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Probiotics Modulate Cell Signaling Pathway and Innate Cytokine Responses to Oral HRV Vaccine in HGM-Transplanted Gn Pigs
Published in Lijuan Yuan, Vaccine Efficacy Evaluation, 2022
Although there is no significant difference in p38 observed among different treatments in immunohistochemistry (Figure 13.4), the AttHRV+LGG9X pigs had significantly higher p-p38 expression levels than the AttHRV and AttHRV+LGG14X pigs. The ERK expression levels of the AttHRV+LGG9X pigs were higher than the AttHRV pigs and significantly higher than the AttHRV+LGG14X pigs. The AttHRV+LGG9X pigs had significantly higher p-ERK expression levels than the AttHRV pigs. There is no significant difference in CD80 or IFN-γ expression levels among different treatment groups in immunohistochemistry (data not shown).
Effects of Lipopolysaccharide on T Cells
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Masayasu Nakano, Teruo Kirikae, Toshimasa Nitta
Mattem et al. (6–8) reported that LPS as well as its hydrophobic part, lipid A, were capable of inducing proliferation of human T cells in the presence of monocytes. The LPS-induced proliferation was strongly dependent on direct cell-to-cell contact, and the interaction of the cell surface molecules CD28 and/or CTLA-4 on T cells with their ligands CD80 and/or CD86 on monocytes was especially important. These ligands were differentially regulated on monocytes of LPS responders and LPS nonresponders. There was a clear correlation of CD80 expression on monocytes after LPS stimulation and their capacity to support T-cell proliferation. The interaction between T cells and monocytes was not MHC-restricted, suggesting that LPS did not act like an antigen, and the proliferative T cells were Th1 type helper T cells, since the proliferative cells expressed mRNA for the Th1 cell-derived cytokines interferon (IFN)-γ and IL-2, but not for the Th2 type of helper T-cell-derived cytokines IL-4, IL-5, and IL-10.
Active Specific Immunization by the Use of Leukemic Dendritic Cell Vaccines
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
Ilse Houtenbos, Gert J. Ossenkoppele, Arjan A. van de Loosdrecht
A second signal termed costimulation is crucial for final T-cell activation. Absence of this second activation signal can lead to T-cell anergy with subsequent tolerance to the presented antigen. A number of molecular interactions contribute to costimulatory signaling. CD28 is the most important costimulatory molecule expressed on naïve T cells and interacts with CD80 and CD86 on APC. Upon activation, T cells will proliferate and differentiate towards effector and memory subtypes. Additionally, T cells upregulate the expression of other costimulatory molecules with either a stimulatory or inhibitory function thereby regulating the immune response.
Targeting the CTLA-4/B7 axes in glioblastoma: preclinical evidence and clinical interventions
Published in Expert Opinion on Therapeutic Targets, 2022
Mehrdad Fathi, Seyed-Mostafa Razavi, Mozhdeh Sojoodi, Armin Ahmadi, Farbod Ebrahimi, Afshin Namdar, Mohammad Hojjat-Farsangi, Sharareh Gholamin, Farhad Jadidi-Niaragh
A novel study on CRISPR/Cas9 mouse model reported that tumors without CD80 provided a hot TME (boosted NK and NKT cells’ infiltration) and improved sensitivity to anti-CTLA-4 monoclonal antibodies (mAbs) when compared to controls. The study suggested CD80 as a biomarker to predict the sensitivity of cancer patients to CTLA-4 blockers [70]. Similarly, in another investigation, it was reported that CD80 inhibition in mouse colon tumors induced strong anti-tumor immune responses in immunocompetent mice, which rejected tumors and immunized against unmodified CT26 tumors when rechallenged after 12 weeks [93]. Unlike previous results, an opposite role of CD80 on tumor cells was reported in the study. Accordingly, CD80 inhibition significantly reduced Lysosome-Associated Membrane Protein (LAMP-1) or CD107a+ T cells (T cell cytolytic activity marker) and increased dysplasia extension in murine models. In other words, CD80 could suppress anti-tumor responses that differ from suppressing tumor progression [94]. It was also reported that CD80 expression could induce anti-tumor responses in human cancer epithelial cells.
Ocular Complications of Checkpoint Inhibitors and Immunotherapeutic Agents: A Case Series
Published in Ocular Immunology and Inflammation, 2021
Ruby A. Parikh, Benjamin C. Chaon, Meghan K. Berkenstock
Understanding how uveitis develops requires an understanding of the mechanism of action of checkpoint inhibition. As a class, the checkpoint inhibitors promote T-cell activation against tumor cell antigens.32,33 The first step in this process occurs within the tumor bed, where antigens from the malignant cells are released and uptaken for processing by antigen-presenting cells (APC). The antigens are placed on the MHC 1 and 2 receptors and transported to the draining lymph nodes. Once inside the lymph node, the APC presents the antigen to waiting T-cells via MHC and T-cell receptor (TCR) interaction.33 In addition to TCR binding, a second stimulatory signal is required for T-cell activation. CTLA-4 and CD28 receptors on the T-cell surface compete to bind the CD80 and CD86 receptors on the APC. Binding of CD28 to CD80 and CD86 comprises the second stimulatory signal for T-cell activation.33 Conversely, if CTLA-4 binds CD80 and CD86, T-cell suppression and T regulatory cell (Treg) formation results. Blocking of this receptor is the mechanism of action of the CTLA-4 inhibitor, ipilimumab, leading to the activation of T-cells against tumor-specific antigens.33
CD80 expression is upregulated by TP53 activation in human cancer epithelial cells
Published in OncoImmunology, 2021
Melania Scarpa, Chiara Marchiori, Marco Scarpa, Ignazio Castagliuolo
Tumor cells employ several immune-suppressive strategies to overcome antitumor immunity. One such method is the modulation on the tumor cell surface of the expression of T cell cosignaling molecules, which are required for effective T cell activation and consequently a successful elimination of cancer cells.5 CD80 is recognized as one of the most potent costimulatory molecules by which immune cells limit malignant growth.6 It is upregulated upon cell stress and it is critical for efficacious immune surveillance during carcinogenesis.7–9 Low surface expression of CD80 was reported as an immune escape mechanism of colon carcinoma;10 on the other hand, its expression resulted enhanced in high-frequency microsatellite instability (MSI) colorectal cancers, a CRC subtype which is highly immunogenic and associated with a better prognosis.11 Both in vivo and in vitro studies showed that the upregulation of CD80 on tumor cell surface successfully activates anti-tumor immune responses, while its expression is frequently lost during tumor progression probably due to selective pressure by the immune system.7,12–14 Thus, to develop effective approaches for cancer immunotherapy, strategies for enhancing CD80 expression in tumors are urgently required.15 However, the current understanding of the regulation of CD80 expression is limited.