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Introduction to basic immunology and vaccine design
Published in Amine Kamen, Laura Cervera, Bioprocessing of Viral Vaccines, 2023
Alaka Mullick, Shantoshini Dash
The innate immune system recognizes molecular patterns associated with pathogens. Such pathogen-associated molecular patterns or PAMPs include various lipopolysaccharide molecules on bacterial surfaces, yeast cell wall components, and structures such as flagella and microbial nucleic acids. The cells of the innate immune system possess special receptors called pattern recognition receptors (PRRs) that can distinguish these general molecular patterns, thereby detecting the presence of foreign organisms in the environment [1]. One such family of receptors is named toll-like receptors (TLR), referring to “toll,” a drosophila receptor, that was the first member of this family to be identified. As shown in Figure 3.2, TLRs 2, 4, 6, and 10 are present on the cell surface and recognize extracellular pathogens. Others, such as TLR 7, 8, and 9 are present on the surface of endosomes and can recognize nucleic acids from intracellular pathogens [2]. Other families of pattern recognition receptors include C-type lectin receptors (CLRs), NOD-like receptors (NLRs), and RIG-like receptors (RLRs) that detect the presence of molecules derived from pathogens in the cytoplasm [1],
Viral Noncoding RNAs in Modulating Cellular Defense and Their Potential for RNA Nanotechnology
Published in Peixuan Guo, Kirill A. Afonin, RNA Nanotechnology and Therapeutics, 2022
Martin Panigaj, Marina A. Dobrovolskaia, Kirill A. Afonin
The innate immune response provides a first line of defense against viral infection while avoiding reactions to its own nucleic acids (NA). Four determinants are considered in the recognition of self from non-self NA: (i) structural patterns (e.g., composition (DNA vs. RNA), sequence, and/or chemical modification of NAs), (ii) intracellular localizations (e.g., occurrence in compartments unusual for NAs presence), (iii) relative quantities (e.g., when compared to physiological conditions), and (iv) threshold (e.g., expression of components for sensing of NAs and downstream signaling) [8]. The frontline of the innate immune response is represented by pattern recognition receptors (PRRs) that in the case of the viral infections detect pathogen-associated molecular patterns, or PAMPs. PRRs sensing PAMPs outside the cellular interior are located on the cell surface and, among others, include Toll-like receptors, or TLRs [9]. TLR9 sensing nucleic acids (TLR3, TLR7, TLR8, and TLR9) are located in the endosomal compartment of a cell. Other groups of NA-sensing receptors reside in the cytoplasm and nucleus and include RNA sensing RIG-I-like receptors (RLRs), and DNA-sensing cyclic GMP-AMP synthase (cGAS) and interferon-γ-inducible protein 16 (IFI16), just to name a few [10]. The presence of individual PRRs differs among various tissues. While TLRs are mostly specific for cells of immune system, intracellular PRRs are expressed broadly.
COVID-19 pathogenesis and host immune response
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Surbhi Bihani, Shalini Aggarwal, Arup Acharjee
Acute respiratory infections (ARI) are among the top five causes of mortality worldwide and respiratory virus infections are significant contributors to that (Legand et al. 2013), causing an enormous burden to the healthcare systems and the socioeconomic conditions. The emerging respiratory viruses such as influenza viruses and coronaviruses, among others, present a continual threat to global health and the economy (Tyrrell, Allen, and Carson 2017). To initiate any response against an invading pathogen, the host has to detect the presence of the pathogen. Pathogen-associated molecular patterns (PAMPs) are distinct molecular structures associated with different classes of pathogens that the host recognizes through pattern recognition receptors (PRRs). Upon sensing the PAMPs, PRRs initiate downstream signaling to trigger the production of mediators that aid in alerting the immune system, propagating the immune response, protecting the neighboring cells, and clearing the infection. Three classes of PRRs, viz., Toll-like receptors (TLRs), a retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), and nucleotide oligomerization domain (NOD)-like receptors (NLRs), are currently known to be involved in sensing of viral components like ssRNA, dsRNA, RNA with 5′-triphosphate ends, and genomic DNA (Takeuchi and Akira 2009). Endoplasmic reticulum (ER) stress induced by virus infection and fusion of viral envelope with cell membrane can also trigger host immune response (Hrincius et al. 2015; Holm et al. 2012).
Inhibitory effect of particulate matter on toll-like receptor 9 stimulated dendritic cells by downregulating mitogen-activated protein kinase and NF-κB pathway
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Madeeha Arooj, Irshad Ali, Hee Kyoung Kang, Jin Won Hyun, Young-Sang Koh
Innate immune cells such as dendritic cells (DCs) and macrophages are key endogenous components to counteract pathogens and serve as a link between innate and adaptive immunity. Antigen-presenting cells (APCs) recognize pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) (Akira and Takeda 2004; Koo et al. 2012). Toll-like receptors (TLRs) interaction with PAMPs activates major signal transduction pathways including mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and induces cytokine production which serves as a trigger to initiate T-cell-mediated immunity (Akira and Takeda 2004). MAPKs including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 kinase play a key role in apoptosis, cell survival, proliferation, differentiation, and inflammation. NF-κB is a rapid-acting transcription factor that aids in the expression of cytokines and cell survival. Under quiescent conditions, NF-κB, a transcription factor within cytosol is coupled with specific inhibitor nuclear factor of kappa light polypeptide gene enhancer in B-cells, alpha (IκBα). Upon TLR stimulation, IκBα is phosphorylated and ubiquitinated, which leads to proteasomal degradation and translocation of NF-κB into the nucleus where it regulates transcription of various inflammatory genes including cytokines (Akira and Takeda 2004; Blasius and Beutler 2010; Koo et al. 2012).
Glycyrrhizin and Omega-3 fatty acids have hepatoprotective roles through toll-like receptor-4
Published in Egyptian Journal of Basic and Applied Sciences, 2019
Nada F. Abo El-Magd, Amro El-Karef, Mamdouh M. El-Shishtawy, Laila A. Eissa
Toll-like receptor-4 (TLR-4) has a critical role in innate immunity as the first line of host defense. Dimerization of two receptor molecules precedes TLR-4 activation [4]. The TLR-4 pathway consists of two different signaling pathways, the myeloid differentiating primary response gene 88 (MyD88)-dependent and the MyD88-independent pathway. (MyD88)-dependent pathway results in the production of pro-inflammatory cytokines through activation of nuclear factor-κB (NF-κB), while the MyD88-independent pathway results in the production of type 1 interferons [5]. Innate immune responses are initiated when danger associated molecule patterns and pathogen-associated molecular patterns (PAMP) are recognized by pattern recognition receptors including TLR-4 [6]. A classical PAMP is a lipopolysaccharide (LPS) from gram-negative bacteria which activates high mobility group box1 (HMGB1). HMGB1 is a highly conserved protein released by injured or dying cells as a result of pathogenic products [7]. HMGB1 may trigger an inflammatory response via activation of TLR-4 pathway which activates NF-κB. This consequently causes an enhancement in the production of tumor necrosis factor α (TNF-α), interleukin-1b (IL-1b) and nitric oxide [8].