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The Human Microbiome: How Our Health is Impacted by Microorganisms
Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
An article published in Nature reported that intestinal commensala bacteria can regulate the differentiation of multiple T cells and thus change the immune system of the intestinal mucosa. F. prazilus is located in the mucosal layer of the intestine and produces butyrate by fermentation. This short-chain fatty acid stimulates and modulates T cells to prevent the development of intestinal inflammation. All Clostridium bacteria have similar mechanism. Another article in Science pointed out that under normal circumstances, dendritic cells do not respond to T-cell inflammation in the intestinal mucosa, so they play an important role in maintaining intestinal immune tolerance.80 However, when the environment changes, dendritic cells can activate T cells, and β-chain proteins on T cells play an important role in regulating dendritic cells. When the β-chain protein is cleared, the activity and resistance of T cells are regulated. The effect of inflammatory cytokines was significantly reduced, while pro-inflammatory helper T cells 1 and 17 and their cytokines increased. Mice lacking beta-catenin in dendritic cells exhibit increased sensitivity to enteritis.
The Human Microbiome: How Our Health is Impacted by Microorganisms
Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
An article published in Nature reported that intestinal commensala bacteria can regulate the differentiation of multiple T cells and thus change the immune system of the intestinal mucosa. F. prazilus is located in the mucosal layer of the intestine and produces butyrate by fermentation. This short-chain fatty acid stimulates and modulates T cells to prevent the development of intestinal inflammation. All Clostridium bacteria have similar mechanism. Another article in Science pointed out that under normal circumstances, dendritic cells do not respond to T-cell inflammation in the intestinal mucosa, so they play an important role in maintaining intestinal immune tolerance.80 However, when the environment changes, dendritic cells can activate T cells, and β-chain proteins on T cells play an important role in regulating dendritic cells. When the β-chain protein is cleared, the activity and resistance of T cells are regulated. The effect of inflammatory cytokines was significantly reduced, while pro-inflammatory helper T cells 1 and 17 and their cytokines increased. Mice lacking betacatenin in dendritic cells exhibit increased sensitivity to enteritis.
Engineering Nanoparticles to Overcome Barriers to Immunotherapy
Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019
Despite this wealth of new technologies, the efficacy and widespread adoption of immunotherapy has been limited. The major challenge lies in delivering an immunotherapy to a specific target without causing harm to healthy tissues or inducing a feedback pathway that counteracts the mechanism of the immunotherapy. Nonspecific delivery of proinflammatory cytokines and monoclonal antibody therapies has the potential to induce systemic toxicity. In a similar fashion, the adoptive transfer of cells potentially can induce autoimmunity at off-target sites [6]. The development of cancer immunotherapies is stifled by the widespread presence of immune tolerance at the tumor site. Low immunogenicity of tumor antigens, the proliferation of immunosuppressive cells (e.g., myeloid-derived suppressor cells, regulatory T-cells), and the increased production of immunosuppressive cytokines (e.g., IL-10, TGF-β) work together to limit the antitumor response elicited by immunotherapies [7]. Autoimmune diseases, conversely, have the opposite problem of inducing systemic immune suppression that renders patients susceptible to infectious disease [8]. The overarching question is, therefore, how do we deliver the optimal amount of immunotherapy to a specific site, with appropriate kinetics and dosing schedule, without inducing deleterious side effects that outweigh the benefits of the therapy?
Epigenotoxicity: a danger to the future life
Published in Journal of Environmental Science and Health, Part A, 2023
Farzaneh Kefayati, Atoosa Karimi Babaahmadi, Taraneh Mousavi, Mahshid Hodjat, Mohammad Abdollahi
Genetic diversity, environmental effects, and epigenetic factors may bring about autoimmune diseases. Enzymes involved in the histone modification process can impair DNA repair processes. Some HDAC inhibitors (HDACi) increase the possibility of transcription of specific genes such as those involved in autoimmune diseases. These enzymes are more active in T cells and cause post-translational changes. Such changes eventually lead to the immune tolerance modulation and autoimmune diseases. lncRNAs control the expression of genes involved in the differentiation of immune cell types. Also, dysregulation of miRNAs was linked with the incidence of many autoimmune diseases by altering epigenetic mechanisms like DNA methylation, RNA-dependent mechanisms, and post-translational histone modifications.[90] Many chemical agents in the environment, such as various types of hydrocarbons, heavy metals, and agricultural chemicals that have already been addressed, are immunotoxic and cause structural, functional, or combined changes in various immune system components and alter the immune response.[176]
An immune cell infiltration landscape classification to predict prognosis and immunotherapy effect in oral squamous cell carcinoma
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
In recent years, the pathogenesis and development of malignant tumors, as well as the response to immunotherapy, have gradually expanded from independent tumor tissue to the combined role of tumor tissue and tumor microenvironment, in which immune and inflammatory factors play a critical role (Mittal et al. 2018). Of the three ICI subtypes obtained during the first cluster analysis, the patients in the subtype with the best prognosis obtained during the first cluster analysis had high levels of T cells, M1 macrophages and a high immune score, which is consistent with previous research (He et al. 2018; Zhang et al. 2020). This highlights that the host immune response may have an antitumor effect and positively influence the response to immunotherapy. However, fewer than 20% of patients responded to immunotherapy compared to other tumor types with low immune invasion (Yarchoan et al. 2017), suggesting that even immune cells in a tumor may not be able to accurately predict response to immunotherapy. The intercellular communication between infiltrating immune cells may be disrupted during tumor development, disturbing the balance between immune tolerance and immune activity (Chen and Mellman 2017).
Tumor growth suppression by implantation of an anti-CD25 antibody-immobilized material near the tumor via regulatory T cell capture
Published in Science and Technology of Advanced Materials, 2021
Tsuyoshi Kimura, Rino Tokunaga, Yoshihide Hashimoto, Naoko Nakamura, Akio Kishida
Cancer immunotherapy can involve enhancement of immune attack or release of immune tolerance [17]. Importantly, FoxP3+ CD25+ CD4+ Tregs have been shown to strongly affect tumor immune tolerance [4]. In the tumor microenvironment, Tregs infiltrate and accumulate through the secretion of chemokines, such as CCL22, from cancer cells and inhibit the attack of immune cells, such as NK cells and effector T cells, to cancer cells [4,5]. In this study, in order to remove Tregs from the tumor and release immune tolerance, we designed and prepared an antibody-immobilized mesh and subsequently investigated the effects of the mesh on tumor growth suppression following implantation in mice. The transcription factor FoxP3 is a specific marker of Tregs and is FoxP3 expressed inside the cells; thus, this specific marker could not be used in our system. CD25 is a surface marker of Tregs; therefore, we chose anti-CD25 antibodies in this study. A recent study showed that three types of Tregs, including naïve Tregs, effector Tregs, and non-Tregs, were present and exhibited variations in immunosuppression. Among these types of Tregs, effector Tregs, which show high immunosuppressive ability, are present as the CD25++FoxP3++ cell population. Moreover, effector Tregs have been identified in proliferative tumors [18]. Therefore, in this study, we designed an anti-CD25 antibody-immobilized material to remove the effector Tregs from tumors.