecting T cell specificity by TCR gene transfer." Nature Immunology 2, no. 10 (October 1, 2001): 900–901. http://dx.doi.org/10.1038/ni1001-900.

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32

Pape, Kathryn A., Elizabeth R. Kearney, Alexander Khoruts, Anna Mondino, Rebecca Merica, Zong-Ming Chen, Elizabeth Ingulli, Jennifer White, Julia G. Johnson, and Marc K. Jenkins. "Use of adoptive transfer of T-cell antigen-receptor-transgenic T cells for the study of T-cell activation in vivo." Immunological Reviews 156, no. 1 (April 1997): 67–78. http://dx.doi.org/10.1111/j.1600-065x.1997.tb00959.x.

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33

Zhang, Jifeng, Brice E. Barefoot, Wenjian Mo, Divino Deoliveira, Jessica Son, Xiuyu Cui, Elizabeth Ramsburg, and Benny J. Chen. "CD62L− memory T cells enhance T-cell regeneration after allogeneic stem cell transplantation by eliminating host resistance in mice." Blood 119, no. 26 (June 28, 2012): 6344–53. http://dx.doi.org/10.1182/blood-2011-03-342055.

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A major challenge in allogeneic hematopoietic cell transplantation is how to transfer T-cell immunity without causing graft-versus-host disease (GVHD). Effector memory T cells (CD62L−) are a cell subset that can potentially address this challenge because they do not induce GVHD. Here, we investigated how CD62L− T cells contributed to phenotypic and functional T-cell reconstitution after transplantation. On transfer into allogeneic recipients, CD62L− T cells were activated and expressed multiple cytokines and cytotoxic molecules. CD62L− T cells were able to deplete host radioresistant T cells and facilitate hematopoietic engraftment, resulting in enhanced de novo T-cell regeneration. Enhanced functional immune reconstitution was demonstrated in CD62L− T-cell recipients using a tumor and an influenza virus challenge model. Even though CD62L− T cells are able to respond to alloantigens and deplete host radioresistant immune cells in GVHD recipients, alloreactive CD62L− T cells lost the reactivity over time and were eventually tolerant to alloantigens as a result of prolonged antigen exposure, suggesting a mechanism by which CD62L− T cells were able to eliminate host resistance without causing GVHD. These data further highlight the unique characteristics of CD62L− T cells and their potential applications in clinical hematopoietic cell transplantation.

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Busch, Annette, Thomas Quast, Sascha Keller, Waldemar Kolanus, Percy Knolle, Peter Altevogt, and Andreas Limmer. "Transfer of T Cell Surface Molecules to Dendritic Cells upon CD4+ T Cell Priming Involves Two Distinct Mechanisms." Journal of Immunology 181, no. 6 (September 3, 2008): 3965–73. http://dx.doi.org/10.4049/jimmunol.181.6.3965.

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Kitamura, K., J. Farber, and B. Kelsall. "Possible role for CCR6+ regulatory T cell in the T cell-transfer model of colitis." Inflammatory Bowel Diseases 17, suppl_1 (January 1, 2011): S5. http://dx.doi.org/10.1093/ibd/17.supplement1.s5a.

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Rifa'i, Muhaimin, Yoshiyuki Kawamoto, Izumi Nakashima, and Haruhiko Suzuki. "Essential Roles of CD8+CD122+ Regulatory T Cells in the Maintenance of T Cell Homeostasis." Journal of Experimental Medicine 200, no. 9 (November 1, 2004): 1123–34. http://dx.doi.org/10.1084/jem.20040395.

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Regulation of immune system is of paramount importance to prevent immune attacks against self-components. Mice deficient in the interleukin (IL)-2/IL-15 receptor β chain, CD122, are model animals of such immune attacks and characteristically have a high number of abnormally activated T cells. Here, we show that the transfer of CD8+CD122+ cells into CD122-deficient neonates totally prevented the development of abnormal T cells. Furthermore, recombination activating gene–2−/− mice that received wild-type mice–derived CD8+CD122− cells died within 10 wk after cell transfer, indicating that normal CD8+CD122− cells become dangerously activated T cells in the absence of CD8+CD122+ T cells. CD8+CD122+ cells could control activated CD8+ or CD4+ T cells both in vivo and in vitro. Our results indicate that the CD8+CD122+ population includes naturally occurring CD8+ regulatory T cells that control potentially dangerous T cells.

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Zhou, Qi, Irene C. Schneider, Inan Edes, Annemarie Honegger, Patricia Bach, Kurt Schönfeld, Axel Schambach, et al. "T-cell receptor gene transfer exclusively to human CD8+ cells enhances tumor cell killing." Blood 120, no. 22 (November 22, 2012): 4334–42. http://dx.doi.org/10.1182/blood-2012-02-412973.

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AbstractTransfer of tumor-specific T-cell receptor (TCR) genes into patient T cells is a promising strategy in cancer immunotherapy. We describe here a novel vector (CD8-LV) derived from lentivirus, which delivers genes exclusively and specifically to CD8+ cells. CD8-LV mediated stable in vitro and in vivo reporter gene transfer as well as efficient transfer of genes encoding TCRs recognizing the melanoma antigen tyrosinase. Strikingly, T cells genetically modified with CD8-LV killed melanoma cells reproducibly more efficiently than CD8+ cells transduced with a conventional lentiviral vector. Neither TCR expression levels, nor the rate of activation-induced death of transduced cells differed between both vector types. Instead, CD8-LV transduced cells showed increased granzyme B and perforin levels as well as an up-regulation of CD8 surface expression in a small subpopulation of cells. Thus, a possible mechanism for CD8-LV enhanced tumor cell killing may be based on activation of the effector functions of CD8+ T cells by the vector particle displaying OKT8-derived CD8-scFv and an increase of the surface density of CD8, which functions as coreceptor for tumor-cell recognition. CD8-LV represents a powerful novel vector for TCR gene therapy and other applications in immunotherapy and basic research requiring CD8+ cell-specific gene delivery.

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Sprague, Wendy S., Melissa Robbiani, Paul R. Avery, Kevin P. O'Halloran, and Edward A. Hoover. "Feline immunodeficiency virus dendritic cell infection and transfer." Journal of General Virology 89, no. 3 (March 1, 2008): 709–15. http://dx.doi.org/10.1099/vir.0.83068-0.

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Feline immunodeficiency virus (FIV) interacts with dendritic cells (DC) during initiation of infection, but whether DC support or transfer FIV infection remains unclear. To address this issue, we studied the susceptibility of feline myeloid DC to FIV infection and assessed potential transfer of infection from DC to CD4+ T cells. FIV was detected in membrane-bound vesicles of DC within 2 h of inoculation, although only low concentrations of FIV DNA were found in virus-exposed isolated DC. Addition of resting CD4+ T cells increased viral DNA levels; however, addition of activated CD4+ T cells resulted in a burst of viral replication manifested by FIV p27 capsid antigen generation. To determine whether transfer of FIV infection required productively infected DC (vs virus bound to DC but not internalized), virus-exposed DC were cultured for 2 days to allow for degradation of uninternalized virus and initiation of infection in the DC, then CD4+ T blasts were added. Infection of T cells remained robust, indicating that T-cell infection is likely to be mediated by de novo viral infection of DC followed by viral transfer during normal DC/T-cell interactions. We conclude that feline DC support restricted FIV infection, which nevertheless is sufficient to efficiently transfer infection to susceptible T cells and trigger the major burst of viral replication. Feline DC/FIV/T-cell interactions (similar to those believed to occur in human immunodeficiency virus and simian immunodeficiency virus infections) highlight the means by which immunodeficiency-inducing lentiviruses exploit normal DC/T-cell interactions to transfer and amplify virus infection.

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Ku, Manching, Eugene Ke, Mohsen Sabouri-Ghomi, Justin R. Abadejos, Brent Freeman, Amy Nham, Nathaniel Phillips, Kevin Y. Yang, Kathy O. Lui, and Oktay Kirak. "Deconstructive somatic cell nuclear transfer reveals novel regulatory T-cell subsets." Journal of Allergy and Clinical Immunology 142, no. 3 (September 2018): 997–1000. http://dx.doi.org/10.1016/j.jaci.2018.04.038.

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Iqbal, Nuzhat, James R. Oliver, Frederic H. Wagner, Audrey J. Lazenby, Charles O. Elson, and Casey T. Weaver. "T Helper 1 and T Helper 2 Cells Are Pathogenic in an Antigen-specific Model of Colitis." Journal of Experimental Medicine 195, no. 1 (January 7, 2002): 71–84. http://dx.doi.org/10.1084/jem.2001889.

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Dysregulated T cell responses to enteric bacteria have been implicated as a common mechanism underlying pathogenesis in rodent models of colitis. However, the bacterial species and T cell specificities that induce disease have been poorly defined. We have developed a model system in which target antigen, bacterial host, and corresponding T cell specificity are defined. OVA-specific T cells from DO11.RAG-2−/− TCR transgenic mice were transferred into RAG-2−/− recipients whose intestinal tracts were colonized with OVA-expressing or control Escherichia coli. Transfer of antigen-naive DO11.RAG-2−/− T cells into recipients colonized with OVA-E. coli resulted in enhanced intestinal recruitment and cell cycling of OVA-specific T cells; however, there was no development of disease. In contrast, transfer of polarized T helper (Th) 1 and Th2 populations resulted in severe wasting and colitis in recipients colonized with OVA-expressing but not control E. coli. The histopathologic features of disease induced by Th1 and Th2 transfers were distinct, but disease severity was comparable. Induction of disease by both Th1 and Th2 transfers was dependent on bacterially associated OVA. These results establish that a single bacterially associated antigen can drive the progression of colitis mediated by both Th1 and Th2 cells and provide a new model for understanding the immunoregulatory interactions between T cells responsive to gut floral antigens.

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Debets, Reno, Ralph Willemsen, and Reinder Bolhuis. "Adoptive transfer of T-cell immunity: gene transfer with MHC-restricted receptors." Trends in Immunology 23, no. 9 (September 2002): 435–36. http://dx.doi.org/10.1016/s1471-4906(02)02290-1.

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Schumacher, Ton N. M., Monika C. Wolkers, and Helmut W. H. G. Kessels. "Adoptive transfer of T-cell immunity: gene transfer with MHC-restricted receptors." Trends in Immunology 23, no. 9 (September 2002): 436–37. http://dx.doi.org/10.1016/s1471-4906(02)02292-5.

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43

Griffioen, Marieke, H. M. Esther van Egmond, Menno A. W. G. van der Hoorn, Renate S. Hagedoorn, Michel Kester, Roelof Willemze, J. H. Frederik Falkenburg, and Mirjam Heemskerk. "T Cell Receptor Gene Transfer to Virus-Specific T Cells for Cellular Anti-Tumor Immunotherapy." Blood 110, no. 11 (November 16, 2007): 2594. http://dx.doi.org/10.1182/blood.v110.11.2594.2594.

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Abstract Patients with relapsed hematological malignancies after allogeneic stem cell transplantation (alloSCT) can be successfully treated by donor lymphocyte infusions (DLI). Since DLI consists of a variety of T cells with different specificities, the benificial anti-leukemic effect of DLI is often accompanied by Graft-versus-Host Disease (GvHD). Genetic modification of T cells to express T cell receptors (TCR) with defined anti-tumor specificity would be an attractive strategy to specifically eradicate the malignant cells without induction of GvHD. We previously demonstrated that transfer of the minor histocompatibility antigen HA-2 specific TCR to CMV specific T cells led to the generation of T cells with dual specificity for CMV as well as HA-2. CMV and EBV specific T cells are ideal target cells for TCR gene transfer, since the majority of human individuals have high frequencies of these T cells due to latent persistence of CMV and EBV. In addition, based on their virus specificity, these T cells do not induce GvHD in an alloSCT setting, and we hypothesize that due to frequent encounter with viral antigens, TCR transferred virus specific T cells will survive for a prolonged period of time in vivo. The aim of this study is to develop a clinical grade method for the generation of TCR transduced virus specific T cells for cellular immunotherapy. CMV and EBV specific T cells were isolated from healthy individuals using pentamers in combination with clinical grade available anti-biotin magnetic beads. Isolation by pentamer-coated beads induced stimulation, expansion and efficient transduction of virus specific T cells, leading to the generation of cell lines with high frequencies of virus specific (>80%) and transduced (20–40%) T cells. T cells were transduced with multi-cistronic retroviral vectors encoding the α and β chains of the HA-2 TCR linked by an IRES or 2A-like sequence. No differences in transduction efficiency and TCR surface expression were observed between the IRES and 2A-like vectors. The transduced virus specific T cells were shown to exhibit dual specificity and tetramer staining of the introduced TCR correlated with specific lysis of target cells endogenously-expressing HA-2. Furthermore, variation in surface expression of the introduced TCR was observed between T cells with different virus specificities. T cells directed against the HLA-A1 epitope of CMV-pp50, for example, efficiently expressed the HA-2 TCR, whereas T cells specific for the HLA-B8 epitope of EBV-EBNA-3A did not express the introduced TCR. Functional analyses demonstrated that TCR-transduced pp50 specific T cells were dual specific, recognizing HA-2 as well as pp50 positive target cells, whereas TCR-engineered EBNA-3A specific T cells were primarily EBNA-3A specific. The efficiency of surface expression of the transferred TCR was shown to be determined by intrinsic properties of the TCRs, illustrating that for TCR gene transfer purposes TCRs need to be selected that exhibit high competition potential, whereas recipient T cells need to express endogenous TCRs with low competition potential. For clinical application, TCRs will be transferred to virus specific T cells selected for their capacity to efficiently express the introduced TCR without loss of virus specificity. The safety, clinical and immunological efficacy of TCR gene transfer to virus specific T cells as cellular anti-tumor immunotherapy after alloSCT will be investigated in a clinical phase I/II study.

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Yu, Shiguang, Gordon C. Sharp, and Helen Braley-Mullen. "CD4+ T cells are required for CD8+ T-cell activation but not for CD8+ T cell effector function for induction of thyrocyte hyperplasia (TEC H/P) and fibrosis (93.7)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 93.7. http://dx.doi.org/10.4049/jimmunol.184.supp.93.7.

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Abstract IFN-γ-/-NOD.H-2h4 mice develop TEC H/P and fibrosis characterized by abnormal proliferation of thyrocytes and infiltration of thyroids by CD4+ and CD8+ T cells. CD8+ T cells are the primary effector cells for TEC H/P. CD4-/- and CD8-/- IFN-γ-/- NOD.H-2h4 mice were generated to determine if CD4+ T cells were required for activation of CD8+ T cells that induce TEC H/P and fibrosis. 60-70% of IFN-γ-/- mice given NaI water for 6-7 mo develop severe TEC H/P and fibrosis, compared to 11 of 53 (21%) CD4-/- mice and only 2 of 42 (5%) CD8-/- mice. TEC H/P incidence in CD4-/- mice given splenocytes from CD8-/- mice is similar to that of IFN-γ-/- mice (60%). Splenocytes from IFN-γ-/- donors with severe TEC H/P transfer severe TEC H/P to SCID recipients after culture in vitro for 72 hr, and purified CD8+ T cells from the same donors also transfer severe TEC H/P to SCID recipients. Splenocytes from some CD4-/- donors with severe TEC H/P can transfer severe TEC H/P to SCID recipients, but more often they transfer only minimal disease. These results suggest that CD4+ T cells are required for optimal activation of CD8+ T cells that induce TEC H/P, and they may also be important for optimal in vitro activation of CD8+ T cells that induce severe TEC H/P. In contrast, after CD8+ T cells are fully activated, CD4+ T cells are not required for their mobilization to thyroids or for effector function leading to TEC H/P and fibrosis.

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Chen, Aoshuang, Shanrong Liu, David Park, Youmin Kang, and Guoxing Zheng. "Depleting Intratumoral CD4+CD25+ Regulatory T Cells via FasL Protein Transfer Enhances the Therapeutic Efficacy of Adoptive T Cell Transfer." Cancer Research 67, no. 3 (February 1, 2007): 1291–98. http://dx.doi.org/10.1158/0008-5472.can-06-2622.

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Kursar, Mischo, Kerstin Bonhagen, Joachim Fensterle, Anne Köhler, Robert Hurwitz, Thomas Kamradt, Stefan H. E. Kaufmann, and Hans-Willi Mittrücker. "Regulatory CD4+CD25+ T Cells Restrict Memory CD8+ T Cell Responses." Journal of Experimental Medicine 196, no. 12 (December 9, 2002): 1585–92. http://dx.doi.org/10.1084/jem.20011347.

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CD4+ T cell help is important for the generation of CD8+ T cell responses. We used depleting anti-CD4 mAb to analyze the role of CD4+ T cells for memory CD8+ T cell responses after secondary infection of mice with the intracellular bacterium Listeria monocytogenes, or after boost immunization by specific peptide or DNA vaccination. Surprisingly, anti-CD4 mAb treatment during secondary CD8+ T cell responses markedly enlarged the population size of antigen-specific CD8+ T cells. After boost immunization with peptide or DNA, this effect was particularly profound, and antigen-specific CD8+ T cell populations were enlarged at least 10-fold. In terms of cytokine production and cytotoxicity, the enlarged CD8+ T cell population consisted of functional effector T cells. In depletion and transfer experiments, the suppressive function could be ascribed to CD4+CD25+ T cells. Our results demonstrate that CD4+ T cells control the CD8+ T cell response in two directions. Initially, they promote the generation of a CD8+ T cell responses and later they restrain the strength of the CD8+ T cell memory response. Down-modulation of CD8+ T cell responses during infection could prevent harmful consequences after eradication of the pathogen.

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Hamad, M., M. Whetsell, and J. R. Klein. "T cell precursors in the spleen give rise to complex T cell repertoires in the thymus and the intestine." Journal of Immunology 155, no. 6 (September 15, 1995): 2866–76. http://dx.doi.org/10.4049/jimmunol.155.6.2866.

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Abstract T cell precursors located in peripheral immune tissues have been studied according to the potential to repopulate the thymus and the gut of lethally irradiated mice. T cell repopulation could be achieved with spleen cells from athymic or euthymic mice thoroughly devoid of mature T cells. Repopulation did not occur with lymph node lymphocytes as determined from studies in congenic mice. The kinetics of T cell repopulation differed in the gut and thymus in that donor-derived T cells appeared in the gut by day 7 after cell transfer, and in the thymus by day 14 after cell transfer. The multipotent nature of splenic T cell precursors was evident from the finding that all major phenotypic subsets of T cells in the thymus and the gut developed after spleen cell transfer. T cell repopulation of the intraepithelial lymphocytes also occurred efficiently in athymic radiation chimeras injected with spleen cells from congenitally athymic nude mice, demonstrating that gut T cell repopulation by those cells does not require a functional thymus. PCR-spectratype analyses of twenty-four V beta TCR genes in thymocytes and intraepithelial lymphocytes revealed extensive TCR-beta repertoires in both tissues 1 to 2 wk after cell transfer, although T cells with rearranged TCR were undetectable in the donor spleen cell population. The minimal phenotype of the splenic T cell precursor was determined to be CD3-, CD4-, CD8-, HSA+.

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Fossati, Gianluca, Anne Cooke, Ruby Quartey Papafio, Kathryn Haskins, and Brigitta Stockinger. "Triggering a Second T Cell Receptor on Diabetogenic T Cells Can Prevent Induction of Diabetes." Journal of Experimental Medicine 190, no. 4 (August 16, 1999): 577–84. http://dx.doi.org/10.1084/jem.190.4.577.

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In this paper, we test the hypothesis that triggering of a second T cell receptor (TCR) expressed on diabetogenic T cells might initiate the onset of diabetes. A cross between two TCR-transgenic strains, the BDC2.5 strain that carries diabetogenic TCRs and the A18 strain that carries receptors specific for C5, was set up to monitor development of diabetes after activation through the C5 TCR. F1 BDC2.5 × A18 mice developed diabetes spontaneously beyond 3–4 mo of age. Although their T cells express both TCRs constitutively, the A18 receptor is expressed at extremely low levels. In vitro activation of dual TCR T cells followed by adoptive transfer into neonatal or adult F1 mice resulted in diabetes onset and death within 10 d after transfer. In contrast, in vivo immunization of F1 mice with different forms of C5 antigen not only failed to induce diabetes but protected mice from the spontaneous onset of diabetes. We propose that antigenic stimulation of cells with low levels of TCR produces signals inadequate for full activation, resulting instead in anergy.

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Autio, Anu, Huan Wang, Francisco Velázquez, Gail Newton, Charles A. Parkos, Pablo Engel, Daniel Engelbertsen, Andrew H. Lichtman, and Francis W. Luscinskas. "SIRPα - CD47 axis regulates dendritic cell-T cell interactions and TCR activation during T cell priming in spleen." PLOS ONE 17, no. 4 (April 12, 2022): e0266566. http://dx.doi.org/10.1371/journal.pone.0266566.

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The SIRPα-CD47 axis plays an important role in T cell recruitment to sites of immune reaction and inflammation but its role in T cell antigen priming is incompletely understood. Employing OTII TCR transgenic mice bred to Cd47-/- (Cd47KO) or SKI mice, a knock-in transgenic animal expressing non-signaling cytoplasmic-truncated SIRPα, we investigated how the SIRPα-CD47 axis contributes to antigen priming. Here we show that adoptive transfer of Cd47KO or SKI Ova-specific CD4+ T cells (OTII) into Cd47KO and SKI recipients, followed by Ova immunization, elicited reduced T cell division and proliferation indices, increased apoptosis, and reduced expansion compared to transfer into WT mice. We confirmed prior reports that splenic T cell zone, CD4+ conventional dendritic cells (cDCs) and CD4+ T cell numbers were reduced in Cd47KO and SKI mice. We report that in vitro derived DCs from Cd47KO and SKI mice exhibited impaired migration in vivo and exhibited reduced CD11c+ DC proximity to OTII T cells in T cell zones after Ag immunization, which correlates with reduced TCR activation in transferred OTII T cells. These findings suggest that reduced numbers of CD4+ cDCs and their impaired migration contributes to reduced T cell-DC proximity in splenic T cell zone and reduced T cell TCR activation, cell division and proliferation, and indirectly increased T cell apoptosis.

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Ptak, W., D. R. Green, and P. Flood. "Cellular interactions in the adoptive transfer of contact sensitivity: characterization of an antigen-nonspecific Vicia villosa-adherent T cell needed for adoptive transfer into naive recipients." Journal of Immunology 137, no. 6 (September 15, 1986): 1822–28. http://dx.doi.org/10.4049/jimmunol.137.6.1822.

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Abstract The adoptive transfer of delayed-type hypersensitivity (DTH) into naive recipients requires the interaction of two functionally distinct Ly-1+ T cells: and I-J- cell effector cell for DTH which transfers antigen-specific DTH only into animals whose suppressive mechanisms have been compromised, and and I-J+ cell which alone never transfers DTH but allows the transfer of DTH by the I-J- DTH effector cell into naive animals. We investigated the phenotypic and functional characteristics of the cell which "protects" the I-J- DTH effector cell from host suppressive mechanisms and allows the transfer of DTH into naive recipients. This cell was found to express the cell surface phenotype Lyt-1+,2-, L3T4+, and I-J+, and, in contrast to the I-J- DTH effector cell, was found to be adherent to the lectin Vicia villosa (VV). These cells routinely are found in the spleens of both immune or naive animals, and regardless of their origin are antigen-nonspecific in their functional activity in that they complement VV-nonadherent cells to transfer DTH responses of both TNP and oxazolone-primed cells. Treatment of recipient mice with cyclophosphamide (to remove host suppressor mechanisms) or Bordetella pertussis vaccine (which stimulates splenic T cells to circulate) abrogates the need for these cells in the transfer population, whereas treatment of donor mice with B. pertussis functionally depletes these cells from splenic T cell populations. Therefore, it appears that in the adoptive transfer of DTH responses, the antigen-specific I-J- VV-nonadherent cell requires an I-J+ VV-adherent cell in the circulation to overcome host suppressive mechanisms. The importance of these I-J+ cells in DTH responses is discussed.

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