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Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
It has been hypothesized by Rossi et al.294 that anti-inflammatory Th2 response caused by allergen sensitization may be suppressed by the competing proinflammatory response elicited by TiO2 exposure. On the other hand, it has been suggested that T-cell dysfunction results in systemic immune suppression in mice exposed to multiwalled carbon nanotubes.315 This T8 cell depression seen in the chemically sensitive must alter this response to the hypersensitivity stage as seen in several chemically sensitive patients. Also in the case of cigarette smoke exposure, reduced T helper function was considered as one possible reason for the suppression of allergic symptoms. Furthermore, consensus exists that Foxp3+ Treg cells are able to control the inflammation thus preventing overactive inflammatory process that harms hosts’ own tissue. Rossi et al.294 therefore also investigated whether the exposure to TiO2 particles induces elevated levels of Foxp3, a marker of Treg ells, as well as regulatory cytokine IL-10. Expression levels of Foxp3 and IL-10 were, however, significantly inhibited in asthmatic mice by the particle exposure excluding the possibility that suppression was mediated mainly via Treg cells and regulatory cytokines.
Host Response to Biomaterials
Published in Claudio Migliaresi, Antonella Motta, Scaffolds for Tissue Engineering, 2014
Sangeetha Srinivasan, Julia E. Babensee
TCRs recognize peptide fragments of antigens bound to MHC molecules. Naive TH cells require a second signal for generation of protective effector functions post TCR stimulation.95109 This second signal is provided by ligation of costimulatory molecules with B7 molecules on APCs. Upon APC maturation, CD80 and CD86 expressions are upregulated, thus supporting their immunostimulatory ability.111 The third signal of the cytokine environment polarizes T-cells responses. Absence of the second signal leads to T-cell anergy. T-cell polarization, for example, toward TH1 or TH2 phenotypes is achieved in response to secreted IL-12 or IL-4. Regulatory T-cells or Tregs with CD4+ CD25+ CTLA4+ or TGF-^-induced CD4+ CD25- FoxP3+112 have the ability of resolving immunity and promoting tolerance with specificity to antigen. The T-lymphocyte antigen 4 (CTLA4), a molecule homologous to CD28, binds to costimulatory B7 molecules.113114
Effects of exercise training on immunological factors in kidney transplant recipients; a randomized controlled trial
Published in Research in Sports Medicine, 2022
Nazi Hemmati, Sohrab Kazemi, Narges Jamshidian-Tehrani, Jamshid Roozbeh, Maryam Koushkie Jahromi, Mohsen Salesi, Meghdad Abdollahpour-Alitappeh, Mohammad Hossein Karimi
Although the exact mechanisms of action of T-cell subsets have not been clearly identified, several pathways are suggested in this context. For example, Th1 cells contribute to the allograft rejection through production of IL-2, resulting in the proliferation of alloreactive cytotoxic CD8+ T cells. In addition, cytotoxic CD8+ T cells can directly exert their cytotoxicity through a Fas/Fas ligand-mediated manner (Ayala Garcia et al., 2012). Other mechanisms of action in allograft rejection mediated by Th-2 and Th-17 include eosinophil activation through Th-2 and Treg suppression by Th-17. Treg cell population, which is known for its transcription factor FOXP3, plays an important role in immune-tolerance and autoimmune stability. Most importantly, the balance or imbalance between Th1/Th2 and Th17/Treg can cause different physiological and pathological effects in the immune function (Dolff et al., 2011; Yang et al., 2017).
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
How Tregs modulate the immune system is not fully understood but one way might be through TLR. TLR were first recognised on the surface of inflammatory cells, especially macrophages where they alert the body to external pathogens, particularly bacteria, and set off an immune response, but it is now well known that they recognise endogenous damage as well. Danger signals arising from injured or altered cells are known as damage–associated molecular patterns (DAMPS) and these are recognised by certain TLRs. Perhaps cancer cells and/or potentially malignant cells release DAMPS? Our group assessed 50 cases each of inflamed irritative hyperplasia (IH), epithelial dysplasia (ED) and OSCC and found that more inflammatory cells expressed TLR2 in the stroma of OSCC than in hyperplastic tissue (Figure 4A,B). No hyperplastic samples showed TLR2+ keratinocytes but keratinocytes in 64% of cases of OSCC were TLR2+. Positive TLR2 expression in the TME suggests that immune surveillance is activated against the altered epithelial cells while TLR2 expression by malignant keratinocytes may correlate with apoptosis resistance and hence the survival of tumour cells (Ng et al. 2011). Double immunofluoresence studies showed that TLR2+FoxP3+ Tregs were present in the OSCC microenvironment (Figure 5) with apparent cell-to-cell contact between TLR2+ and FoxP3+ cells. The presence of FoxP3+TLR2+ cells may represent a dendritic cell-dependent pathway capable of inhibiting Treg suppressive activity, potentially beneficial to the anti-tumour response (Hussaini et al. 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 treatment can be classified into surgical treatment, chemotherapy, radiotherapy, and immunotherapy. Cancer immunotherapy is a method for treating cancer using the immune system. To date, various cancer immunotherapies have been proposed, including vaccine therapy using autologous cancer vaccines [1], dendritic cell vaccines [2], and adoptive immunotherapy using natural killer (NK) cells and cytotoxic T cells [3]. Among these approaches, cancer immunotherapy related to regulatory T cells (Tregs) has recently become a major research focus. Tregs, i.e., CD4-, CD25-, and FoxP3-positive T cells, are key players in immune suppression [4] and function by controlling the activation of antigen-presenting cells via cytotoxic T lymphocyte antigen (CTLA)-4 and immunosuppressive cytokines (e.g., interleukin-10). In addition, Tregs play roles in suppressing the attack of T cells and other immune cells by modulating the production of transforming growth factor-β [5]. Furthermore, in the tumor microenvironment, which is formed by various components, including cancer cells, immune cells, and the extracellular matrix, Treg accumulation is induced by secretion of the chemokine C-C motif chemokine ligand 22 (CCL22) from cancer cells and tumor-infiltrating macrophages, resulting in an antitumor immune response [6,7]. Several treatments that inhibit immunosuppressive signal transduction by immune checkpoint inhibitors (e.g., anti-CTLA-4 and anti-programmed death-1 antibodies) and depletion of Tregs by administration of anti-C-C motif chemokine receptor 4 antibodies have been proposed as Treg-related cancer immunotherapies [8,9]. The development of selective Treg removal methods is also proposed [10,11]. Although the efficacies of these treatments have been demonstrated, treatment with immune checkpoint inhibitors can induce serious side effects owing to activation of T cells [12]. In addition, because Tregs are strongly related to autoimmunity, Treg-removing treatments may cause systemic autoimmune diseases. Therefore, the development of a method for local Treg removal at the tumor is essential.