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Journal articles on the topic 'Innate immune signalling'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Guillamot, Maria, and Iannis Aifantis. "Splicing the innate immune signalling in leukaemia." Nature Cell Biology 21, no. 5 (April 22, 2019): 536–37. http://dx.doi.org/10.1038/s41556-019-0323-4.

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2

Yu, Xiaoyu, Liyuan Zhang, Jingxiang Shen, Yanfang Zhai, Qifei Jiang, Mengran Yi, Xiaobing Deng, et al. "The STING phase-separator suppresses innate immune signalling." Nature Cell Biology 23, no. 4 (April 2021): 330–40. http://dx.doi.org/10.1038/s41556-021-00659-0.

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3

Weidenbusch, Marc, Onkar P. Kulkarni, and Hans-Joachim Anders. "The innate immune system in human systemic lupus erythematosus." Clinical Science 131, no. 8 (March 28, 2017): 625–34. http://dx.doi.org/10.1042/cs20160415.

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Although the role of adaptive immune mechanisms, e.g. autoantibody formation and abnormal T-cell activation, has been long noted in the pathogenesis of human systemic lupus erythematosus (SLE), the role of innate immunity has been less well characterized. An intricate interplay between both innate and adaptive immune elements exists in protective anti-infective immunity as well as in detrimental autoimmunity. More recently, it has become clear that the innate immune system in this regard not only starts inflammation cascades in SLE leading to disease flares, but also continues to fuel adaptive immune responses throughout the course of the disease. This is why targeting the innate immune system offers an additional means of treating SLE. First trials assessing the efficacy of anti-type I interferon (IFN) therapy or modulators of pattern recognition receptor (PRR) signalling have been attempted. In this review, we summarize the available evidence on the role of several distinct innate immune elements, especially neutrophils and dendritic cells as well as the IFN system, as well as specific innate PRRs along with their signalling pathways. Finally, we highlight recent clinical trials in SLE addressing one or more of the aforementioned components of the innate immune system.
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4

Hopcraft, Sharon E., and Blossom Damania. "Tumour viruses and innate immunity." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1732 (September 11, 2017): 20160267. http://dx.doi.org/10.1098/rstb.2016.0267.

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Host cells sense viral infection through pattern recognition receptors (PRRs), which detect pathogen-associated molecular patterns (PAMPs) and stimulate an innate immune response. PRRs are localized to several different cellular compartments and are stimulated by viral proteins and nucleic acids. PRR activation initiates signal transduction events that ultimately result in an inflammatory response. Human tumour viruses, which include Kaposi's sarcoma-associated herpesvirus, Epstein–Barr virus, human papillomavirus, hepatitis C virus, hepatitis B virus, human T-cell lymphotropic virus type 1 and Merkel cell polyomavirus, are detected by several different PRRs. These viruses engage in a variety of mechanisms to evade the innate immune response, including downregulating PRRs, inhibiting PRR signalling, and disrupting the activation of transcription factors critical for mediating the inflammatory response, among others. This review will describe tumour virus PAMPs and the PRRs responsible for detecting viral infection, PRR signalling pathways, and the mechanisms by which tumour viruses evade the host innate immune system. This article is part of the themed issue ‘Human oncogenic viruses’.
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5

Triantafilou, Martha, Philipp M. Lepper, Robin Olden, Ivo de Seabra Rodrigues Dias, and Kathy Triantafilou. "Location, Location, Location: Is Membrane Partitioning Everything When It Comes to Innate Immune Activation?" Mediators of Inflammation 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/186093.

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In the last twenty years, the general view of the plasma membrane has changed from a homogeneous arrangement of lipids to a mosaic of microdomains. It is currently thought that islands of highly ordered saturated lipids and cholesterol, which are laterally mobile, exist in the plane of the plasma membrane. Lipid rafts are thought to provide a means to explain the spatial segregation of certain signalling pathways emanating from the cell surface. They seem to provide the necessary microenvironment in order for certain specialised signalling events to take place, such as the innate immune recognition. The innate immune system seems to employ germ-lined encoded receptors, called pattern recognition receptors (PRRs), in order to detect pathogens. One family of such receptors are the Toll-like receptors (TLRs), which are the central “sensing” apparatus of the innate immune system. In recent years, it has become apparent that TLRs are recruited into membrane microdomains in response to ligands. These nanoscale assemblies of sphingolipid, cholesterol, and TLRs stabilize and coalesce, forming signalling platforms, which transduce signals that lead to innate immune activation. In the current paper, we will investigate all past and current literature concerning recruitment of extracellular and intracellular TLRs into lipid rafts and how this membrane organization modulates innate immune responses.
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6

Eades, Lauren, Michael Drozd, and Richard M. Cubbon. "Hypoxia signalling in the regulation of innate immune training." Biochemical Society Transactions 50, no. 1 (January 11, 2021): 413–22. http://dx.doi.org/10.1042/bst20210857.

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Innate immune function is shaped by prior exposures in a phenomenon often referred to as ‘memory’ or ‘training’. Diverse stimuli, ranging from pathogen-associated molecules to atherogenic lipoproteins, induce long-lasting training, impacting on future responses, even to distinct stimuli. It is now recognised that epigenetic modifications in innate immune cells, and their progenitors, underpin these sustained behavioural changes, and that rewired cellular metabolism plays a key role in facilitating such epigenetic marks. Oxygen is central to cellular metabolism, and cells exposed to hypoxia undergo profound metabolic rewiring. A central effector of these responses are the hypoxia inducible factors (or HIFs), which drive transcriptional programmes aiming to adapt cellular homeostasis, such as by increasing glycolysis. These metabolic shifts indirectly promote post-translational modification of the DNA-binding histone proteins, and also of DNA itself, which are retained even after cellular oxygen tension and metabolism normalise, chronically altering DNA accessibility and utilisation. Notably, the activity of HIFs can be induced in some normoxic circumstances, indicating their broad importance to cell biology, irrespective of oxygen tension. Some HIFs are implicated in innate immune training and hypoxia is present in many disease states, yet many questions remain about the association between hypoxia and training, both in health and disease. Moreover, it is now appreciated that cellular responses to hypoxia are mediated by non-HIF pathways, suggesting that other mechanisms of training may be possible. This review sets out to define what is already known about the topic, address gaps in our knowledge, and provide recommendations for future research.
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7

Boudsocq, Marie, Matthew R. Willmann, Matthew McCormack, Horim Lee, Libo Shan, Ping He, Jenifer Bush, Shu-Hua Cheng, and Jen Sheen. "Differential innate immune signalling via Ca2+ sensor protein kinases." Nature 464, no. 7287 (February 17, 2010): 418–22. http://dx.doi.org/10.1038/nature08794.

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8

Zhang, Yaxing, Zan Huang, and Hongliang Li. "Insights into innate immune signalling in controlling cardiac remodelling." Cardiovascular Research 113, no. 13 (July 3, 2017): 1538–50. http://dx.doi.org/10.1093/cvr/cvx130.

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9

Shadel, Gerald S. "Mitochondrial DNA stress in innate immune signalling and cancer." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1857 (August 2016): e5-e6. http://dx.doi.org/10.1016/j.bbabio.2016.04.408.

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10

Sprenger, Hans-Georg, Thomas MacVicar, Amir Bahat, Kai Uwe Fiedler, Steffen Hermans, Denise Ehrentraut, Katharina Ried, et al. "Cellular pyrimidine imbalance triggers mitochondrial DNA–dependent innate immunity." Nature Metabolism 3, no. 5 (April 26, 2021): 636–50. http://dx.doi.org/10.1038/s42255-021-00385-9.

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AbstractCytosolic mitochondrial DNA (mtDNA) elicits a type I interferon response, but signals triggering the release of mtDNA from mitochondria remain enigmatic. Here, we show that mtDNA-dependent immune signalling via the cyclic GMP–AMP synthase‒stimulator of interferon genes‒TANK-binding kinase 1 (cGAS–STING–TBK1) pathway is under metabolic control and is induced by cellular pyrimidine deficiency. The mitochondrial protease YME1L preserves pyrimidine pools by supporting de novo nucleotide synthesis and by proteolysis of the pyrimidine nucleotide carrier SLC25A33. Deficiency of YME1L causes inflammation in mouse retinas and in cultured cells. It drives the release of mtDNA and a cGAS–STING–TBK1-dependent inflammatory response, which requires SLC25A33 and is suppressed upon replenishment of cellular pyrimidine pools. Overexpression of SLC25A33 is sufficient to induce immune signalling by mtDNA. Similarly, depletion of cytosolic nucleotides upon inhibition of de novo pyrimidine synthesis triggers mtDNA-dependent immune responses in wild-type cells. Our results thus identify mtDNA release and innate immune signalling as a metabolic response to cellular pyrimidine deficiencies.
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11

Lin, Rui. "Crosstalk between Vitamin D Metabolism, VDR Signalling, and Innate Immunity." BioMed Research International 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/1375858.

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The primary function of vitamin D is to regulate calcium homeostasis, which is essential for bone formation and resorption. Although diet is a source of vitamin D, most foods are naturally lacking vitamin D. Vitamin D is also manufactured in the skin through a photolysis process, leading to a process called the “sunshine vitamin.” The active form of vitamin D, 1,25-dihydroxyvitamin D (calcitriol), is biosynthesised in the kidney through the hydroxylation of 25-hydroxycholecalciferol by the CYP27B1 enzyme. It has been found that several immune cells express the vitamin D receptor (VDR) and CYP27B1; of the latter, synthesis is determined by several immune-specific signals. The realisation that vitamin D employs several molecular mechanisms to regulate innate immune responses is more recent. Furthermore, evidence collected from intervention studies indicates that vitamin D supplements may boost clinical responses to infections. This review considers the current knowledge of how immune signals regulate vitamin D metabolism and how innate immune system function is modulated by ligand-bound VDR.
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12

van de Vosse, Esther, Jaap T. van Dissel, and Tom HM Ottenhoff. "Genetic deficiencies of innate immune signalling in human infectious disease." Lancet Infectious Diseases 9, no. 11 (November 2009): 688–98. http://dx.doi.org/10.1016/s1473-3099(09)70255-5.

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13

Chew, A. C., M. K. Tulic, D. Mallon, G. L. Radford-Smith, S. L. Prescott, and I. C. Lawrance. "P298 Dysregulation of the innate immune signalling in ulcerative colitis." Journal of Crohn's and Colitis 6 (February 2012): S128—S129. http://dx.doi.org/10.1016/s1873-9946(12)60318-3.

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14

Wang, Lihui, and Petros Ligoxygakis. "Pathogen recognition and signalling in the Drosophila innate immune response." Immunobiology 211, no. 4 (June 2006): 251–61. http://dx.doi.org/10.1016/j.imbio.2006.01.001.

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15

Creagh, Emma M. "Caspase crosstalk: integration of apoptotic and innate immune signalling pathways." Trends in Immunology 35, no. 12 (December 2014): 631–40. http://dx.doi.org/10.1016/j.it.2014.10.004.

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16

Ragab, Anan, Tina Buechling, Viola Gesellchen, Kerstin Spirohn, Anna-Lisa Boettcher, and Michael Boutros. "DrosophilaRas/MAPK signalling regulates innate immune responses in immune and intestinal stem cells." EMBO Journal 30, no. 6 (February 4, 2011): 1123–36. http://dx.doi.org/10.1038/emboj.2011.4.

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17

Kumar, Himanshu, Taro Kawai, and Shizuo Akira. "Pathogen recognition in the innate immune response." Biochemical Journal 420, no. 1 (April 28, 2009): 1–16. http://dx.doi.org/10.1042/bj20090272.

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Immunity against microbial pathogens primarily depends on the recognition of pathogen components by innate receptors expressed on immune and non-immune cells. Innate receptors are evolutionarily conserved germ-line-encoded proteins and include TLRs (Toll-like receptors), RLRs [RIG-I (retinoic acid-inducible gene-I)-like receptors] and NLRs (Nod-like receptors). These receptors recognize pathogens or pathogen-derived products in different cellular compartments, such as the plasma membrane, the endosomes or the cytoplasm, and induce the expression of cytokines, chemokines and co-stimulatory molecules to eliminate pathogens and instruct pathogen-specific adaptive immune responses. In the present review, we will discuss the recent progress in the study of pathogen recognition by TLRs, RLRs and NLRs and their signalling pathways.
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18

Katholnig, Karl, Monika Linke, Ha Pham, Markus Hengstschläger, and Thomas Weichhart. "Immune responses of macrophages and dendritic cells regulated by mTOR signalling." Biochemical Society Transactions 41, no. 4 (July 18, 2013): 927–33. http://dx.doi.org/10.1042/bst20130032.

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The innate myeloid immune system is a complex network of cells that protect against disease by identifying and killing pathogens and tumour cells, but it is also implicated in homoeostatic mechanisms such as tissue remodelling and wound healing. Myeloid phagocytes such as monocytes, macrophages or dendritic cells are at the basis of controlling these immune responses in all tissues of the body. In the present review, we summarize recent studies demonstrating that mTOR [mammalian (or mechanistic) target of rapamycin] regulates innate immune reactions in macrophages and dendritic cells. The mTOR pathway serves as a decision maker to control the cellular response to pathogens and tumours by regulating the expression of inflammatory mediators such as cytokines, chemokines or interferons. In addition to various in vivo mouse models, kidney transplant patients under mTOR inhibitor therapy allowed the elucidation of important innate immune functions regulated by mTOR in humans. The role of the mTOR pathway in macrophages and dendritic cells enhances our understanding of the immune system and suggests new therapeutic avenues for the regulation of pro- versus anti-inflammatory mediators with potential relevance to cancer therapy, the design of novel adjuvants and the control of distinct infectious and autoimmune diseases.
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19

Krzyzowska, Malgorzata, Weronika Swiatek, Beata Fijalkowska, Marek Niemialtowski, and Ada Schollenberger. "The Role of Map Kinases in Immune Response." Advances in Cell Biology 2, no. 3 (April 1, 2010): 125–38. http://dx.doi.org/10.2478/v10052-010-0007-5.

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Summary The MAP kinases (MAPKs), including ERK, JNK and p38 families comprise part of the intracellular signalling network, which is essential for signal transduction from receptors and stimuli to the biological reaction. Activity of MAPKs plays a crucial role in normal functioning of the immune system. By taking part in cytokine production upon signalling from activated TLR receptors, MAPKs are involved in initiation of innate immunity and in responses to binding of cytokines by appropriate receptors. MAPKs activity is also important for T and B lymphocyte differentiation, by the ITAM signalling pathway. Moreover, their involvement in apoptosis supports lymphocyte T cytotoxicity and enables the removal of damaged, infected or transformed cells. Correct functioning of the MAPK signalling is crucial for effective immune response, and therefore MAPKs’ inhibitors constitute a promising therapeutic goal
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20

Elshina, Elizaveta, and Aartjan J. W. te Velthuis. "The influenza virus RNA polymerase as an innate immune agonist and antagonist." Cellular and Molecular Life Sciences 78, no. 23 (October 22, 2021): 7237–56. http://dx.doi.org/10.1007/s00018-021-03957-w.

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AbstractInfluenza A viruses cause a mild-to-severe respiratory disease that affects millions of people each year. One of the many determinants of disease outcome is the innate immune response to the viral infection. While antiviral responses are essential for viral clearance, excessive innate immune activation promotes lung damage and disease. The influenza A virus RNA polymerase is one of viral proteins that affect innate immune activation during infection, but the mechanisms behind this activity are not well understood. In this review, we discuss how the viral RNA polymerase can both activate and suppress innate immune responses by either producing immunostimulatory RNA species or directly targeting the components of the innate immune signalling pathway, respectively. Furthermore, we provide a comprehensive overview of the polymerase residues, and their mutations, associated with changes in innate immune activation, and discuss their putative effects on polymerase function based on recent advances in our understanding of the influenza A virus RNA polymerase structure.
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Lara-Reyna, Samuel, Jonathan Holbrook, Heledd H. Jarosz-Griffiths, Daniel Peckham, and Michael F. McDermott. "Dysregulated signalling pathways in innate immune cells with cystic fibrosis mutations." Cellular and Molecular Life Sciences 77, no. 22 (May 4, 2020): 4485–503. http://dx.doi.org/10.1007/s00018-020-03540-9.

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Abstract Cystic fibrosis (CF) is one of the most common life-limiting recessive genetic disorders in Caucasians, caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR). CF is a multi-organ disease that involves the lungs, pancreas, sweat glands, digestive and reproductive systems and several other tissues. This debilitating condition is associated with recurrent lower respiratory tract bacterial and viral infections, as well as inflammatory complications that may eventually lead to pulmonary failure. Immune cells play a crucial role in protecting the organs against opportunistic infections and also in the regulation of tissue homeostasis. Innate immune cells are generally affected by CFTR mutations in patients with CF, leading to dysregulation of several cellular signalling pathways that are in continuous use by these cells to elicit a proper immune response. There is substantial evidence to show that airway epithelial cells, neutrophils, monocytes and macrophages all contribute to the pathogenesis of CF, underlying the importance of the CFTR in innate immune responses. The goal of this review is to put into context the important role of the CFTR in different innate immune cells and how CFTR dysfunction contributes to the pathogenesis of CF, highlighting several signalling pathways that may be dysregulated in cells with CFTR mutations.
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22

Toka, Felix N., Patryk Dolega, Karolina Gregorczyk, Magdalena Bossowska, Matylda Mielcarska, and Lidia Szulc-Dabrowska. "Influence of Ectromelia virus (ECTV-Mos) infection on mRNA transcript levels of selected genes encoding antiviral proteins in a macrophage cell line RAW 264.7 (in vitro studies)." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 63.2. http://dx.doi.org/10.4049/jimmunol.196.supp.63.2.

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Abstract Poxviruses have evolved a number of mechanisms to avoid immune response by the infected host. We investigated the impact of poxvirus infection on the level of mRNA transcripts of selected genes encoding antiviral proteins in the macrophage cell line (RAW 264.7). We observed reduction of mRNA transcript level in four groups of signalling pathways (Toll-like receptor signalling, NOD-like receptor signalling, RIG-I-like receptor signalling, and Type I interferon signalling) involved in innate immune response. Seventy-three genes had a statistically significantly decreased mRNA expression, 4 genes had a statistically significantly sustained mRNA expression. Only Cxcl11 and Ifna2 were statistically significantly increased. The results confirmed that the mouse poxvirus ECTV may interfere with or inhibit many signalling pathways, which are involved in inducing an antiviral immune response in infected macrophages.
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23

Bakshi, S., B. Holzer, A. Bridgen, G. McMullan, D. G. Quinn, and M. D. Baron. "Dugbe virus ovarian tumour domain interferes with ubiquitin/ISG15-regulated innate immune cell signalling." Journal of General Virology 94, no. 2 (February 1, 2013): 298–307. http://dx.doi.org/10.1099/vir.0.048322-0.

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The ovarian tumour (OTU) domain of the nairovirus L protein has been shown to remove ubiquitin and interferon-stimulated gene 15 protein (ISG15) from host cell proteins, which is expected to have multiple effects on cell signalling pathways. We have confirmed that the OTU domain from the L protein of the apathogenic nairovirus Dugbe virus has deubiquitinating and deISGylating activity and shown that, when expressed in cells, it is highly effective at blocking the TNF-α/NF-κB and interferon/JAK/STAT signalling pathways even at low doses. Point mutations of the catalytic site of the OTU [C40A, H151A and a double mutant] both abolished the ability of the OTU domain to deubiquitinate and deISGylate proteins and greatly reduced its effect on cell signalling pathways, confirming that it is this enzymic activity that is responsible for blocking the two signalling pathways. Expression of the inactive mutants at high levels could still block signalling, suggesting that the viral OTU can still bind to its substrate even when mutated at its catalytic site. The nairovirus L protein is a very large protein that is normally confined to the cytoplasm, where the virus replicates. When the OTU domain was prevented from entering the nucleus by expressing it as part of the N-terminal 205 kDa of the viral L protein, it continued to block type I interferon signalling, but no longer blocked the TNF-α-induced activation of NF-κB.
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24

Jarosz-Griffiths, Heledd H., Jonathan Holbrook, Samuel Lara-Reyna, and Michael F. McDermott. "TNF receptor signalling in autoinflammatory diseases." International Immunology 31, no. 10 (March 6, 2019): 639–48. http://dx.doi.org/10.1093/intimm/dxz024.

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Abstract Autoinflammatory syndromes are a group of disorders characterized by recurring episodes of inflammation as a result of specific defects in the innate immune system. Patients with autoinflammatory disease present with recurrent outbreaks of chronic systemic inflammation that are mediated by innate immune cells, for the most part. A number of these diseases arise from defects in the tumour necrosis factor receptor (TNFR) signalling pathway leading to elevated levels of inflammatory cytokines. Elucidation of the molecular mechanisms of these recently defined autoinflammatory diseases has led to a greater understanding of the mechanisms of action of key molecules involved in TNFR signalling, particularly those involved in ubiquitination, as found in haploinsufficiency of A20 (HA20), otulipenia/OTULIN-related autoinflammatory syndrome (ORAS) and linear ubiquitin chain assembly complex (LUBAC) deficiency. In this review, we also address other TNFR signalling disorders such as TNFR-associated periodic syndrome (TRAPS), RELA haploinsufficiency, RIPK1-associated immunodeficiency and autoinflammation, X-linked ectodermal dysplasia and immunodeficiency (X-EDA-ID) and we review the most recent advances surrounding these diseases and therapeutic approaches currently used to target these diseases. Finally, we explore therapeutic advances in TNF-related immune-based therapies and explore new approaches to target disease-specific modulation of autoinflammatory diseases.
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25

Maruta, Natsumi, Hayden Burdett, Bryan Y. J. Lim, Xiahao Hu, Sneha Desa, Mohammad Kawsar Manik, and Bostjan Kobe. "Structural basis of NLR activation and innate immune signalling in plants." Immunogenetics 74, no. 1 (January 4, 2022): 5–26. http://dx.doi.org/10.1007/s00251-021-01242-5.

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AbstractAnimals and plants have NLRs (nucleotide-binding leucine-rich repeat receptors) that recognize the presence of pathogens and initiate innate immune responses. In plants, there are three types of NLRs distinguished by their N-terminal domain: the CC (coiled-coil) domain NLRs, the TIR (Toll/interleukin-1 receptor) domain NLRs and the RPW8 (resistance to powdery mildew 8)-like coiled-coil domain NLRs. CC-NLRs (CNLs) and TIR-NLRs (TNLs) generally act as sensors of effectors secreted by pathogens, while RPW8-NLRs (RNLs) signal downstream of many sensor NLRs and are called helper NLRs. Recent studies have revealed three dimensional structures of a CNL (ZAR1) including its inactive, intermediate and active oligomeric state, as well as TNLs (RPP1 and ROQ1) in their active oligomeric states. Furthermore, accumulating evidence suggests that members of the family of lipase-like EDS1 (enhanced disease susceptibility 1) proteins, which are uniquely found in seed plants, play a key role in providing a link between sensor NLRs and helper NLRs during innate immune responses. Here, we summarize the implications of the plant NLR structures that provide insights into distinct mechanisms of action by the different sensor NLRs and discuss plant NLR-mediated innate immune signalling pathways involving the EDS1 family proteins and RNLs.
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26

Rosenthal, Kenneth L. "Tweaking Innate Immunity: The Promise of Innate Immunologicals as Anti-Infectives." Canadian Journal of Infectious Diseases and Medical Microbiology 17, no. 5 (2006): 307–14. http://dx.doi.org/10.1155/2006/195957.

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New and exciting insights into the importance of the innate immune system are revolutionizing our understanding of immune defense against infections, pathogenesis, and the treatment and prevention of infectious diseases. The innate immune system uses multiple families of germline-encoded pattern recognition receptors (PRRs) to detect infection and trigger a variety of antimicrobial defense mechanisms. PRRs are evolutionarily highly conserved and serve to detect infection by recognizing pathogen-associated molecular patterns that are unique to microorganisms and essential for their survival. Toll-like receptors (TLRs) are transmembrane signalling receptors that activate gene expression programs that result in the production of proinflammatory cytokines and chemokines, type I interferons and antimicrobial factors. Furthermore, TLR activation facilitates and guides activation of adaptive immune responses through the activation of dendritic cells. TLRs are localized on the cell surface and in endosomal/lysosomal compartments, where they detect bacterial and viral infections. In contrast, nucleotide-binding oligomerization domain proteins and RNA helicases are located in the cell cytoplasm, where they serve as intracellular PRRs to detect cytoplasmic infections, particularly viruses. Due to their ability to enhance innate immune responses, novel strategies to use ligands, synthetic agonists or antagonists of PRRs (also known as 'innate immunologicals') can be used as stand-alone agents to provide immediate protection or treatment against bacterial, viral or parasitic infections. Furthermore, the newly appreciated importance of innate immunity in initiating and shaping adaptive immune responses is contributing to our understanding of vaccine adjuvants and promises to lead to improved next-generation vaccines.
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Preiss, S., A. Thompson, X. Chen, S. Rodgers, V. Markovska, P. Desmond, K. Visvanathan, K. Li, S. Locarnini, and P. Revill. "Characterization of the innate immune signalling pathways in hepatocyte cell lines." Journal of Viral Hepatitis 15, no. 12 (July 28, 2008): 888–900. http://dx.doi.org/10.1111/j.1365-2893.2008.01001.x.

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28

Ishikawa, Hiroki, and Glen N. Barber. "STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling." Nature 455, no. 7213 (August 24, 2008): 674–78. http://dx.doi.org/10.1038/nature07317.

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Wood, L. G., J. L. Simpson, P. A. B. Wark, H. Powell, and P. G. Gibson. "Characterization of innate immune signalling receptors in virus-induced acute asthma." Clinical & Experimental Allergy 41, no. 5 (December 3, 2010): 640–48. http://dx.doi.org/10.1111/j.1365-2222.2010.03669.x.

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30

Gitlin, Alexander D., Klaus Heger, Alexander F. Schubert, Rohit Reja, Donghong Yan, Victoria C. Pham, Eric Suto, et al. "Integration of innate immune signalling by caspase-8 cleavage of N4BP1." Nature 587, no. 7833 (September 24, 2020): 275–80. http://dx.doi.org/10.1038/s41586-020-2796-5.

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Roberts, Amy, Tim Vyse, and Benjamin Rhodes. "243. Modulating Innate Immune Signalling Using a Complement Receptor 3 Agonist." Rheumatology 53, suppl_1 (April 2014): i150—i151. http://dx.doi.org/10.1093/rheumatology/keu119.001.

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32

Ding, Chengming, Jun He, Jun Zhao, Junhua Li, Jie Chen, Wenyan Liao, Yi Zeng, et al. "β-catenin regulates IRF3-mediated innate immune signalling in colorectal cancer." Cell Proliferation 51, no. 5 (July 13, 2018): e12464. http://dx.doi.org/10.1111/cpr.12464.

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33

Pott, Johanna, and Mathias Hornef. "Innate immune signalling at the intestinal epithelium in homeostasis and disease." EMBO reports 13, no. 8 (July 17, 2012): 684–98. http://dx.doi.org/10.1038/embor.2012.96.

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34

García Bueno, B., J. R. Caso, J. L. M. Madrigal, and J. C. Leza. "Innate immune receptor Toll-like receptor 4 signalling in neuropsychiatric diseases." Neuroscience & Biobehavioral Reviews 64 (May 2016): 134–47. http://dx.doi.org/10.1016/j.neubiorev.2016.02.013.

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Polinski, Mark, Julia Bradshaw, Sabrina Inkpen, Matthew Rise, Rosemarie Ganassin, Kyle Garver, and Stewart Johnson. "Effects of piscine reovirus infection on innate immune signalling in salmon." Fish & Shellfish Immunology 53 (June 2016): 92–93. http://dx.doi.org/10.1016/j.fsi.2016.03.145.

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36

Smith, Dylan G. M., Yuki Hosono, Masahiro Nagata, Sho Yamasaki, and Spencer J. Williams. "Design of potent Mincle signalling agonists based on an alkyl β-glucoside template." Chemical Communications 56, no. 31 (2020): 4292–95. http://dx.doi.org/10.1039/d0cc00670j.

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37

Toka, Felix, Patryk Dolega, Matylda Mielcarska, and Magdalena Bossowska. "Comparison of messenger RNA expression profile of antiviral innate immune response genes in peritoneal macrophages from BALB/c and C57BL/6 mice infected with ectromelia virus (INM3P.413)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 127.18. http://dx.doi.org/10.4049/jimmunol.194.supp.127.18.

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Abstract Although a few mechanisms have explained how, for instance ectromelia virus (ECTV), is successful in causing fatal disease in certain strains of mice and how other strains are not susceptible, a global transcription overview of innate immunity genes is not entirely known. Poxviruses have evolved several mechanisms to avoid immune response of an infected host. Here we have studied the innate gene transcriptional response of BALB/c and C57BL/6 mice peritoneal macrophages to infection with ECTV Moscow strain (ECTV-Mos). Indeed, assessment of four categories of antiviral innate immune response receptors, downstream signalling and responsive components revealed generalized down regulation of many genes in both strains of mice. Of the 84 genes assessed in each mouse strain only 3 and 15 were significantly upregulated in BALB/c and C57BL/6 mice, respectively. The remaining genes were more or less down-regulated. Surprisingly, type I interferon genes were substantially upregulated. The observed upregulation strongly correlated with protein expression in the case of cathepsin genes as well as TLR genes. ECTV-Mos inhibits receptors and signalling components of the innate immune response in mice. Results provide an insight into initial factors that presumably lead to an ineffective antiviral immune response of BALB/c and C57BL/6 mice in the light of infection with ECTV.
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Holms, Rupert Donald. "The COVID-19 Cell Signalling Problem: Spike, RAGE, PKC, p38, NFκB & IL-6 Hyper-Expression and the Human Ezrin Peptide, VIP, PKA-CREB Solution." Immuno 2, no. 2 (March 23, 2022): 260–82. http://dx.doi.org/10.3390/immuno2020017.

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SARS-CoV-2 infection inhibits interferon expression, while hyper-activating innate-immune signalling and expression of pro-inflammatory cytokines. SARS-CoV-2 proteins: Spike, M and nsp6, nsp12 and nsp13 inhibit IFR3-mediated Type-1-interferon defence, but hyper-activate intracellular signalling, which leads to dysfunctional expression of pro-inflammatory cytokines, particularly IL-1β IL-6, IL-8, and TNFα. Ezrin, a sub-membrane adaptor-protein, organises multi-protein-complexes such as ezrin+NHERF1+NHE+CFTR, which control the density and location of ACE2 receptor expression on the luminal surface of airway-epithelial-cells, as well as determining susceptibility to SARS-CoV-2 infection. This protein complex is vital for lung-surfactant production for efficient gas-exchange. Ezrin also forms multi-protein-complexes that regulate signalling kinases; Ras, PKC, PI3K, and PKA. m-RAGE is a pattern-recognition-receptor of the innate immune system that is triggered by AGEs, which are chemically modified proteins common in the elderly and obese. m-RAGE forms multi-protein complexes with ezrin and TIRAP, a toll-like-receptor adaptor-protein. The main cause of COVID-19 is not viral infection but pro-inflammatory p38MAPK signalling mediated by TLRs and RAGE. In contrast, it appears that activated ezrin+PKA signalling results in the activation of transcription-factor CREB, which suppresses NFκB mediated pro-inflammatory cytokine expression. In addition, competition between ezrin and TIRAP to form multi-protein-complexes on membrane PIP2-lipid-rafts is a macromolecular-switch that changes the priority from innate immune activation programs to adaptive immune activation programs. Human Vasoactive Intestinal Peptide (VIP), and Human Ezrin Peptides (HEP-1 and RepG3) probably inhibit COVID-19 by activating the ezrin+PKA and ras>Raf>MEK>ERK>RSK>CREB>IL-10 signalling, which favours activation of adaptive immunity programs and inhibition of the dysfunctional innate-inflammation, the cause of COVID-19. HEP-1, RepG3, and VIP in individual human volunteers and in small clinical studies have been shown to be effective COVID-19 therapies, and seem to have a closely related mechanism of action.
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39

Basatvat, Shaghayegh, Deborah Angela Louise Carter, Endre Kiss-Toth, and Alireza Fazeli. "Tribbles role in reproduction." Biochemical Society Transactions 43, no. 5 (October 1, 2015): 1116–21. http://dx.doi.org/10.1042/bst20150121.

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Tribbles (TRIB) proteins, a family of evolutionary conserved psuedokinase proteins, modulate various signalling pathways within the cell. The regulatory roles of TRIB make them an important part of a number of biological processes ranging from cell proliferation to metabolism, immunity, inflammation and carcinogenesis. Innate immune system plays a pivotal role during the regulation of reproductive processes that allows successful creation of an offspring. Its involvement initiates from fertilization of the oocyte by spermatozoon and lasts throughout early embryonic development, pregnancy and labour. Therefore, there is a close cooperation between the reproductive system and the innate immune system. Evidence from our lab has demonstrated that improper activation of the innate immune system can reduce embryo implantation, thus leading to infertility. Therefore, control mechanisms regulating the innate immune system function can be critical for successful reproductive events.
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Fischer, Lena, David C. Hay, and Cliona O'Farrelly. "Innate immunity in stem cell-derived hepatocytes." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1750 (May 21, 2018): 20170220. http://dx.doi.org/10.1098/rstb.2017.0220.

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Stem cell-derived hepatocyte-like cells (HLCs) offer great opportunities for studies of host–pathogen interactions and tissue regeneration, as well as hepatotoxicity. To reliably predict the outcome of infection or to enhance graft survival, a finely tuned innate immune system is essential. Hepatocytes have long been considered solely metabolic and their critical innate immune potential is only recently gaining attention. Viral infection studies show that pathogen detection by cytosolic receptors leads to interferon (IFN) induction in primary hepatocytes and HLCs. IFN expression in HLCs is characterized by strong expression of type III IFN and low expression of type I IFN which is also a characteristic of primary hepatocytes. The response to IFN differs in HLCs with lower interferon-stimulated gene (ISG)-expression levels than in primary hepatocytes. Tumour necrosis factor-alpha (TNF-α) signalling is less studied in HLCs, but appears to be functional. Expression of toll-like receptors (TLR) 2–5, 7 and 9 has been reported in primary hepatocytes but has been poorly studied in HLCs. In summary, although they retain some immature features, HLCs are in many ways superior to hepatoma cell lines for cell-based modelling. In this review, we will provide an overview of innate immune signalling in HLCs and how this compares with primary hepatocytes. This article is part of the themed issue ‘Designer human tissue: coming to a lab near you’.
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Ferreira, Ana Rita, Ana Catarina Ramalho, Mariana Marques, and Daniela Ribeiro. "The Interplay between Antiviral Signalling and Carcinogenesis in Human Papillomavirus Infections." Cancers 12, no. 3 (March 10, 2020): 646. http://dx.doi.org/10.3390/cancers12030646.

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Human papillomaviruses (HPV) are the causative agents of the most common sexually transmitted infection worldwide. While infection is generally asymptomatic and can be cleared by the host immune system, when persistence occurs, HPV can become a risk factor for malignant transformation. Progression to cancer is actually an unintended consequence of the complex HPV life cycle. Different antiviral defence mechanisms recognize HPV early in infection, leading to the activation of the innate immune response. However, the virus has evolved several specific strategies to efficiently evade the antiviral immune signalling. Here, we review and discuss the interplay between HPV and the host cell innate immunity. We further highlight the evasion strategies developed by different HPV to escape this cellular response and focus on the correlation with HPV-induced persistence and tumorigenesis.
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Schröder, M., and A. G. Bowie. "An arms race: innate antiviral responses and counteracting viral strategies." Biochemical Society Transactions 35, no. 6 (November 23, 2007): 1512–14. http://dx.doi.org/10.1042/bst0351512.

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Viral recognition is mediated by different classes of PRRs (pattern-recognition receptors) among which the TLRs (Toll-like receptors) and the RLHs [RIG (retinoic-acid-inducible)-like helicases] play major roles. The detection of PAMPs (pathogen-associated molecular patterns) by these PRRs leads to the initiation of signalling pathways that ultimately result in the activation of transcription factors such as NF-κB (nuclear factor κB) and IRF-3 [IFN (interferon) regulatory factor-3] and IRF-7 and the induction of pro-inflammatory cytokines and type I IFNs. Viruses have evolved a fine-tuned mechanism to evade detection by the immune system or to interfere with the resulting signalling pathways. Here, we discuss viral evasion proteins that specifically interfere with TLR and/or RLH signalling.
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Byrne, Jennifer C., Joan Ní Gabhann, Elisa Lazzari, Rebecca Mahony, Siobhán Smith, Kevin Stacey, Claire Wynne, and Caroline A. Jefferies. "Genetics of SLE: Functional Relevance for Monocytes/Macrophages in Disease." Clinical and Developmental Immunology 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/582352.

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Genetic studies in the last 5 years have greatly facilitated our understanding of how the dysregulation of diverse components of the innate immune system contributes to pathophysiology of SLE. A role for macrophages in the pathogenesis of SLE was first proposed as early as the 1980s following the discovery that SLE macrophages were defective in their ability to clear apoptotic cell debris, thus prolonging exposure of potential autoantigens to the adaptive immune response. More recently, there is an emerging appreciation of the contribution both monocytes and macrophages play in orchestrating immune responses with perturbations in their activation or regulation leading to immune dysregulation. This paper will focus on understanding the relevance of genes identified as being associated with innate immune function of monocytes and macrophages and development of SLE, particularly with respect to their role in (1) immune complex (IC) recognition and clearance, (2) nucleic acid recognition via toll-like receptors (TLRs) and downstream signalling, and (3) interferon signalling. Particular attention will be paid to the functional consequences these genetic associations have for disease susceptibility or pathogenesis.
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44

Chittezhath, Manesh, Cho M. M. Wai, Vanessa S. Y. Tay, Minni Chua, Sarah R. Langley, and Yusuf Ali. "TLR4 signals through islet macrophages to alter cytokine secretion during diabetes." Journal of Endocrinology 247, no. 1 (October 2020): 87. http://dx.doi.org/10.1530/joe-20-0131.

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Toll-like receptors (TLRs), particularly TLR4, may act as immune sensors for metabolic stress signals such as lipids and link tissue metabolic changes to innate immunity. TLR signalling is not only tissue-dependent but also cell-type dependent and recent studies suggest that TLRs are not restricted to innate immune cells alone. Pancreatic islets, a hub of metabolic hormones and cytokines, respond to TLR signalling. However, the source of TLR signalling within the islet remain poorly understood. Uncovering the specific cell source and its role in mediating TLR signalling, especially within type 2 diabetes (T2D) islet will yield new targets to tackle islet inflammation, hormone secretion dysregulation and ultimately diabetes. In the present study, we immuno-characterised TLRs linked to pancreatic islets in both healthy and obese diabetic mice. We found that while TLRs1–4 and TLR9 were expressed in mouse islets, these TLRs did not co-localise with insulin-producing β-cells. β-Cells from obese diabetic mice were also devoid of these TLRs. While TLR immunoreactivity in obese mice islets increased, this was driven mostly by increased islet endothelial cell and islet macrophage presence. Analysis of human islet single-cell RNA-seq databases revealed that macrophages were an important source of islet TLRs. However, only TLR4 and TLR8 showed variation and cell-type specificity in their expression patterns. Cell depletion experiments in isolated mouse islets showed that TLR4 signalled through macrophages to alter islet cytokine secretome. Together, these studies suggest that islet macrophages are a dominant source of TLR4-mediated signalling in both healthy and diabetic islets.
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45

Chen, Wei-Yu, Tzu-Hsien Tsai, Jenq-Lin Yang, and Lung-Chih Li. "Therapeutic Strategies for Targeting IL-33/ST2 Signalling for the Treatment of Inflammatory Diseases." Cellular Physiology and Biochemistry 49, no. 1 (2018): 349–58. http://dx.doi.org/10.1159/000492885.

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Interleukin (IL)-33, a member of the IL-1 family of cytokines, is involved in innate and adaptive immune responses via interaction with its receptor, ST2. Activation of ST2 signalling by IL-33 triggers pleiotropic immune functions in multiple ST2-expressing immune cells, including macrophages, neutrophils, eosinophils, basophils, mast cells, type 2 helper T cells, regulatory T cells, and group 2 innate lymphoid cells. IL-33-mediated effector functions contribute to the tissue inflammatory and reparative responses in various organs including lung, skin, kidney, central nerve system, cardiovascular system, and gastrointestinal system. Endogenous IL-33/ ST2 signaling exhibits diverse immune regulatory functions during progression of different diseases. IL-33 likely functions as a disease sensitizer and plays pathological roles in inflamed tissues in allergic disorders that involve hyperreactive immune responses in the context of skin and pulmonary allergy. However, IL-33 also mediates tissue-protective functions during the recovery phase following tissue injury in the central nerve system and gastrointestinal system. Modulation of the IL-33/ST2 axis, therefore, represents a promising strategy for treating immune disorders that involve dysregulation of the cytokine signalling. In the past two decades, therapeutic strategies blocking IL-33/ST2 have been extensively studied for the treatment of diseases in animal models. In this review, the current progress on the development of therapeutic biologics for targeting IL-33/ST2 signalling in inflammatory diseases is summarized.
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46

Weis, Sabrina, and Aartjan J. W. te Velthuis. "Influenza Virus RNA Synthesis and the Innate Immune Response." Viruses 13, no. 5 (April 28, 2021): 780. http://dx.doi.org/10.3390/v13050780.

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Infection with influenza A and B viruses results in a mild to severe respiratory tract infection. It is widely accepted that many factors affect the severity of influenza disease, including viral replication, host adaptation, innate immune signalling, pre-existing immunity, and secondary infections. In this review, we will focus on the interplay between influenza virus RNA synthesis and the detection of influenza virus RNA by our innate immune system. Specifically, we will discuss the generation of various RNA species, host pathogen receptors, and host shut-off. In addition, we will also address outstanding questions that currently limit our knowledge of influenza virus replication and host adaption. Understanding the molecular mechanisms underlying these factors is essential for assessing the pandemic potential of future influenza virus outbreaks.
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47

Wilkinson, Hannah, Daxin Chen, and Anthony Dorling. "Thrombin fine tunes innate immune cell function." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 74.2. http://dx.doi.org/10.4049/jimmunol.204.supp.74.2.

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Abstract Thrombin is the main effector protease in the coagulation cascade. It can also signal via protease activating receptors (PAR). The presence of these receptors on the surface of innate immune cells has been well reported but the functional consequence of activation has yet to be fully defined. This study aims to investigate the role thrombin has on innate immune cell function using murine bone marrow macrophages (BMM). In Vitro, stimulating mature MCSF-cultured BMM with thrombin did not affect gross markers of macrophage polarisation (iNOS or CD206). The stimulated cell supernatants contained increased amounts of Interferon gamma (IFNγ) but reduced IL10. Thrombin increased IFNγ receptor expression at the cell surface. Thrombin-treated cells had increased lipid rich microdomains by Cholera Toxin B staining and increased co-localisation of the LPS receptor within the lipid rafts. Compared to untreated cells, thrombin stimulated cells were highly sensitive to low dose M1 polarising stimuli, as evidenced by iNOS expression. The thrombin treated cells down regulated surface ABCA1 expression, but this was prevented by transfecting cells with siRNA against Cullin 3. This preserved ABCA1 expression and prevented the increase in lipid rich microdomains after thrombin stimulation and was associated with the loss of heightened sensitivity to low dose M1 stimuli. Taken together this shows a clear pro inflammatory signal on the thrombin treated cells and to date the first description of ABCA1’s key role in thrombin mediated inflammatory signalling.
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48

Clark, Kristopher. "Protein kinase networks that limit TLR signalling." Biochemical Society Transactions 42, no. 1 (January 23, 2014): 11–24. http://dx.doi.org/10.1042/bst20130124.

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TLRs (Toll-like receptors) detect invading micro-organisms which triggers the production of pro-inflammatory mediators needed to combat infection. Although these signalling networks are required to protect the host against invading pathogens, dysregulation of TLR pathways contributes to the development of chronic inflammatory diseases and autoimmune disorders. Molecular mechanisms have therefore evolved to restrict the strength of TLR signalling. In the present review, I highlight recent advances in our understanding of the protein kinase networks required to suppress the innate immune response by negatively regulating TLR signalling and/or promoting the secretion of anti-inflammatory cytokines. I present my discoveries on the key roles of the IKK (inhibitor of nuclear factor κB kinase)-related kinases and the SIKs (salt-inducible kinases) in limiting innate immunity within the greater context of the field.
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Akthar, Ihshan, Mohamed A. Marey, Yejin Kim, Masayuki Shimada, Susan S. Suarez, and Akio Miyamoto. "Sperm interaction with the uterine innate immune system: toll-like receptor 2 (TLR2) is a main sensor in cattle." Reproduction, Fertility and Development 34, no. 2 (2022): 139. http://dx.doi.org/10.1071/rd21265.

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During the passage through the female reproductive tract, sperm interact with various compartments and their immune systems. The immune system that protects the female against pathogens also could destroy sperm or prevent them from reaching the site of fertilisation. In particular, the uterine innate immune response is crucial from the perspectives of both the sperm and the uterus. Following insemination, sperm immediately start to trigger inflammation in the uterus by entering uterine glands and activating an innate immune response. In cattle, the activation occurs mainly via TLR2 signalling, if not the only one, between sperm and the uterine epithelium lining the glands. This acute immune response is manifested as the upregulation of mRNA expression of IL8, TNFA, IL1B, and PGES. As a consequence, many sperm are trapped by polymorphonuclear neutrophils, the first and major component of innate immunity. The sperm-induced uterine innate immune responses apparently serve to clear the uterus of excess sperm and, importantly, prepare the endometrium for implantation. Pathophysiological conditions in the uterus seriously disrupt this phenomenon, and thus could directly decrease fertility.
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Lafyatis, Robert. "New Insights into the Mechanisms of Innate Immune Receptor Signalling in Fibrosis." Open Rheumatology Journal 6, no. 1 (June 15, 2012): 72–79. http://dx.doi.org/10.2174/1874312901206010072.

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