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Journal articles on the topic 'Anti-CTLA-4'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Robert, Caroline, and Christine Mateus. "Anticorps anti-CTLA-4." médecine/sciences 27, no. 10 (2011): 850–58. http://dx.doi.org/10.1051/medsci/20112710013.

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2

&NA;. "Anti-CTLA-4 monoclonal antibody." Reactions Weekly &NA;, no. 1042 (2005): 6–7. http://dx.doi.org/10.2165/00128415-200510420-00013.

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3

Cepero, Enrique, H. James Hnatyszyn, Günter Kraus, and Mathias G. Lichtenheld. "Potent Inhibition of CTLA-4 Expression by an Anti-CTLA-4 Ribozyme." Biochemical and Biophysical Research Communications 247, no. 3 (1998): 838–43. http://dx.doi.org/10.1006/bbrc.1998.8889.

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4

Killock, David. "Interferon in anti-CTLA-4 responses." Nature Reviews Clinical Oncology 13, no. 11 (2016): 653. http://dx.doi.org/10.1038/nrclinonc.2016.166.

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5

Bapodra, Anuj, Ines Esteves Domingues Pires Da Silva, Kevin P. Lui, et al. "Clinical outcome and CD4+ differentiation in anti-CTLA-4/radiation and anti-CTLA-4/steroid therapy." Journal of Clinical Oncology 32, no. 15_suppl (2014): 3019. http://dx.doi.org/10.1200/jco.2014.32.15_suppl.3019.

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6

Damle, N. K., K. Klussman, G. Leytze, et al. "Costimulation of T lymphocytes with integrin ligands intercellular adhesion molecule-1 or vascular cell adhesion molecule-1 induces functional expression of CTLA-4, a second receptor for B7." Journal of Immunology 152, no. 6 (1994): 2686–97. http://dx.doi.org/10.4049/jimmunol.152.6.2686.

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Abstract Costimulation by the CD28 ligand B7/BB1 plays an important role during T cell proliferation primarily by augmenting synthesis of IL-2 and other cytokines. Resting CD4+ T cells express CD28 but not CTLA-4 on their surface. Costimulation of T cells with ICAM-1 or VCAM-1 induced CTLA-4 expression and up-regulated CD28 expression. CD28 and CTLA-4 were independently distributed on the surface of activated T lymphoblasts. When co-immobilized with anti-TCR mAb both anti-CD28 and anti-CTLA-4 mAb augmented T cell proliferation. Although anti-CD28-mediated augmentation of T cell proliferation w

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7

Hong, Megan M. Y., and Saman Maleki Vareki. "Addressing the Elephant in the Immunotherapy Room: Effector T-Cell Priming versus Depletion of Regulatory T-Cells by Anti-CTLA-4 Therapy." Cancers 14, no. 6 (2022): 1580. http://dx.doi.org/10.3390/cancers14061580.

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Cytotoxic T-lymphocyte Associated Protein 4 (CTLA-4) is an immune checkpoint molecule highly expressed on regulatory T-cells (Tregs) that can inhibit the activation of effector T-cells. Anti-CTLA-4 therapy can confer long-lasting clinical benefits in cancer patients as a single agent or in combination with other immunotherapy agents. However, patient response rates to anti-CTLA-4 are relatively low, and a high percentage of patients experience severe immune-related adverse events. Clinical use of anti-CTLA-4 has regained interest in recent years; however, the mechanism(s) of anti-CTLA-4 is not

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Korman, Alan J., John Engelhardt, Vafa Shahabi, et al. "Role of the immunoglobulin constant region in the antitumor activity of antibodies to cytotoxic T-lymphocyte antigen-4 (CTLA-4)." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9055. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9055.

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9055 Background: Anti-CTLA-4 therapy enhances antitumor T-cell responses by both cell-intrinsic and cell-extrinsic mechanisms. Effector T-cell (Teff) activation is increased directly by interfering with CTLA-4-B7 interactions that negatively regulate T cells and by interfering with CTLA-4 expressed on regulatory T cells (Tregs), which function to inhibit immune responses. To analyze in greater detail the mechanism of action of anti-CTLA-4 antibodies (Abs), we examined the role of the immunoglobulin constant region in the antitumor activity of anti-CTLA-4 Abs in mouse tumor models. Methods: The

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9

Zhang, Peng, Xinxin Xiong, Christian Rolfo, et al. "Mechanism- and Immune Landscape-Based Ranking of Therapeutic Responsiveness of 22 Major Human Cancers to Next Generation Anti-CTLA-4 Antibodies." Cancers 12, no. 2 (2020): 284. http://dx.doi.org/10.3390/cancers12020284.

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Background: CTLA-4 was the first immune checkpoint targeted for cancer therapy and the first target validated by the FDA (Food and Drug Administration) after approval of the anti-CTLA-4 antibody, Ipilimumab. However, clinical response rates to anti-CTLA-4 antibodies are lower while the rates of immunotherapy-related adverse events (irAE) are higher than with anti-PD-1 antibodies. As a result, the effort to target CTLA-4 for cancer immunotherapy has stagnated. To reinvigorate CTLA-4-targeted immunotherapy, we and others have reported that rather than blocking CTLA-4 interaction with its cognate

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10

Wang, Bin, Lei Qin, Mei Ren, and Hao Sun. "Effects of Combination of Anti-CTLA-4 and Anti-PD-1 on Gastric Cancer Cells Proliferation, Apoptosis and Metastasis." Cellular Physiology and Biochemistry 49, no. 1 (2018): 260–70. http://dx.doi.org/10.1159/000492876.

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Background/Aims: Gastric cancer (GC) is one of the most common and lethal varieties of cancers. Anticancer activities of anti-CTLA-4 and anti-PD-1 antibodies have been explored in different cancers, including GC. The study aimed to explore the role of combination therapy with anti-CTLA-4 and anti-PD-1 antibodies in GC cells, and understand the possible underlying molecular mechanism. Methods: MKN-45 and MGC-803 cells were divided into four groups, namely control, CTLA-4, PD-1, and CTLA-4&PD-1. Cell viability, cell cycle, apoptosis, migration and invasion were measured by MTT, flow cytometr

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11

Linsley, P. S., J. L. Greene, P. Tan, et al. "Coexpression and functional cooperation of CTLA-4 and CD28 on activated T lymphocytes." Journal of Experimental Medicine 176, no. 6 (1992): 1595–604. http://dx.doi.org/10.1084/jem.176.6.1595.

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T cell costimulation by molecules on the antigen presenting cell (APC) is required for optimal T cell proliferation. The B7 molecule on APC binds the T lymphocyte receptor CD28, triggering increased interleukin 2 (IL-2) production and subsequent T cell proliferation. CTLA-4 is a predicted T cell membrane receptor homologous to CD28, which also binds the B7 counter receptor, but whose distribution and function are unknown. Here we have developed monoclonal antibodies (mAbs) specific for CTLA-4 and have investigated these questions. mAbs were produced that bound CTLA-4 but not CD28, and that blo

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Guazzelli, Alice, Emyr Bakker, Marija Krstic-Demonacos, Michael P. Lisanti, Federica Sotgia, and Luciano Mutti. "Anti-CTLA-4 therapy for malignant mesothelioma." Immunotherapy 9, no. 3 (2017): 273–80. http://dx.doi.org/10.2217/imt-2016-0123.

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13

Blank, C. U., and A. Enk. "Therapeutic use of anti-CTLA-4 antibodies." International Immunology 27, no. 1 (2014): 3–10. http://dx.doi.org/10.1093/intimm/dxu076.

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14

Sharma, P., D. Tsavachidou, A. Kamat, et al. "Immunologic impact of anti-CTLA-4 therapy." Journal of Clinical Oncology 27, no. 15_suppl (2009): 3019. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.3019.

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3019 Background: Blockade of the T-cell inhibitory molecule known as cytotoxic T lymphocyte antigen-4 (CTLA-4) results in antitumor responses. To date, trials have been conducted with over 4,000 patients with various malignancies in the metastatic disease setting, which allow for correlation of therapy with clinical outcome but do not provide analyses of relevant biomarkers in the systemic circulation that reflect changes within the tumor microenvironment. Approximately 10% of treated patients respond to therapy. Why some patients respond while others do not remains unknown. The identification

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15

Zhang, Anli, Zhenhua Ren, Kuo-fu Tseng, et al. "800 Dual targeting of CTLA-4 and CD47 on Treg cells rejuvenates immunity against solid tumors." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A835—A837. http://dx.doi.org/10.1136/jitc-2021-sitc2021.800.

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BackgroundAlthough approved by FDA, anti-CTLA-4 treatment has severe side effect that limits its clinical usage. Blockade of CD47, the “don't eat me” signal, has limited effects in solid tumors despite its potent anti-tumor effects in hematopoietic malignancies. Targeted delivery of immune blockers into tumor tissues are desireble.MethodsTaking advantage of the high expression of CTLA-4 on Treg cells and abundant Fc receptor+ active phagocytes inside the tumor microenvironment (TME), we design and test an anti-CTLA-4×SIRPα (CD47 ligand)-Fc heterodimer that selectively blocks CD47 on intratumor

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Du, Xuexiang, Mingyue Liu, Yan Zhang, Fei Tang, Pan Zheng, and Yang Liu. "Exploring the main mechanisms of anti-tumor and immunotherapy-related adverse events for safer and effective anti-CTLA-4 immunotherapy." Journal of Immunology 204, no. 1_Supplement (2020): 244.10. http://dx.doi.org/10.4049/jimmunol.204.supp.244.10.

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Abstract Targeting CTLA-4 has shown remarkable long-term benefit and thus remains a valuable tool for cancer immunotherapy if the immunotherapy-related adverse effects (irAEs) can be brought under control. Here, we systematically studied the immunotherapeutic effect of anti-human CTLA-4 mAbs and suggest that Fc/Fc receptor mediated intra-tumor Treg depletion rather than the widely held mechanism of checkpoint blockade contribute to the cancer immunotherapeutic effect, which raised the reappraisal of CTLA-4 checkpoint blockade in cancer immunotherapy. Meanwhile, an animal model, which recapitul

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17

Gao, Jianjun, Hong Chen, Derek Ng Tang, and Padmanee Sharma. "Investigating genes and micro-RNAs that may predict clinical benefits of anti-CTLA-4 therapy." Journal of Clinical Oncology 31, no. 15_suppl (2013): 3043. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3043.

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3043 Background: Blockade of T cell co-inhibitory receptor CTLA-4 with a monoclonal antibody, ipilimumab, has led to augmented anti-tumor immune responses, clinical benefit, and FDA approval of ipilimumab for the treatment of metastatic melanoma. Only a subset of patients benefit from anti-CTLA-4 therapy. In order to identify genes, microRNAs, and signaling pathways that are modulated by anti-CTLA-4, which may be used for potential correlation with clinical outcomes or provide additional targets for therapy, we purified and analyzed CD4+T cells from patients treated with anti-CTLA-4 for change

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18

Matsui, Toshihiro, Manae Kurokawa, Tetsuji Kobata, et al. "Autoantibodies to T Cell Costimulatory Molecules in Systemic Autoimmune Diseases." Journal of Immunology 162, no. 7 (1999): 4328–35. http://dx.doi.org/10.4049/jimmunol.162.7.4328.

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Abstract To determine whether antilymphocyte Abs to T cell costimulatory molecules are generated in patients with autoimmune diseases and, if they exist, to clarify the mechanism of their production and pathological roles, we investigated the presence of autoantibodies to CTLA-4 (CD152), CD28, B7-1 (CD80), and B7-2 (CD86) in serum samples obtained from patients with various autoimmune diseases and from normal subjects using recombinant fusion proteins. In ELISAs, anti-CD28, anti-B7-1, and anti-B7-2 Abs were rarely seen, whereas anti-CTLA-4 Abs were detected in 8.2% of the patients with systemi

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19

Mok, Stephen, and James P. Allison. "Abstract 662: Late CTLA-4 Ig treatment improves antitumor efficacy of immunotherapy." Cancer Research 82, no. 12_Supplement (2022): 662. http://dx.doi.org/10.1158/1538-7445.am2022-662.

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Abstract The promising approach of combining immune checkpoint therapies such as anti-CTLA-4 and anti-PD-1 increases antitumor response and overall survival rate relative to single treatments. However, it also increases the frequency and severity of immune-related adverse events (irAEs), such as cardiotoxicity. Our previous results showed that CTLA-4 Ig (abatacept), an inhibitor of T cell costimulation through CD28, can reverse those irAEs in patients with cancer, however, its effect on the antitumor response remains unclear. In the B16F10 melanoma model, we injected mice with CTLA-4 Ig antibo

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Alegre, Maria-Luisa, Helena Shiels, Craig B. Thompson, and Thomas F. Gajewski. "Expression and Function of CTLA-4 in Th1 and Th2 Cells." Journal of Immunology 161, no. 7 (1998): 3347–56. http://dx.doi.org/10.4049/jimmunol.161.7.3347.

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Abstract CTLA-4 is expressed on T cells after activation and shares homology with the CD28 costimulatory receptor. In contrast to CD28, CTLA-4 is thought to be a negative regulator of T cell activation. Cross-linking of CTLA-4 during activation of peripheral T cells reduces IL-2 production and arrests T cells in G1. Much less is known about the function of CTLA-4 in differentiated T cells. We have investigated the expression and function of CTLA-4 in established Th1 and Th2 clones and in bulk populations of Th1 and Th2 cells freshly derived in vitro from TCR transgenic splenocytes. We found th

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Ha, Danbee, Atsushi Tanaka, Tatsuya Kibayashi, et al. "Differential control of human Treg and effector T cells in tumor immunity by Fc-engineered anti–CTLA-4 antibody." Proceedings of the National Academy of Sciences 116, no. 2 (2018): 609–18. http://dx.doi.org/10.1073/pnas.1812186116.

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Anti–CTLA-4 mAb is efficacious in enhancing tumor immunity in humans. CTLA-4 is expressed by conventional T cells upon activation and by naturally occurring FOXP3+CD4+ Treg cells constitutively, raising a question of how anti–CTLA-4 mAb can differentially control these functionally opposing T cell populations in tumor immunity. Here we show that FOXP3high potently suppressive effector Treg cells were abundant in melanoma tissues, expressing CTLA-4 at higher levels than tumor-infiltrating CD8+ T cells. Upon in vitro tumor-antigen stimulation of peripheral blood mononuclear cells from healthy in

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Harui, Airi, and Michael D. Roth. "Hyaluronidase Enhances Targeting of Hydrogel-Encapsulated Anti-CTLA-4 to Tumor Draining Lymph Nodes and Improves Anti-Tumor Efficacy." Gels 8, no. 5 (2022): 284. http://dx.doi.org/10.3390/gels8050284.

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Immunotherapy targeting checkpoint inhibitors, such as CTLA-4 and/or PD-1, has emerged as a leading cancer therapy. While their combination produces superior efficacy compared to monotherapy, it also magnifies inflammatory and autoimmune toxicity that limits clinical utility. We previously reported that a peri-tumor injection of low-dose hydrogel-encapsulated anti-CTLA-4 produced anti-tumor responses that were equal to, or better than, systemic dosing despite a >80% reduction in total dose. Injection of hydrogel-encapsulated anti-CTLA-4 was associated with low serum exposure and limited aut

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23

Allison, James. "Cytotoxic T-lymphocyte-associated Protein 4 and Cancer Therapy." Blood 126, no. 23 (2015): SCI—7—SCI—7. http://dx.doi.org/10.1182/blood.v126.23.sci-7.sci-7.

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Abstract The existence of multiple non-redundant l inhibitory pathways that limit T cell responses offers novel strategies for mobilizing the immune system to attack cancer cells. The best characterized of these immune checkpoints is CTLA-4, which inhibits CD28 mediated costimulation. Antibodies to CTLA-4 have proven effective against multiple tumor types in both pre-clinical and clinical studies. Ipilimumab, an antibody to human CTLA-4, showed long term (>4.5 years) survival benefit in about 23% of patients in a randomized, placebo-controlled trial in late stage melanoma. In 2011 it was ap

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Semmrich, Monika, Jean-Baptiste Marchand, Matilda Rehn, et al. "746 Vectorized Treg-depleting anti-CTLA-4 elicits antigen cross-presentation and CD8+ T cell immunity to reject “cold” tumors." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A777. http://dx.doi.org/10.1136/jitc-2021-sitc2021.746.

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BackgroundImmune checkpoint blockade (ICB) is a clinically proven concept to treat cancer. Still, a majority of cancer patients including those with poorly immune infiltrated “cold” tumors are resistant to currently available ICB therapies. CTLA-4 is one of few clinically validated targets for ICB, but toxicities linked to efficacy in approved anti-CTLA-4 regimens have restricted their use and precluded full therapeutic dosing. At a mechanistic level, accumulating preclinical and clinical data indicate dual mechanisms for anti-CTLA-4; immune checkpoint blockade and Treg depletion are both thou

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Smyth, Mark J., Hideo Yagita, and Grant A. McArthur. "Combination Anti-CTLA-4 and Anti-RANKL in Metastatic Melanoma." Journal of Clinical Oncology 34, no. 12 (2016): e104-e106. http://dx.doi.org/10.1200/jco.2013.51.3572.

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van Bijnen, Sandra, Maria Rogkoti, Marian Withaar, Theo de Witte, Petra Muus, and Harry Dolstra. "Anti-CTLA-4 Antibody Is Not Able to Trigger Apoptosis in CTLA-4 Expressing Myeloid Tumor Cells." Blood 118, no. 21 (2011): 5054. http://dx.doi.org/10.1182/blood.v118.21.5054.5054.

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Abstract Abstract 5054 Cytoxic T-lymphocyte-associated antigen-4 (CTLA-4) is a co-inhibitory molecule normally expressed on activated effector T cells and a subset of regulatory T cells. However, it has been reported also to be expressed on acute myeloid leukemia (AML) cells, CD34+ hematopoietic progenitor cells after stimulation as well as several solid tumor cell types. Furthermore, CTLA-4 engagement with recombinant CD80 and CD86 ligands has been shown to induce apoptosis in AML cells (Laurent et al. Br J Haematol 2007). In this study, we investigated CTLA-4 expression on different cell pop

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Lühder, Fred, Petter Höglund, James P. Allison, Christophe Benoist, and Diane Mathis. "Cytotoxic T Lymphocyte–associated Antigen 4 (CTLA-4) Regulates the Unfolding of Autoimmune Diabetes." Journal of Experimental Medicine 187, no. 3 (1998): 427–32. http://dx.doi.org/10.1084/jem.187.3.427.

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Evidence has been accumulating that shows that insulin-dependent diabetes is subject to immunoregulation. To determine whether cytotoxic T lymphocyte–associated antigen 4 (CTLA-4) is involved, we injected anti–CTLA-4 mAb into a TCR transgenic model of diabetes at different stages of disease. When injected into young mice, months before they would normally become diabetic, anti–CTLA-4 induced diabetes rapidly and essentially universally; this was not the result of a global activation of T lymphocytes, but did reflect a much more aggressive T cell infiltrate in the pancreatic islets. These effec

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Abdallah, Kald, Boris Shulgin, Kirill Peskov, et al. "Model-based meta-analysis of safety for immune checkpoint inhibitor combinations and monotherapy." Journal of Clinical Oncology 35, no. 7_suppl (2017): 89. http://dx.doi.org/10.1200/jco.2017.35.7_suppl.89.

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89 Background: Immune checkpoint inhibitors (ICIs) have shown efficacy across multiple cancer types; however, ICIs are also associated with immune-mediated (im) adverse events (AEs) especially when used in combination. Methods: Published safety data from 35 melanoma and non-small cell lung cancer clinical trials was normalized for drug exposure using drug concentrations at 50% inhibition (IC50). Pharmacokinetic models from FDA, EMEA, and our own model were used to compare AEs across 4 ICIs: anti-PD-1 (nivolumab, pembrolizumab) and anti-CTLA-4 (ipilumumab, tremelimumab). Data was analyzed by IC

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Ubaldi, Vanessa, Lucia Gatta, Luigia Pace, Gino Doria, and Claudio Pioli. "CTLA-4 Engagement Inhibits Th2 but not Th1 Cell Polarisation." Clinical and Developmental Immunology 10, no. 1 (2003): 13–17. http://dx.doi.org/10.1080/10446670310001598519.

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CTLA-4 deficient mice show severe lymphoproliferative disorders with T helper sub-population skewed toward the Th2 phenotype. In the present work, we investigated the role of CTLA-4 in T helper cell subset differentiation. Naïve CD4+cells were stimulated with anti-CD3 and anti-CD28 mAbs in the presence of either IL-12 or IL-4 to induce polarisation to Th1 or Th2 cells, respectively. Under these two polarising conditions cells express comparable levels of CTLA-4. CTLA-4 was stimulated by plastic-bound mAb. The frequency of IFN-γ- and IL-4-producing cells were estimated by FACS analysis. In para

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Ingram, Jessica R., Olga S. Blomberg, Mohammad Rashidian, et al. "Anti–CTLA-4 therapy requires an Fc domain for efficacy." Proceedings of the National Academy of Sciences 115, no. 15 (2018): 3912–17. http://dx.doi.org/10.1073/pnas.1801524115.

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Ipilimumab, a monoclonal antibody that recognizes cytotoxic T lymphocyte antigen (CTLA)-4, was the first approved “checkpoint”-blocking anticancer therapy. In mouse tumor models, the response to antibodies against CTLA-4 depends entirely on expression of the Fcγ receptor (FcγR), which may facilitate antibody-dependent cellular phagocytosis, but the contribution of simple CTLA-4 blockade remains unknown. To understand the role of CTLA-4 blockade in the complete absence of Fc-dependent functions, we developed H11, a high-affinity alpaca heavy chain-only antibody fragment (VHH) against CTLA-4. Th

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Miller, William L., Valerie Contrad, Iliana Gonzalez, et al. "Increased CD4+ T cell proliferation upon treatment correlates with improved overall survival of patients with metastatic melanoma upon anti-CTLA-4 therapy." Journal of Immunology 196, no. 1_Supplement (2016): 214.17. http://dx.doi.org/10.4049/jimmunol.196.supp.214.17.

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Abstract Blockade of cytotoxic T-lymphocyte antigen 4 (CTLA-4) augments anti-tumor immunity and has shown success in treating patients with metastatic melanoma. Mechanisms of anti-CTLA-4 efficacy have been proposed in animal models, yet the mechanisms in humans remain to be elucidated. Increased frequency of ICOS+ CD4+ T cells has been shown to be a marker of drug bioactivity, but discovery of prognostic indicators and baseline indicators of which patients are most likely to benefit from CTLA-4 blockade remains a priority. PBMCs from 29 metastatic melanoma patients in a multicenter compassiona

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Liu, Yang, Yan Zhang, Xuexiang Du, et al. "231 Molecular insights on safety and anti-tumor activity of a non-irAE-inducing anti-CTLA-4 monoclonal antibody ONC-392." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A246. http://dx.doi.org/10.1136/jitc-2021-sitc2021.231.

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BackgroundAnti-CTLA-4 antibodies have brought about limited clinical benefit because severe toxicity limits dosing levels and/or duration. We used CTLA-4 knockin mice to screen for antibodies with higher anti-tumor activity but lower autoimmunity. We have revealed that the key for better safety and preclinical efficacy is preservation of CTLA-4 for immune tolerance and intratumorial Treg depletion. Our work established that, independent of blocking activities, mAbs that preserve CTLA-4 recycling maintain the physiological immune tolerance checkpoint function while allowing more efficient and s

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Karandikar, N. J., C. L. Vanderlugt, T. L. Walunas, S. D. Miller, and J. A. Bluestone. "CTLA-4: a negative regulator of autoimmune disease." Journal of Experimental Medicine 184, no. 2 (1996): 783–88. http://dx.doi.org/10.1084/jem.184.2.783.

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CTLA-4, a CD28 homologue expressed on activated T cells, binds with high affinity to the CD28 ligands, B7-1 (CD80) and B7-2 (CD86). This study was designed to examine the role of CTLA-4 in regulating autoimmune disease. Murine relapsing-remitting experimental autoimmune encephalomyelitis (R-EAE) is a demyelinating disease mediated by PLP139-151-specific CD4+ T cells in SJL/J mice. Anti-CTLA-4 mAbs (or their F(ab) fragments) enhanced in vitro proliferation and pro-inflammatory cytokine production by PLP139-151-primed lymph node cells. Addition of either reagent to in vitro activation cultures p

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Oosterwegel, Mariette A., Didier A. Mandelbrot, Scott D. Boyd, et al. "The Role of CTLA-4 in Regulating Th2 Differentiation." Journal of Immunology 163, no. 5 (1999): 2634–39. http://dx.doi.org/10.4049/jimmunol.163.5.2634.

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Abstract To examine the role of CTLA-4 in Th cell differentiation, we used two newly generated CTLA-4-deficient (CTLA-4−/−) mouse strains: DO11.10 CTLA-4−/− mice carrying a class II restricted transgenic TCR specific for OVA, and mice lacking CTLA-4, B7.1 and B7.2 (CTLA-4−/− B7.1/B7.2−/− ). When purified naive CD4+ DO11.10 T cells from CTLA-4−/− and wild-type mice were primed and restimulated in vitro with peptide Ag, CTLA-4−/− DO11.10 T cells developed into Th2 cells, whereas wild-type DO11.10 T cells developed into Th1 cells. Similarly, when CTLA-4−/− CD4+ T cells from mice lacking CTLA-4, B

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Pol, Jonathan, and Guido Kroemer. "Anti-CTLA-4 immunotherapy: uncoupling toxicity and efficacy." Cell Research 28, no. 5 (2018): 501–2. http://dx.doi.org/10.1038/s41422-018-0031-9.

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Eggermont, Alexander M. M., Alessandro Testori, Michele Maio, and Caroline Robert. "Anti–CTLA-4 Antibody Adjuvant Therapy in Melanoma." Seminars in Oncology 37, no. 5 (2010): 455–59. http://dx.doi.org/10.1053/j.seminoncol.2010.09.009.

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Ren, Zhenhua, Jingya Guo, Jing Liao, et al. "CTLA-4 Limits Anti-CD20–Mediated Tumor Regression." Clinical Cancer Research 23, no. 1 (2016): 193–203. http://dx.doi.org/10.1158/1078-0432.ccr-16-0040.

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38

Postow, M. "SP019 Monitoring response to anti CTLA-4 therapy." European Journal of Cancer 49 (November 2013): S5. http://dx.doi.org/10.1016/s0959-8049(13)70097-2.

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Marabelle, Aurélien, and Alexander Eggermont. "How should we use anti-CTLA-4 antibodies?" European Journal of Cancer 51, no. 17 (2015): 2686–88. http://dx.doi.org/10.1016/j.ejca.2015.09.002.

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Ren, Zhenhua, Hua Peng, and Yang-Xin Fu. "CTLA-4 limits anti-CD20-mediated tumor regression." Journal of Immunology 200, no. 1_Supplement (2018): 122.3. http://dx.doi.org/10.4049/jimmunol.200.supp.122.3.

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Abstract The inhibition of tumor growth by anti-CD20 antibody (Ab) treatment is mediated by antibody- and complement-dependent cytotoxicity in xenograft tumor models. Additionally, anti-CD20 therapy for B-cell lymphoma can result in intrinsic and extrinsic tumor resistance to further Ab treatment. However, adaptive immune response-related resistance has not been well studied in anti-CD20-mediated tumor control, and adaptive immunity has long been underestimated. However, using a syngeneic mouse B-cell lymphoma model, we observed that CD8+ T cells played an essential role for anti-CD20-mediated

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Murphy, Michaela L., Sara E. J. Cotterell, Patricia M. A. Gorak, Christian R. Engwerda, and Paul M. Kaye. "Blockade of CTLA-4 Enhances Host Resistance to the Intracellular Pathogen, Leishmania donovani." Journal of Immunology 161, no. 8 (1998): 4153–60. http://dx.doi.org/10.4049/jimmunol.161.8.4153.

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Abstract CTLA-4 has recently been shown to act as a negative regulator of T cell activation. Here we provide evidence that blockade of CTLA-4 can result in enhanced host resistance to an intracellular pathogen. The administration of anti-CTLA-4 mAb 4F10 to BALB/c mice, 1 day following infection with Leishmania donovani, enhanced the frequency of IFN-γ and IL-4 producing cells in both spleen and liver, and dramatically accelerated the development of a hepatic granulomatous response. The expression of mRNA for the CXC chemokine γIP-10 was also elevated above that seen in control Ab treated mice,

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Jenkins, Kurt, Parker Johnson, Minjie Zhang, et al. "587 Tumor-activated Fc-engineered anti-CTLA-4 monoclonal antibody, XTX101, demonstrates tumor-selective PD and efficacy in preclinical models." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A622. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0587.

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BackgroundThe clinical benefit of CTLA-4 blockade to cancer patients has been well established. However, the promising antitumor activity shown by anti-CTLA-4 monoclonal antibodies (mAb) has been limited by the occurrence of immune-mediated adverse reactions, especially when CTLA-4 inhibition is used in combination with anti-PD-1 therapy. These dose-limiting toxicities restrict the therapeutic use of CTLA-4 blockade. To overcome these limitations, we have developed a potent anti-CTLA-4 antibody that is selectively active in the tumor microenvironment (TME). This antibody is engineered with an

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Shulgin, Boris, Yuri Kosinsky, Alexandra Smirnova, Gabriel Helmlinger, and Kirill Peskov. "Quantification of dose dependence and frequency of checkpoint inhibitor immune-mediated adverse events: A Bayesian model-based meta-analysis." Journal of Clinical Oncology 38, no. 5_suppl (2020): 83. http://dx.doi.org/10.1200/jco.2020.38.5_suppl.83.

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83 Background: Immune checkpoint inhibitors (ICIs) are associated with immune-mediated adverse events (imAEs). The objective of this study was to use a Bayesian model-based meta-analysis to quantify dose dependence and compare imAE frequencies for PD-1, PD-L1 and CTLA-4 inhibitor monotherapies and their combinations. Methods: We searched PubMed, TrialTrove, ASCO and ESMO databases and retrieved relevant ICI safety data. In order to quantitatively compare safety across doses and drugs against a given target, we converted the various dose regimens used into drug exposures derived from pharmacoki

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Walunas, Theresa L., and Jeffrey A. Bluestone. "CTLA-4 Regulates Tolerance Induction and T Cell Differentiation In Vivo." Journal of Immunology 160, no. 8 (1998): 3855–60. http://dx.doi.org/10.4049/jimmunol.160.8.3855.

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Abstract Cytotoxic T lymphocyte Ag-4 (CTLA-4; CD152) is an important T cell regulatory molecule. In vitro experiments have shown that the blockade of signals through CTLA-4 augments T cell expansion, while CTLA-4 cross-linking results in decreased T cell proliferation due to decreased IL-2 production. However, less is known about the role of CTLA-4 in regulating an ongoing immune response. In this study, we examined the role of CTLA-4 in the expansion, decline, tolerization, and differentiation of T cells following treatment with staphylococcal enterotoxin B (SEB). Anti-CTLA-4 treatment result

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McCoy, Kathy D., Ian F. Hermans, J. Henry Fraser, Graham Le Gros, and Franca Ronchese. "Cytotoxic T Lymphocyte–associated Antigen 4 (CTLA-4) Can Regulate Dendritic Cell–induced Activation and Cytotoxicity of CD8+ T Cells Independently of CD4+T Cell Help." Journal of Experimental Medicine 189, no. 7 (1999): 1157–62. http://dx.doi.org/10.1084/jem.189.7.1157.

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The mechanisms that regulate the strength and duration of CD8+ cytotoxic T cell activity determine the effectiveness of an antitumor immune response. To better understand the antitumor effects of anti-cytotoxic T lymphocyte–associated antigen 4 (CTLA-4) antibody treatment, we analyzed the effect of CTLA-4 signaling on CD8+ T cells in vitro and in vivo. In vitro, cross-linking of CTLA-4 on purified CD8+ T cells caused decreased proliferative responses to anti-CD3 stimulation and rapid loss of activation marker expression. In vivo, blockade of CTLA-4 by neutralizing anti–CTLA-4 mAb greatly enhan

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Do, Priscilla, Kyle A. Beckwith, Larry Beaver, et al. "Leukemic Cell Expressed CTLA-4 Suppresses T Cells Via Down-Modulation of CD80 By Trans-Endocytosis." Blood 128, no. 22 (2016): 3221. http://dx.doi.org/10.1182/blood.v128.22.3221.3221.

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Abstract The function of CTLA-4 on non-T cells is largely ignored and currently ill defined despite rapidly growing interest in targeting this immune checkpoint protein in several cancers. While anti-CTLA-4 therapy is proposed to work through inhibition of the immunosuppressive effect of CTLA-4 on T cells, multiple examples of non-T cell expressed CTLA-4 have been reported. These cells include tumor cells of hematological and non-hematological origin and normal B cells. In this study, we have defined a novel immune suppressive role for non-T cell, tumor expressed CTLA-4 in Chronic Lymphocytic

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Gao, Jianjun, Lewis Shi, Liangwen Xiong, et al. "Expression of IFNgR on tumor cells impact response to anti-CTLA-4 (TUM2P.1034)." Journal of Immunology 194, no. 1_Supplement (2015): 69.31. http://dx.doi.org/10.4049/jimmunol.194.supp.69.31.

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Abstract Blockade of T cell co-inhibitory receptor CTLA-4 with a monoclonal antibody, Ipilimumab (BMS), has led to augmented anti-tumor immune responses, clinical benefit, and FDA approval of Ipilimumab for the treatment of metastatic melanoma. Our published data indicate that anti-CTLA-4 treatment resulted in marked increase of IFN-gamma (IFNg) production by CD4 T cells expressing inducible costimulator (ICOS). Studies in mice have demonstrated the importance of IFNg for effective anti-tumor responses. We hypothesized that tumor cell expression of IFNg-receptor (IFNg-R) would be necessary for

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Grubczak, Kamil, Anna Kretowska-Grunwald, Dawid Groth, et al. "Differential Response of MDA-MB-231 and MCF-7 Breast Cancer Cells to In Vitro Inhibition with CTLA-4 and PD-1 through Cancer-Immune Cells Modified Interactions." Cells 10, no. 8 (2021): 2044. http://dx.doi.org/10.3390/cells10082044.

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Drugs targeting immune checkpoint molecules have been found effective in melanoma, lung cancer, and other malignancies treatment. Recent studies on breast cancer demonstrated the significance of inhibitory anti-CTLA-4 and anti-PD-1 in the regulation of disease progression. However, seemingly the same types of breast cancer do not always respond unambiguously to immunotherapy. Thus, here we set out to analyze the in vitro effects of inhibiting CTLA-4 and PD-1 on interactions between co-cultured lymphocytes and two selected breast adenocarcinoma cell lines. Breast cancer cells were co-cultured w

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DU, XUEXIANG, Fei Tang, Mingyue Liu, Yang Liu, and Pan Zheng. "Uncoupling Therapeutic from Immunotherapy-related Adverse Effects for Safer and Effective Anti-CTLA-4 Antibodies in CTLA4 Humanized Mice." Journal of Immunology 200, no. 1_Supplement (2018): 57.34. http://dx.doi.org/10.4049/jimmunol.200.supp.57.34.

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Abstract Anti-CTLA-4 monoclonal antibodies (mAbs) confer cancer immunotherapeutic effect (CITE) but cause severe immunotherapy-related adverse effect (irAE). The irAE greatly limited application of immunotherapy targeting the CTLA-4 molecules. However, targeting CTLA-4 has shown remarkable long-term benefit and thus remains a valuable tool for cancer immunotherapy, especially if the irAE can be brought under control. A major obstacle to this goal is lack of animal model that recapitulate clinical irAE. Here we report that mice with the humanized CTLA4 gene recapitulated cardinal features of cl

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Blazar, Bruce R., Patricia A. Taylor, Angela Panoskaltsis-Mortari, Arlene H. Sharpe, and Daniel A. Vallera. "Opposing Roles of CD28:B7 and CTLA-4:B7 Pathways in Regulating In Vivo Alloresponses in Murine Recipients of MHC Disparate T Cells." Journal of Immunology 162, no. 11 (1999): 6368–77. http://dx.doi.org/10.4049/jimmunol.162.11.6368.

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Abstract Blockade with B7 antagonists interferes with CD28:B7 and CTLA-4:B7 interactions, which may have opposing effects. We have examined the roles of CD28:B7 and CTLA-4:B7 on in vivo alloresponses. A critical role of B7:CD28 was demonstrated by markedly compromised expansion of CD28-deficient T cells and diminished graft-versus-host disease lethality of limited numbers of purified CD4+ or CD8+ T cells. When high numbers of T cells were infused, the requirement for CD28:B7 interaction was lessened. In lethally irradiated recipients, anti-CTLA-4 mAb enhanced in vivo donor T cell expansion, bu

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