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Small Interfering RNAs, MicroRNAs, and NPs in Gynecological Cancers
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
The specificity of action carried out by siRNA molecules depends upon the uniqueness of the selected sequences; however, many other factors may also have an impact on a lack of specificity [70]. Several types involving siRNA off-target effects have been described and thoroughly reviewed [71]. It is well known that mammalian immune cells tend to express a family of receptors so-called Toll-like receptors (TLRs) which also have the ability to recognize pathogens and molecules derived from microbes. In addition, some synthetic siRNA sequences as well as their non-viral vehicles have proved to promote the activation of immune system cells, producing inflammatory cytokines and Type I interferon in vitro and in vivo by activating TLR7 and TLR8 in a sequence-dependent manner [72].
Assessment of Quercetin Isolated from Enicostemma Littorale Against Few Cancer Targets: An in Silico Approach
Published in A. K. Haghi, Ana Cristina Faria Ribeiro, Lionello Pogliani, Devrim Balköse, Francisco Torrens, Omari V. Mukbaniani, Applied Chemistry and Chemical Engineering, 2017
Toll-like receptor 7 also known as TLR7 is an immune gene possessed by humans and other mammals. The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on SCC, and mediate the production of cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. This gene is predominantly expressed in lung, placenta and spleen, and lies in close proximity to another family member.43
A porous Co-MOF for CO2 conversion and protective activity on infectious fever by reducing bacterial inflammatory response
Published in Journal of Coordination Chemistry, 2021
LI-Ying Yan, Hong-Chao Zhu, Yan-Qu Ma, Ling Tao, Ling-Li Quan, Qing Zhang
Fever is one of the important clinical manifestations in the progression of many diseases. Among them, most fever is caused by bacterial infection, which is called infectious fever [1]. There are also other kinds of fever, such as viral fever. When the exogenous pyrogen enters into the human body, it acts on monocytes, lymphocytes, macrophages and other immune active cells, producing a great quantity of the pyrogen cytokines, which is also called endogenous pyrogens [2]. These cytokines act indirectly or directly on the thermoregulatory center of body via the central mediators, causing a relative high level of the body temperature [3]. After infected with the bacteria, the TLR on the cell membranes would be activated, then leading to activation of the NF-κB signaling pathway, which finally caused the production of the inflammatory cytokines. Thus, how to control body temperature during bacterial infection is the objective of this research.
Gender-specific associations between polymorphisms in the Toll-like receptor (TLR) genes and lung function among workers in swine operations
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Zhiwei Gao, James A. Dosman, Donna C. Rennie, David A. Schwartz, Ivana V. Yang, Jeremy Beach, Ambikaipakan Senthilselvan
Workers in animal confinement facilities are at higher risk of lung dysfunction due to exposure to a large variety of hazards including bacteria (gram-positive and gram-negative), viruses, fungi, dust particles, and gases (Dosman et al. 2004; Eduard, Pearce, and Douwes 2009; Harting et al. 2012; May, Romberger, and Poole 2012, 2007; Senthilselvan et al. 1997; Viegas et al. 2013). Several investigators showed that the involvement of TLR2 in the airway diseases among workers in swine operation and the important role of TLR9 in lung inflammation following exposure to chicken barn air (Gao et al. 2013; Harting et al. 2012; Just, Duchaine, and Singh 2009; May, Romberger, and Poole 2012; Schneberger et al. 2016). TLR2 mainly responds to cell wall structure components such as peptidoglycan from gram-positive bacteria, and the ligand of TLR9 is un-methylated DNA which is found in bacterial and viral DNA (Hemmi et al. 2000; Iwasaki and Medzhitov 2004). The activation of TLR induces a series of intracellular signaling cascades to produce both pro- and anti-inflammatory cytokines and chemokines, which all work together to respond to invading pathogens (Hemmi et al. 2000; Iwasaki and Medzhitov 2004; Tipping 2006).
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).