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Journal articles on the topic 'Immune signalling'

Author: Grafiati

Published: 25 May 2024

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1

Hegde, Sushmitha, Amarendranath Soory, Bhagyashree Kaduskar, and Girish S. Ratnaparkhi. "SUMO conjugation regulates immune signalling." Fly 14, no. 1-4 (August 31, 2020): 62–79. http://dx.doi.org/10.1080/19336934.2020.1808402.

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2

GOODRIDGE, H. S., and M. M. HARNETT. "Introduction to immune cell signalling." Parasitology 130, S1 (March 2005): S3—S9. http://dx.doi.org/10.1017/s0031182005008115.

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The dynamic interaction of cells of the immune system with other cells, antigens and secreted factors determines the nature of an immune response. The response of individual cells is governed by the sequence of intracellular signalling events triggered following the association of cell surface molecules during cell-cell contact or the detection of soluble molecules of host or pathogen origin. In this review we will first outline the general principles of intracellular signal transduction. We will then describe the signalling pathways triggered following the recognition of antigen, as well as the detection of cytokines, and discuss how the signalling pathways activated regulate the effector response.

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3

Kumar, Santosh, and Shweta Jain. "Immune signalling by supramolecular assemblies." Immunology 155, no. 4 (September 24, 2018): 435–45. http://dx.doi.org/10.1111/imm.12995.

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4

Pittman, Quentin J., and Abdeslam Mouihate. "Immune Signalling to the Brain." Journal of Physiology 550, no. 1 (July 2003): 1. http://dx.doi.org/10.1113/jphysiol.2003.045609.

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5

Burnstock, Geoffrey, and Jean-Marie Boeynaems. "Purinergic signalling and immune cells." Purinergic Signalling 10, no. 4 (October 29, 2014): 529–64. http://dx.doi.org/10.1007/s11302-014-9427-2.

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6

Dragoni, Silvia, and Patric Turowski. "Vascular Signalling." Cells 12, no. 16 (August 10, 2023): 2038. http://dx.doi.org/10.3390/cells12162038.

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7

Maurya, Rashmi, Deepti Srivastava, Munna Singh, and Samir V. Sawant. "Envisioning the immune interactome in Arabidopsis." Functional Plant Biology 47, no. 6 (2020): 486. http://dx.doi.org/10.1071/fp19188.

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During plant–pathogen interaction, immune targets were regulated by protein–protein interaction events such as ligand-receptor/co-receptor, kinase-substrate, protein sequestration, activation or repression via post-translational modification and homo/oligo/hetro-dimerisation of proteins. A judicious use of molecular machinery requires coordinated protein interaction among defence components. Immune signalling in Arabidopsis can be broadly represented in successive or simultaneous steps; pathogen recognition at cell surface, Ca2+ and reactive oxygen species signalling, MAPK signalling, post-translational modification, transcriptional regulation and phyto-hormone signalling. Proteome wide interaction studies have shown the existence of interaction hubs associated with physiological function. So far, a number of protein interaction events regulating immune targets have been identified, but their understanding in an interactome view is lacking. We focussed specifically on the integration of protein interaction signalling in context to plant–pathogenesis and identified the key targets. The present review focuses towards a comprehensive view of the plant immune interactome including signal perception, progression, integration and physiological response during plant pathogen interaction.

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8

Kee, Tay Hwee, Patricia Vit, and Alirio J. Melendez. "Sphingosine kinase signalling in immune cells." Clinical and Experimental Pharmacology and Physiology 32, no. 3 (March 2005): 153–61. http://dx.doi.org/10.1111/j.1440-1681.2005.04166.x.

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9

Barragan, A., J. M. Weidner, Z. Jin, E. R. Korpi, and B. Birnir. "GABAergic signalling in the immune system." Acta Physiologica 213, no. 4 (March 1, 2015): 819–27. http://dx.doi.org/10.1111/apha.12467.

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10

Fiil, Berthe K., and Mads Gyrd‐Hansen. "Met1‐linked ubiquitination in immune signalling." FEBS Journal 281, no. 19 (August 12, 2014): 4337–50. http://dx.doi.org/10.1111/febs.12944.

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11

Ballou, Leslie R., Stanley J. F. Laulederkind, Edward F. Rosloniec, and Rajendra Raghow. "Ceramide signalling and the immune response." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1301, no. 3 (June 1996): 273–87. http://dx.doi.org/10.1016/0005-2760(96)00004-5.

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12

Shaw, Andrey S., and Erin L. Filbert. "Scaffold proteins and immune-cell signalling." Nature Reviews Immunology 9, no. 1 (January 2009): 47–56. http://dx.doi.org/10.1038/nri2473.

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13

Melendez, Alirio J., and Janet M. Allen. "Phospholipase D and immune receptor signalling." Seminars in Immunology 14, no. 1 (February 2002): 49–55. http://dx.doi.org/10.1006/smim.2001.0341.

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14

Gleeson, Deborah J. "Context-dependent effect of social environment on immune response and sexual signalling in male zebra finches." Australian Journal of Zoology 54, no. 6 (2006): 375. http://dx.doi.org/10.1071/zo06001.

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Variation in avian immune response can be influenced by social environment. This is of particular interest in the context of immunomediated sexual behaviour because social environment may subsequently affect a bird’s relative investment in immunocompetence versus sexual signalling. I tested whether the effect of social environment on immune response and sexual signalling depends on socio-sexual status using male zebra finches (Taeniopygia guttata). To do this, I manipulated social environment (‘same sex’ versus ‘dual sex’) and socio-sexual status (‘high’ versus ‘low’) of the males. I then determined what effect these manipulations had on an index of immunocompetence, namely cell-mediated immune response, and two indices of sexual signalling (bill colour and song rate). I found that social environment influenced cell-mediated immune response and sexual signalling in low-status males. These males had lower immune responses and increased sexual signalling in the dual-sex environment compared with the same-sex environment. In contrast, high-status males had similar immune responses and sexual signalling regardless of social environment. These results suggest that social environment can influence immune response and sexual signalling; however, the nature of this effect was context-dependent, with low-status males more affected than high-status males.

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15

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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16

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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17

Liu, Keying. "Immune, metabolism and therapeutic targets in RA (Rheumatoid Arthritis)." BIO Web of Conferences 55 (2022): 01016. http://dx.doi.org/10.1051/bioconf/20225501016.

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Rheumatoid arthritis is a classic autoimmune disease, the pathogenesis of which is closely linked to the auto-reactivity of immune cells and joint inflammation. Three cell types, namely T cells, macrophages and fibroblast-like synoviocytes (FLS), play an important role in the pathogenesis of RA. Numerous studies have pointed to a metabolic reprogramming of T cells, macrophages and FLS in the pathogenesis of RA arthritis, with alterations in different metabolic pathways of cells, mainly producing a shift from oxidative phosphorylation (OXPHOS) to glycolysis, in addition to lipid metabolism and amino acid metabolism which are also altered in the cellular activation state. Metabolic changes are regulated by metabolism-related signalling pathways, and RA is associated with two representative signalling pathways, namely the mTOR signalling pathway and the AMPK signalling pathway. In RA, both signalling pathways are activated or inhibited, and through a series of cascade reactions, different gene expressions are ultimately induced, altering intracellular metabolic pathways and promoting pro-inflammatory functions (e.g. pro-inflammatory cytokine release and FLS phenotypes), or inhibiting the expression of genes related to immune tolerance. Targeting key components of metabolic signalling pathways and key enzymes in cellular metabolic pathways in RA has emerged as a new way of finding drugs for RA, and many modulators targeting these targets have been extensively studied for their therapeutic effects in RA. In this article, we focus on cellular metabolic alterations in RA, related signalling pathways and possible drugs targeting RA metabolic pathways.

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18

Sanz-Ezquerro, Juan José, and Ana Cuenda. "p38 Signalling Pathway." International Journal of Molecular Sciences 22, no. 3 (January 20, 2021): 1003. http://dx.doi.org/10.3390/ijms22031003.

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p38 Mitogen activated protein kinases (p38MAPK) are a highly evolutionary conserved group of protein kinases, which are central for cell adaptation to environmental changes as well as for immune response, inflammation, tissue regeneration, and tumour formation [...]

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19

Smith, Vicky, Dave Lee, Mark Reardon, Rekaya Shabbir, Sudhakar Sahoo, Peter Hoskin, Ananya Choudhury, Timothy Illidge, and Catharine M. L. West. "Hypoxia Is Associated with Increased Immune Infiltrates and Both Anti-Tumour and Immune Suppressive Signalling in Muscle-Invasive Bladder Cancer." International Journal of Molecular Sciences 24, no. 10 (May 18, 2023): 8956. http://dx.doi.org/10.3390/ijms24108956.

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Hypoxia and a suppressive tumour microenvironment (TME) are both independent negative prognostic factors for muscle-invasive bladder cancer (MIBC) that contribute to treatment resistance. Hypoxia has been shown to induce an immune suppressive TME by recruiting myeloid cells that inhibit anti-tumour T cell responses. Recent transcriptomic analyses show hypoxia increases suppressive and anti-tumour immune signalling and infiltrates in bladder cancer. This study sought to investigate the relationship between hypoxia-inducible factor (HIF)-1 and -2, hypoxia, and immune signalling and infiltrates in MIBC. ChIP-seq was performed to identify HIF1α, HIF2α, and HIF1β binding in the genome of the MIBC cell line T24 cultured in 1% and 0.1% oxygen for 24 h. Microarray data from four MIBC cell lines (T24, J82, UMUC3, and HT1376) cultured under 1%, 0.2%, and 0.1% oxygen for 24 h were used. Differences in the immune contexture between high- and low-hypoxia tumours were investigated using in silico analyses of two bladder cancer cohorts (BCON and TCGA) filtered to only include MIBC cases. GO and GSEA were used with the R packages “limma” and “fgsea”. Immune deconvolution was performed using ImSig and TIMER algorithms. RStudio was used for all analyses. Under hypoxia, HIF1α and HIF2α bound to ~11.5–13.5% and ~4.5–7.5% of immune-related genes, respectively (1–0.1% O2). HIF1α and HIF2α both bound to genes associated with T cell activation and differentiation signalling pathways. HIF1α and HIF2α had distinct roles in immune-related signalling. HIF1 was associated with interferon production specifically, whilst HIF2 was associated with generic cytokine signalling as well as humoral and toll-like receptor immune responses. Neutrophil and myeloid cell signalling was enriched under hypoxia, alongside hallmark pathways associated with Tregs and macrophages. High-hypoxia MIBC tumours had increased expression of both suppressive and anti-tumour immune gene signatures and were associated with increased immune infiltrates. Overall, hypoxia is associated with increased inflammation for both suppressive and anti-tumour-related immune signalling and immune infiltrates, as seen in vitro and in situ using MIBC patient tumours.

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20

David, Rachel. "HopU1 puts a stop to immune signalling." Nature Reviews Microbiology 11, no. 4 (March 4, 2013): 222–23. http://dx.doi.org/10.1038/nrmicro2993.

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21

HARNETT, WILLIAM, and L. H. CHAPPELL. "Subversion of immune cell signalling by parasites." Parasitology 130, S1 (March 2005): S1—S2. http://dx.doi.org/10.1017/s0031182005008334.

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22

MAULE, A. G., T. A. DAY, and L. H. CHAPPELL. "Subversion of immune cell signalling by parasites." Parasitology 131, S1 (March 29, 2006): S1. http://dx.doi.org/10.1017/s0031182005009388.

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23

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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24

Wilkinson, Beverley, Jocelyn S. Downey, and Christopher E. Rudd. "T-cell signalling and immune system disorders." Expert Reviews in Molecular Medicine 7, no. 29 (December 19, 2005): 1–29. http://dx.doi.org/10.1017/s1462399405010264.

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T-cell receptor (TCR) engagement initiates intracellular signalling cascades that lead to T-cell proliferation, cytokine production and differentiation into effector cells. These cascades comprise an array of protein-tyrosine kinases, phosphatases, GTP-binding proteins and adaptor proteins that regulate generic and specialised functions. The integration of these signals is essential for the normal development, homeostasis and function of T cells. Defects in a single mediator can produce T cells that are unable to participate fully in an immune response and/or that mount an inappropriate response, which leads to immunodeficiency, autoimmunity or leukaemia/lymphomas. This review highlights some of the key players in T-cell signalling and their involvement in the development of various clinical disease states. Some of these immune-specific signalling proteins are attractive potential targets in the development of therapies to augment T-cell responses to antigen or tumours, and to treat immune cell disorders.

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25

Zhang, Yanbo, and Hongyan Wang. "Integrin signalling and function in immune cells." Immunology 135, no. 4 (March 2, 2012): 268–75. http://dx.doi.org/10.1111/j.1365-2567.2011.03549.x.

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26

Ayub, Khurram, and Maurice B. Hallett. "Signalling shutdown strategies in aging immune cells." Aging Cell 3, no. 4 (July 9, 2004): 145–49. http://dx.doi.org/10.1111/j.1474-9728.2004.00100.x.

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27

Thomas, Hugh. "OX40 signalling mediates effective HBV immune responses." Nature Reviews Gastroenterology & Hepatology 15, no. 5 (April 6, 2018): 256. http://dx.doi.org/10.1038/nrgastro.2018.31.

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28

Levy, Shoshana, and Tsipi Shoham. "The tetraspanin web modulates immune-signalling complexes." Nature Reviews Immunology 5, no. 2 (February 2005): 136–48. http://dx.doi.org/10.1038/nri1548.

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29

Yoshimura, Akihiko, Tetsuji Naka, and Masato Kubo. "SOCS proteins, cytokine signalling and immune regulation." Nature Reviews Immunology 7, no. 6 (May 18, 2007): 454–65. http://dx.doi.org/10.1038/nri2093.

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30

Junger, Wolfgang G. "Immune cell regulation by autocrine purinergic signalling." Nature Reviews Immunology 11, no. 3 (February 18, 2011): 201–12. http://dx.doi.org/10.1038/nri2938.

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31

Przybyła, Tomasz, Monika Sakowicz-Burkiewicz, and Tadeusz Pawełczyk. "Purinergic signalling in B cells." Acta Biochimica Polonica 65, no. 1 (May 27, 2018): 1–7. http://dx.doi.org/10.18388/abp.2017_1588.

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Adenosine and adenosine triphosphate are involved in purinergic signalling which plays important role in control of immune system. Much data have been obtained regarding impact of purinergic signalling on dendritic cells, macrophages, monocytes and T lymphocytes, however less attention has been paid to purinergic regulation of B cells. This review summarizes present knowledge about ATP- and Ado-dependant signalling in B lymphocytes. Human B cells have been shown to express A2A-R and A3-R and each subtype of P2 receptors. Surface of B cells exhibits two antagonistic ectoenzymatic pathways, one relays on constitutive secretion and resynthesis of ATP while the second one depends on degradation of adenosine nucleotides to nucleosides and their subsequent degradation. Inactivated B cells remain under suppressive impact of autocrine and paracrine Ado however activated B lymphocytes increase ATP release and production. ATP protects B cells from suppressive impact of Ado and exerts pro-inflammatory impact on target tissues, it is also involved in IgM release. Ado synthesis however is related with optimal development, implantation and maintenance of plasmocyte population in bone marrow during primary immune response. Moreover Ado plays important role in immunoglobulin class switching which is a key mechanism of humoral immune response. Disruption of purinergic signalling is related with severe clinical implications. Impairment of Ado production in environment of B cells is one of the factors responsible for common variable immunodeficiency. List of evidence suggests also that dysfunction of immune system observed during diabetes may in part depend on disrupted ATP and Ado metabolism in B cells.

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32

Wilmink, Marijn, and Marianne Rebecca Spalinger. "SKAP2—A Molecule at the Crossroads for Integrin Signalling and Immune Cell Migration and Function." Biomedicines 11, no. 10 (October 14, 2023): 2788. http://dx.doi.org/10.3390/biomedicines11102788.

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Src-kinase associated protein 2 (SKAP2) is an intracellular scaffolding protein that is broadly expressed in immune cells and is involved in various downstream signalling pathways, including, but not limited to, integrin signalling. SKAP2 has a wide range of binding partners and fine-tunes the rearrangement of the cytoskeleton, thereby regulating cell migration and immune cell function. Mutations in SKAP2 have been associated with several inflammatory disorders such as Type 1 Diabetes and Crohn’s disease. Rodent studies showed that SKAP2 deficient immune cells have diminished pathogen clearance due to impaired ROS production and/or phagocytosis. However, there is currently no in-depth understanding of the functioning of SKAP2. Nevertheless, this review summarises the existing knowledge with a focus of its role in signalling cascades involved in cell migration, tissue infiltration and immune cell function.

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33

Zhang, Lei, Jun Yu, Chun Wang, and Wei Wei. "The effects of total glucosides of paeony (TGP) and paeoniflorin (Pae) on inflammatory-immune responses in rheumatoid arthritis (RA)." Functional Plant Biology 46, no. 2 (2019): 107. http://dx.doi.org/10.1071/fp18080.

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Rheumatoid arthritis (RA) is a chronic inflammatory and systemic autoimmune disease with an unknown aetiology. Accumulative studies suggest that the pathogenesis of RA involves the excessive activation of synoviocytes and immune cells, increasing the secretion of inflammatory mediators and cytokines in synoviocytes, causing dysfunctional E-prostanoid (EP)-G-protein-cyclic adenosine monophosphate (cAMP) and mitogen-associated-protein kinase (MAPK) signalling in synoviocytes. Total glucosides of paeony (TGP) extracted from the roots of Paeonia lactiflora Pall, was approved by the China Food and Drug Administration as an anti-inflammatory and immuno-modulator drug in 1998. Paeoniflorin (Pae), a water-soluble monoterpene glucoside,is the main effective component of TGP. TGP and Pae produce anti-inflammatory and immuno-regulatory effects by suppressing immune cells and synoviocytes activation, decreasing inflammatory substance production and restoring abnormal signalling in synoviocytes. In this review, the regulation of the inflammatory-immune responses and the therapeutic mechanism between RA and TGP and Pae are discussed in detail. The aim of this review was to provide novel insights into the treatment of RA.

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34

Nadolni, Wiebke, and Susanna Zierler. "The Channel-Kinase TRPM7 as Novel Regulator of Immune System Homeostasis." Cells 7, no. 8 (August 17, 2018): 109. http://dx.doi.org/10.3390/cells7080109.

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The enzyme-coupled transient receptor potential channel subfamily M member 7, TRPM7, has been associated with immunity and immune cell signalling. Here, we review the role of this remarkable signalling protein in lymphocyte proliferation, differentiation, activation and survival. We also discuss its role in mast cell, neutrophil and macrophage function and highlight the potential of TRPM7 to regulate immune system homeostasis. Further, we shed light on how the cellular signalling cascades involving TRPM7 channel and/or kinase activity culminate in pathologies as diverse as allergic hypersensitivity, arterial thrombosis and graft versus host disease (GVHD), stressing the need for TRPM7 specific pharmacological modulators.

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35

Bordon, Yvonne. "Immune cells freeze in response to stress signalling." Nature Reviews Immunology 21, no. 6 (May 5, 2021): 344–45. http://dx.doi.org/10.1038/s41577-021-00559-2.

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36

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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37

Aspinall, Richard, Antonio Lapenna, Christopher B-Lynch, and Pierre O. Lang. "Cellular signalling pathways in immune aging and regeneration." Biochemical Society Transactions 42, no. 3 (May 22, 2014): 651–56. http://dx.doi.org/10.1042/bst20140021.

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The thymus is one of the cornerstones of an effective immune system. It produces new T-cells for the naïve T-cell pool, thus refreshing the peripheral repertoire. As we age, the thymus atrophies and there is a decrease in the area of active T-cell production. A decline in the output of the thymus eventually leads to changes in the peripheral T-cell pool which includes increases in the number of cells at or near their replicative limit and contraction of the repertoire. Debate about the age-associated changes in the thymus leading to functional decline centres on whether this is due to problems with the environment provided by the thymus or with defects in the progenitor cell compartment. In mice, the evidence points towards problems in the epithelial component of the thymus and the production of IL-7 (interleukin 7). But there are discussions about how appropriate mouse models are for human aging. We have developed a simple system that utilizes both human keratinocyte and fibroblast cell lines arrayed on a synthetic tantalum-coated matrix to provide a permissive environment for the maturation of human CD34+ haemopoietic progenitor cells into mature CD4+ or CD8+ T-lymphocytes. We have characterized the requirements for differentiation within these cultures and used this system to compare the ability of CD34+ cells derived from different sources to produce mature thymocytes. The TREC (T-cell receptor excision circle) assay was used as a means of identifying newly produced thymocytes.

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38

Brodsky, Igor E., and Ruslan Medzhitov. "Targeting of immune signalling networks by bacterial pathogens." Nature Cell Biology 11, no. 5 (May 2009): 521–26. http://dx.doi.org/10.1038/ncb0509-521.

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39

Gerlach, Björn, Stefanie M. Cordier, Anna C. Schmukle, Christoph H. Emmerich, Eva Rieser, Tobias L. Haas, Andrew I. Webb, et al. "Linear ubiquitination prevents inflammation and regulates immune signalling." Nature 471, no. 7340 (March 2011): 591–96. http://dx.doi.org/10.1038/nature09816.

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40

Huyer, Gregory, and Denis R. Alexander. "Immune signalling: SHP-2 docks at multiple ports." Current Biology 9, no. 4 (February 1999): R129—R132. http://dx.doi.org/10.1016/s0960-9822(99)80080-3.

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41

Goldstein, Byron, James R. Faeder, and William S. Hlavacek. "Mathematical and computational models of immune-receptor signalling." Nature Reviews Immunology 4, no. 6 (June 2004): 445–56. http://dx.doi.org/10.1038/nri1374.

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42

Beug, Shawn T., Herman H. Cheung, Eric C. LaCasse, and Robert G. Korneluk. "Modulation of immune signalling by inhibitors of apoptosis." Trends in Immunology 33, no. 11 (November 2012): 535–45. http://dx.doi.org/10.1016/j.it.2012.06.004.

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43

Treanor, Bebhinn, Naomi E. Harwood, and Facundo D. Batista. "Microsignalosomes: spatially resolved receptor signalling." Biochemical Society Transactions 37, no. 5 (September 21, 2009): 1014–18. http://dx.doi.org/10.1042/bst0371014.

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B-cells are a critical component of the adaptive immune system. As such, B-cells survey the body and mount appropriate protective responses to pathogen-derived antigens, resulting in the production of specific antibodies and induction of immunological memory. Given the effectiveness of these responses in selectively eliminating pathogenic infections, it is clear that the processes underlying antigen-induced B-cell activation must be highly regulated. Somewhat surprisingly given the specialized function of these immune cells, the BCR (B-cell receptor) functions similarly to receptors of the tyrosine kinase family that are commonplace in biology, as BCR ligation with antigen leads to B-cell proliferation and differentiation. In the Lymphocyte Interaction Laboratory, we are particularly interested in characterizing the very early molecular events underlying B-cell activation using a combination of cutting-edge high-resolution and in vivo imaging techniques.

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44

Bähler, Martin, Kerstin Elfrink, Peter J. Hanley, Sabine Thelen, and Yan Xu. "Cellular functions of class IX myosins in epithelia and immune cells." Biochemical Society Transactions 39, no. 5 (September 21, 2011): 1166–68. http://dx.doi.org/10.1042/bst0391166.

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Mammals contain two class IX myosins, Myo9a and Myo9b. They are actin-based motorized signalling molecules that negatively regulate RhoA signalling. Myo9a has been implicated in the regulation of epithelial cell morphology and differentiation, whereas Myo9b has been shown to play an important role in the regulation of macrophage shape and motility.

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Morgan, Ethan L., and Andrew Macdonald. "Manipulation of JAK/STAT Signalling by High-Risk HPVs: Potential Therapeutic Targets for HPV-Associated Malignancies." Viruses 12, no. 9 (September 3, 2020): 977. http://dx.doi.org/10.3390/v12090977.

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Human papillomaviruses (HPVs) are small, DNA viruses that cause around 5% of all cancers in humans, including almost all cervical cancer cases and a significant proportion of anogenital and oral cancers. The HPV oncoproteins E5, E6 and E7 manipulate cellular signalling pathways to evade the immune response and promote virus persistence. The Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway has emerged as a key mediator in a wide range of important biological signalling pathways, including cell proliferation, cell survival and the immune response. While STAT1 and STAT2 primarily drive immune signalling initiated by interferons, STAT3 and STAT5 have widely been linked to the survival and proliferative potential of a number of cancers. As such, the inhibition of STAT3 and STAT5 may offer a therapeutic benefit in HPV-associated cancers. In this review, we will discuss how HPV manipulates JAK/STAT signalling to evade the immune system and promote cell proliferation, enabling viral persistence and driving cancer development. We also discuss approaches to inhibit the JAK/STAT pathway and how these could potentially be used in the treatment of HPV-associated disease.

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Wong, Ee Tsin, and Vinay Tergaonkar. "Roles of NF-κB in health and disease: mechanisms and therapeutic potential." Clinical Science 116, no. 6 (February 12, 2009): 451–65. http://dx.doi.org/10.1042/cs20080502.

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The NF-κB (nuclear factor κB) family of transcription factors are involved in a myriad of activities, including the regulation of immune responses, maturation of immune cells, development of secondary lymphoid organs and osteoclastogenesis. Fine tuning by positive and negative regulators keeps the NF-κB signalling pathway in check. Microbial products and genetic alterations in NF-κB and other signalling pathway components can lead to deregulation of NF-κB signalling in several human diseases, including cancers and chronic inflammatory disorders. NF-κB-pathway-specific therapies are being actively investigated, and these hold promises as interventions of NF-κB-related ailments.

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Roliano, Gabriela Gonçalves, Juliana Hofstätter Azambuja, Veronica Toniazzo Brunetto, Hannah Elizabeth Butterfield, Antonio Nochi Kalil, and Elizandra Braganhol. "Colorectal Cancer and Purinergic Signalling: An Overview." Cancers 14, no. 19 (October 6, 2022): 4887. http://dx.doi.org/10.3390/cancers14194887.

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Colorectal cancer (CRC) is among the most common cancers and exhibits a high fatality rate. Gut inflammation is related to CRC, with loss of homeostasis in immune cell activities. The cells of the innate and adaptive immune system, including macrophages, neutrophils, mast cells, and lymphocytes, are present in most solid tumors. Purinergic signaling allows for communication between immune cells within the tumor microenvironment (TME) and can alter the TME to promote tumor progression. This system is regulated by the availability of extracellular purines to activate purinoceptors (P1 and P2) and is tightly controlled by ectonucleotidases (E-NPP, CD73/CD39, ADA) and kinases, which interact with and modify nucleotides and nucleosides availability. In this review, we compiled articles detailing the relationship of the purinergic system with CRC progression. We found that increased expression of CD73 leads to the suppression of effector immune cell functions and tumor progression in CRC. The P1 family purinoceptors A1, A2A, and A2B were positively associated with tumor progression, but A2B resulted in increased cancer cell apoptosis. The P2 family purinoceptors P2X5, P2X7, P2Y2, P2Y6, and P2Y12 were factors primarily associated with promoting CRC progression. In summary, CD39/CD73 axis and the purinergic receptors exhibit diagnostic and prognostic value and have potential as therapeutic targets in CRC.

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Chinchilla, Blanca, Paloma Encinas, Julio M. Coll, and Eduardo Gomez-Casado. "Differential Immune Transcriptome and Modulated Signalling Pathways in Rainbow Trout Infected with Viral Haemorrhagic Septicaemia Virus (VHSV) and Its Derivative Non-Virion (NV) Gene Deleted." Vaccines 8, no. 1 (January 30, 2020): 58. http://dx.doi.org/10.3390/vaccines8010058.

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Viral haemorrhagic septicaemia virus (VHSV) is one of the worst viral threats to fish farming. Non-virion (NV) gene-deleted VHSV (dNV-VHSV) has been postulated as an attenuated virus, because the absence of the NV gene leads to lower induced pathogenicity. However, little is known about the immune responses driven by dNV-VHSV and the wild-type (wt)-VHSV in the context of infection. Here, we obtained the immune transcriptome profiling in trout infected with dNV-VHSV and wt-VHSV and the pathways involved in immune responses. As general results, dNV-VHSV upregulated more trout immune genes than wt-VHSV (65.6% vs 45.7%, respectively), whereas wt-VHSV maintained more non-regulated genes than dNV-VHSV (45.7% vs 14.6%, respectively). The modulated pathways analysis (Gene-Set Enrichment Analysis, GSEA) showed that, when compared to wt-VHSV infected trout, the dNV-VHSV infected trout upregulated signalling pathways (n = 19) such as RIG-I (retinoic acid-inducible gene-I) like receptor signalling, Toll-like receptor signalling, type II interferon signalling, and nuclear factor kappa B (NF-kappa B) signalling, among others. The results from individual genes and GSEA demonstrated that wt-VHSV impaired the activation at short stages of infection of pro-inflammatory, antiviral, proliferation, and apoptosis pathways, delaying innate humoral response and cellular crosstalk, whereas dNV-VHSV promoted the opposite effects. Therefore, these results might support future studies on using dNV-VHSV as a potential live vaccine.

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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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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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