Journal articles: 'Molecular immunity'

1

Weiss, R. "Maternal Immunity via Molecular Ferry." Science News 135, no. 2 (January 14, 1989): 20. http://dx.doi.org/10.2307/3973428.

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Toka, Felix N., Christopher D. Pack, and Barry T. Rouse. "Molecular adjuvants for mucosal immunity." Immunological Reviews 199, no. 1 (June 2004): 100–112. http://dx.doi.org/10.1111/j.0105-2896.2004.0147.x.

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Blank, Miri, Ori Barzilai, and Yehuda Shoenfeld. "Molecular mimicry and auto-immunity." Clinical Reviews in Allergy & Immunology 32, no. 1 (February 2007): 111–18. http://dx.doi.org/10.1007/s12016-007-0025-8.

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Chan, Siew Leong, Lieh Yoon Low, Simon Hsu, Sheng Li, Tong Liu, Eugenio Santelli, Gaelle Le Negrate, John C. Reed, Virgil L. Woods, and Jaime Pascual. "Molecular Mimicry in Innate Immunity." Journal of Biological Chemistry 284, no. 32 (June 17, 2009): 21386–92. http://dx.doi.org/10.1074/jbc.c109.007591.

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5

Ulevitch, Richard J. "Molecular Mechanisms of Innate Immunity." Immunologic Research 21, no. 2-3 (2000): 49–54. http://dx.doi.org/10.1385/ir:21:2-3:49.

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Blank, Miri, Ori Barzilai, and Yehuda Shoenfeld. "Molecular mimicry and auto-immunity." Clinical Reviews in Allergy & Immunology 32, no. 1 (February 2007): 111–18. http://dx.doi.org/10.1007/bf02686087.

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Ip, Y. Tony, and Michael Levine. "Molecular genetics of Drosophila immunity." Current Opinion in Genetics & Development 4, no. 5 (October 1994): 672–77. http://dx.doi.org/10.1016/0959-437x(94)90133-n.

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Wu, Hao, and Joseph R. Arron. "TRAF6, a molecular bridge spanning adaptive immunity, innate immunity and osteoimmunology." BioEssays 25, no. 11 (October 17, 2003): 1096–105. http://dx.doi.org/10.1002/bies.10352.

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Pavlov, Valentin A., Sangeeta S. Chavan, and Kevin J. Tracey. "Molecular and Functional Neuroscience in Immunity." Annual Review of Immunology 36, no. 1 (April 26, 2018): 783–812. http://dx.doi.org/10.1146/annurev-immunol-042617-053158.

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Goncharova, Larisa B., and Alexander O. Tarakanov. "Molecular networks of brain and immunity." Brain Research Reviews 55, no. 1 (August 2007): 155–66. http://dx.doi.org/10.1016/j.brainresrev.2007.02.003.

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Burckstummer, Tilmann, Evren Karayel, Evelyn Dixit, Adriana Goncalves, Gerhard Durnberger, Hannah Jahn, Melanie Planyavsky, Jacques Colinge, Keiryn L. Bennett, and Giulio Superti-Furga. "311 Molecular networks in innate immunity." Cytokine 43, no. 3 (September 2008): 317. http://dx.doi.org/10.1016/j.cyto.2008.07.394.

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Černý, Jan, and Ilja Stříž. "Adaptive innate immunity or innate adaptive immunity?" Clinical Science 133, no. 14 (July 2019): 1549–65. http://dx.doi.org/10.1042/cs20180548.

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Abstract The innate immunity is frequently accepted as a first line of relatively primitive defense interfering with the pathogen invasion until the mechanisms of ‘privileged’ adaptive immunity with the production of antibodies and activation of cytotoxic lymphocytes ‘steal the show’. Recent advancements on the molecular and cellular levels have shaken the traditional view of adaptive and innate immunity. The innate immune memory or ‘trained immunity’ based on metabolic changes and epigenetic reprogramming is a complementary process insuring adaptation of host defense to previous infections. Innate immune cells are able to recognize large number of pathogen- or danger- associated molecular patterns (PAMPs and DAMPs) to behave in a highly specific manner and regulate adaptive immune responses. Innate lymphoid cells (ILC1, ILC2, ILC3) and NK cells express transcription factors and cytokines related to subsets of T helper cells (Th1, Th2, Th17). On the other hand, T and B lymphocytes exhibit functional properties traditionally attributed to innate immunity such as phagocytosis or production of tissue remodeling growth factors. They are also able to benefit from the information provided by pattern recognition receptors (PRRs), e.g. γδT lymphocytes use T-cell receptor (TCR) in a manner close to PRR recognition. Innate B cells represent another example of limited combinational diversity usage participating in various innate responses. In the view of current knowledge, the traditional black and white classification of immune mechanisms as either innate or an adaptive needs to be adjusted and many shades of gray need to be included.

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Destoumieux-Garzón, Delphine, Denis Saulnier, Julien Garnier, Céline Jouffrey, Philippe Bulet, and Evelyne Bachère. "Crustacean Immunity." Journal of Biological Chemistry 276, no. 50 (October 11, 2001): 47070–77. http://dx.doi.org/10.1074/jbc.m103817200.

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We report here the isolation from plasma of two penaeid shrimp species of novel peptides/polypeptides with exclusive antifungal activities. A set of three molecules was purified with molecular masses at 2.7 kDa (Penaeus vannamei), 7.9 kDa, and 8.3 kDa (Penaeus stylirostris). Primary structure determination was performed by a combination of Edman degradation and mass spectrometry. The peptides display 95–100% sequence identity with a C-terminal sequence of hemocyanin, indicating that they are cleaved fragments of the shrimp respiratory protein. Specific immunodetection of the hemocyanin-derived (poly)peptides revealed that experimental microbial infections increase their relative concentration in plasma as compared with nonstimulated animals. Thus, the production of antifungal (poly)peptides by limited proteolysis of hemocyanin could be relevant to a shrimp immune reaction that would confer a new function to the multifunctional respiratory pigment of crustaceans.

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14

Wang, Longhao, Wei Yuan, Lifeng Li, Zhibo Shen, Qishun Geng, Yuanyuan Zheng, and Jie Zhao. "Immunogenomic-Based Analysis of Hierarchical Clustering of Diffuse Large Cell Lymphoma." Journal of Immunology Research 2022 (August 9, 2022): 1–16. http://dx.doi.org/10.1155/2022/9544827.

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Diffuse large B cell lymphoma (DLBCL) is one of the most usual types of adult lymphoma with heterogeneousness in histological morphology, prognosis, and clinical indications. Prior to this, several studies were carried out to determine the DLBCL subtype based on the analysis of the genome profile. However, classification based on assessment of genes related to the immune system has limited clinical significance for DLBCL. We systematically explored the DLBCL gene expression dataset and provided publicly available clinical information on patients with GEO. In this research, 928 DLBCL samples were applied, and we calculated 29 immune-related genomes’ enrichment levels in each sample and stratified them into high immunity (Immunity_H, n = 135 , 28.7%), moderate immunity (Immunity_M, n = 135 , 28.7%), and low immunity (Immunity_L, n = 12 , 2.6%) that was based on ssGSEA score. The ESTIMATE algorithm was used to calculate stromal scores (range 586.88 to 1982.43), immune scores, estimated scores (range 2,618.2 to 8,098.14), and tumor purity (range 0.216 to 0.976). All of them were significantly correlated with immune subtypes (Kruskal-Wallis test, p < 0.001 ). At the same time, the correlation of related genes was analyzed by immunohistochemistry staining. In addition, DLBCL cells were cultured in transfected and in vitro with siRNA to verify correlation analysis and gene expression. Finally, human peripheral blood lymphocytes were incubated with DLBCL cells and stained. Flow cytometry was applied to analyze genes’ influence on immune function. By analysis, immune checkpoint and HLA gene expression levels were higher in the Immunity_H group (Kruskal-Wallis test, p < 0.05 ). The levels of Tfhs (follicular helper T cells), monocytes, CD8+ T cells, M1 macrophages, M2 macrophages, and CD4+ memory-activated T cells were the most excellent in Immunity_H, and the total survival rate was higher in the Immunity_L. Through analysis, IRF4 (MUM1) was identified by us as immunotherapeutic target and a potential prognostic marker for DLBCL, which was made sure by using molecular biology experimentations. To conclude, immunosignature made a connection between DLBCL subtypes playing a position in DLBCL prognostic stratification. Immunocharacteristics-related DLBCL subtypes’ construction predicts expected patient results and supplies conceivable immunotherapy candida.

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15

Weetman, Anthony P. "Immunity, thyroid function and pregnancy: molecular mechanisms." Nature Reviews Endocrinology 6, no. 6 (April 27, 2010): 311–18. http://dx.doi.org/10.1038/nrendo.2010.46.

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16

Gasiunas, Giedrius, Tomas Sinkunas, and Virginijus Siksnys. "Molecular mechanisms of CRISPR-mediated microbial immunity." Cellular and Molecular Life Sciences 71, no. 3 (August 20, 2013): 449–65. http://dx.doi.org/10.1007/s00018-013-1438-6.

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Gerdol, Marco, and Paola Venier. "An updated molecular basis for mussel immunity." Fish & Shellfish Immunology 46, no. 1 (September 2015): 17–38. http://dx.doi.org/10.1016/j.fsi.2015.02.013.

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18

Zipfel, Cyril. "Early molecular events in PAMP-triggered immunity." Current Opinion in Plant Biology 12, no. 4 (August 2009): 414–20. http://dx.doi.org/10.1016/j.pbi.2009.06.003.

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19

Zhang, Jie, and Jian-Min Zhou. "Plant Immunity Triggered by Microbial Molecular Signatures." Molecular Plant 3, no. 5 (September 2010): 783–93. http://dx.doi.org/10.1093/mp/ssq035.

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20

Hoffmann, D., and J. A. Hoffmann. "Cellular and molecular aspects of insect immunity." Research in Immunology 141, no. 8 (January 1990): 895–96. http://dx.doi.org/10.1016/0923-2494(90)90045-z.

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21

Hoffmann, D., and J. A. Hoffmann. "Cellular and molecular aspects of insect immunity." Research in Immunology 141, no. 9 (January 1990): 895–96. http://dx.doi.org/10.1016/0923-2494(90)90189-6.

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22

Peng, Yujun, Rowan van Wersch, and Yuelin Zhang. "Convergent and Divergent Signaling in PAMP-Triggered Immunity and Effector-Triggered Immunity." Molecular Plant-Microbe Interactions® 31, no. 4 (April 2018): 403–9. http://dx.doi.org/10.1094/mpmi-06-17-0145-cr.

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Plants use diverse immune receptors to sense pathogen attacks. Recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors localized on the plasma membrane leads to PAMP-triggered immunity (PTI). Detection of pathogen effectors by intracellular or plasma membrane–localized immune receptors results in effector-triggered immunity (ETI). Despite the large variations in the magnitude and duration of immune responses triggered by different PAMPs or pathogen effectors during PTI and ETI, plasma membrane–localized immune receptors activate similar downstream molecular events such as mitogen-activated protein kinase activation, oxidative burst, ion influx, and increased biosynthesis of plant defense hormones, indicating that defense signals initiated at the plasma membrane converge at later points. On the other hand, activation of ETI by immune receptors localized to the nucleus appears to be more directly associated with transcriptional regulation of defense gene expression. Here, we review recent progress in signal transductions downstream of different groups of plant immune receptors, highlighting the converging and diverging molecular events.

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23

von Hertzen, Leena, Ilkka Hanski, and Tari Haahtela. "Natural immunity." EMBO reports 12, no. 11 (October 7, 2011): 1089–93. http://dx.doi.org/10.1038/embor.2011.195.

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24

Min, Kyung-Jin, and Marc Tatar. "Unraveling the Molecular Mechanism of Immunosenescence in Drosophila." International Journal of Molecular Sciences 19, no. 9 (August 21, 2018): 2472. http://dx.doi.org/10.3390/ijms19092472.

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A common feature of the aging process is a decline in immune system performance. Extensive research has sought to elucidate how changes in adaptive immunity contribute to aging and to provide evidence showing that changes in innate immunity have an important role in the overall decline of net immune function. Drosophila is an emerging model used to address questions related to immunosenescence via research that integrates its capacity for genetic dissection of aging with groundbreaking molecular biology related to innate immunity. Herein, we review information on the immunosenescence of Drosophila and suggest its possible mechanisms that involve changes in insulin/IGF(insulin-like growth factor)-1 signaling, hormones such as juvenile hormone and 20-hydroxyecdysone, and feedback system degeneration. Lastly, the emerging role of microbiota on the regulation of immunity and aging in Drosophila is discussed.

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25

Lamberty, Mireille, Daniel Zachary, René Lanot, Christian Bordereau, Alain Robert, Jules A. Hoffmann, and Philippe Bulet. "Insect Immunity." Journal of Biological Chemistry 276, no. 6 (October 26, 2000): 4085–92. http://dx.doi.org/10.1074/jbc.m002998200.

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26

VanHook, Annalisa M. "Immunity pipelines." Science Signaling 8, no. 385 (July 14, 2015): ec191-ec191. http://dx.doi.org/10.1126/scisignal.aac9914.

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27

Charlet, Maurice, Serguey Chernysh, Hervé Philippe, Charles Hetru, Jules A. Hoffmann, and Philippe Bulet. "Innate Immunity." Journal of Biological Chemistry 271, no. 36 (September 6, 1996): 21808–13. http://dx.doi.org/10.1074/jbc.271.36.21808.

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28

Kaaya, Godwin P., Casper Flyg, and Hans G. Boman. "Insect immunity." Insect Biochemistry 17, no. 2 (January 1987): 309–15. http://dx.doi.org/10.1016/0020-1790(87)90073-4.

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29

Flyg, Casper, Gunnel Dalhammar, Bertil Rasmuson, and Hans G. Boman. "Insect immunity." Insect Biochemistry 17, no. 1 (January 1987): 153–60. http://dx.doi.org/10.1016/0020-1790(87)90155-7.

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30

Lamberty, Mireille, Sarah Ades, Sandrine Uttenweiler-Joseph, Gary Brookhart, Dean Bushey, Jules A. Hoffmann, and Philippe Bulet. "Insect Immunity." Journal of Biological Chemistry 274, no. 14 (April 2, 1999): 9320–26. http://dx.doi.org/10.1074/jbc.274.14.9320.

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31

Pag, Ulrike, Christoph Heidrich, Gabriele Bierbaum, and Hans-Georg Sahl. "Molecular Analysis of Expression of the Lantibiotic Pep5 Immunity Phenotype." Applied and Environmental Microbiology 65, no. 2 (February 1, 1999): 591–98. http://dx.doi.org/10.1128/aem.65.2.591-598.1999.

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ABSTRACT The lantibiotic Pep5 is produced by Staphylococcus epidermidis 5. Within its biosynthetic gene cluster, the immunity gene pepI, providing producer self-protection, is localized upstream of the structural gene pepA. Pep5 production and the immunity phenotype have been found to be tightly coupled (M. Reis, M. Eschbach-Bludau, M. I. Iglesias-Wind, T. Kupke, and H.-G. Sahl, Appl. Environ. Microbiol. 60:2876–2883, 1994). To study this phenomenon, we analyzed pepA and pepItranscription and translation and constructed a number of strains containing various fragments of the gene cluster and expressing different levels of immunity. Complementation of apepA-expressing strain with pepI intrans did not result in phenotypic immunity or production of PepI. On the other hand, neither pepA nor its product was found to be involved in immunity, since suppression of the translation of the pepA mRNA by mutation of the ATG start codon did not reduce the level of immunity. Moreover, homologous and heterologous expression of pepI from a xylose-inducible promoter resulted in significant Pep5 insensitivity. Most important for expression of the immunity phenotype was the stability ofpepI transcripts, which in the wild-type strain, is achieved by an inverted repeat with a free energy of −56.9 kJ/mol, localized downstream of pepA. We performed site-directed mutagenesis to study the functional role of PepI and constructed F13D PepI, I17R PepI, and PepI 1-65; all mutants showed reduced levels of immunity. Western blot analysis indicated that F13D PepI and PepI 1-65 were not produced correctly or were partially degraded, while I17R PepI apparently was less efficient in providing self-protection than the wild-type PepI.

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Chan, Yvonne Gar-Yun, Sean Phillip Riley, Emily Chen, and Juan José Martinez. "Molecular Basis of Immunity to Rickettsial Infection Conferred through Outer Membrane Protein B." Infection and Immunity 79, no. 6 (March 28, 2011): 2303–13. http://dx.doi.org/10.1128/iai.01324-10.

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ABSTRACTPathogenic rickettsiae are the causative agents of Rocky Mountain spotted fever, typhus, and other human diseases with high mortality and an important impact on society. Although survivors of rickettsial infections are considered immune to disease, the molecular basis of this immunity or the identification of protective antigens that enable vaccine development was hitherto not known. By exploring the molecular pathogenesis ofRickettsia conorii, the agent of Mediterranean spotted fever, we report here that the autotransporter protein, rickettsial outer membrane protein B (rOmpB), constitutes a protective antigen for this group of pathogens. A recombinant, purified rOmpB passenger domain fragment comprised of amino acids 36 to 1334 is sufficient to elicit humoral immune responses that protect animals against lethal disease. Protective immunity requires folded antigen and production of antibodies that recognize conformational epitopes on the rickettsial surface. Monoclonal antibodies (MAbs) 5C7.27 and 5C7.31, which specifically recognize a conformation present in the folded, intact rOmpB passenger domain, are sufficient to confer immunityin vivo. Analysesin vitroindicate this protection involves a mechanism of complement-mediated killing in mammalian blood, a means of rickettsial clearance that has not been previously described. Considering the evolutionary conservation of rOmpB and its crucial contribution to bacterial invasion of host cells, we propose that rOmpB antibody-mediated killing confers immunity to rickettsial infection.

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33

Zhao, Haoxin, Lydia N. Raines, and Stanley Ching-Cheng Huang. "Molecular Chaperones: Molecular Assembly Line Brings Metabolism and Immunity in Shape." Metabolites 10, no. 10 (October 3, 2020): 394. http://dx.doi.org/10.3390/metabo10100394.

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Molecular chaperones are a set of conserved proteins that have evolved to assist the folding of many newly synthesized proteins by preventing their misfolding under conditions such as elevated temperatures, hypoxia, acidosis and nutrient deprivation. Molecular chaperones belong to the heat shock protein (HSP) family. They have been identified as important participants in immune functions including antigen presentation, immunostimulation and immunomodulation, and play crucial roles in metabolic rewiring and epigenetic circuits. Growing evidence has accumulated to indicate that metabolic pathways and their metabolites influence the function of immune cells and can alter transcriptional activity through epigenetic modification of (de)methylation and (de)acetylation. However, whether molecular chaperones can regulate metabolic programs to influence immune activity is still largely unclear. In this review, we discuss the available data on the biological function of molecular chaperones to immune responses during inflammation, with a specific focus on the interplay between molecular chaperones and metabolic pathways that drive immune cell fate and function.

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34

Momcheva, Irina, I. Kazmin, S. Hristova, and V. Madjova. "OSTEOARTHRITIS AND IMMUNITY." Revmatologiia (Bulgaria) 29, no. 1 (May 26, 2021): 44–51. http://dx.doi.org/10.35465/29.1.2021.pp44-51.

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Abstract Low-grade inflammation is part of the pathogenesis of osteoarthritis (OA) from its earliest stages and contributes to the acceleration of the degenerative process. Innate immunity has a leading role in it. Activation of the innate immune response is initiated by stimulation of the receptors on the cell membrane to recognize the secreted PAMPs (pathogen-associated molecular patterns). However, PAMPs can also be activated by endogenous damage-related molecular patterns (DAMPs). The group of DAMPs also includes toll-like receptors (TLRs).The disruption of matrix homeostasis in the course of OA is an example of activation of these receptors in chronic damage. The complement system is a key element of the innate immune system. It is one of the serum enzyme systems whose function is to opsonize antigens. The complement receptors on the surface of the cell membranes adhere to the targets for phagocytosis. The C3R fraction activates the complement cascade itself, as well as the oxygen metabolism of the cell, which is essential for the phagocytosis. The cartilage damage products released during joint damage are a separate class of potent complement modulators. Complement fractions bind to complement receptors on the surface of the chondrocyte and the synoviocyte cell membranes by TLR. The complement system is involved in many processes in the course of osteoarthritis: chondrocyte degeneration, ECM degradation, low-grade inflammation in the osteoarthritis, cell lysis, unbalanced bone remodeling, osteophyte formation, and neoangiogenesis. Whether drug control of complement activation may be a future therapeutic strategy in the treatment of OA and prevent its progression is a subject of future studies.

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35

Rua, Rejane, and Dorian B. McGavern. "Advances in Meningeal Immunity." Trends in Molecular Medicine 24, no. 6 (June 2018): 542–59. http://dx.doi.org/10.1016/j.molmed.2018.04.003.

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36

Gross, Roy, Fabrice Vavre, Abdelaziz Heddi, Gregory D. D. Hurst, Einat Zchori-Fein, and Kostas Bourtzis. "Immunity and symbiosis." Molecular Microbiology 73, no. 5 (September 2009): 751–59. http://dx.doi.org/10.1111/j.1365-2958.2009.06820.x.

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37

Hasing, Maria E., and Xiaoli L. Pang. "Norovirus: Molecular Epidemiology, Viral Culture, Immunity, and Vaccines." Clinical Microbiology Newsletter 43, no. 5 (March 2021): 33–43. http://dx.doi.org/10.1016/j.clinmicnews.2021.02.002.

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38

Awad, Wael, Geraldine Ler, Jeffrey Y. W. Mak, Jérôme Le Nours, James McCluskey, Alexandra J. Corbett, David P. Fairlie, and Jamie Rossjohn. "Molecular basis underpinning metabolite-mediated T-cell immunity." Acta Crystallographica Section A Foundations and Advances 77, a2 (August 14, 2021): C110. http://dx.doi.org/10.1107/s0108767321095702.

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39

Akira, Shizuo. "Pathogen Associated Molecular Pattern Recognition in Innate Immunity." Ensho Saisei 23, no. 4 (2003): 211–17. http://dx.doi.org/10.2492/jsir.23.211.

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Sahni, Sanjeev K., Hema P. Narra, Abha Sahni, and David H. Walker. "Recent molecular insights into rickettsial pathogenesis and immunity." Future Microbiology 8, no. 10 (October 2013): 1265–88. http://dx.doi.org/10.2217/fmb.13.102.

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41

Göhre, Vera, Alexandra M. E. Jones, Jan Sklenář, Silke Robatzek, and Andreas P. M. Weber. "Molecular Crosstalk Between PAMP-Triggered Immunity and Photosynthesis." Molecular Plant-Microbe Interactions® 25, no. 8 (August 2012): 1083–92. http://dx.doi.org/10.1094/mpmi-11-11-0301.

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The innate immune system allows plants to respond to potential pathogens in an appropriate manner while minimizing damage and energy costs. Photosynthesis provides a sustained energy supply and, therefore, has to be integrated into the defense against pathogens. Although changes in photosynthetic activity during infection have been described, a detailed and conclusive characterization is lacking. Here, we addressed whether activation of early defense responses by pathogen-associated molecular patterns (PAMPs) triggers changes in photosynthesis. Using proteomics and chlorophyll fluorescence measurements, we show that activation of defense by PAMPs leads to a rapid decrease in nonphotochemical quenching (NPQ). Conversely, NPQ also influences several responses of PAMP-triggered immunity. In a mutant impaired in NPQ, apoplastic reactive oxygen species production is enhanced and defense gene expression is differentially affected. Although induction of the early defense markers WRKY22 and WRKY29 is enhanced, induction of the late markers PR1 and PR5 is completely abolished. We propose that regulation of NPQ is an intrinsic component of the plant's defense program.

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GRUNIG, G., A. BANZ, and R. DEWAALMALEFYT. "Molecular regulation of Th2 immunity by dendritic cells." Pharmacology & Therapeutics 106, no. 1 (April 2005): 75–96. http://dx.doi.org/10.1016/j.pharmthera.2004.11.004.

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43

Boulanger, Lisa M., Gene S. Huh, and Carla J. Shatz. "Neuronal plasticity and cellular immunity: shared molecular mechanisms." Current Opinion in Neurobiology 11, no. 5 (October 2001): 568–78. http://dx.doi.org/10.1016/s0959-4388(00)00251-8.

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Boulanger, Lisa M., Gene S. Huh, and Carla J. Shatz. "Neuronal plasticity and cellular immunity: shared molecular mechanisms." Current Opinion in Neurobiology 12, no. 1 (February 2002): 119. http://dx.doi.org/10.1016/s0959-4388(02)00300-8.

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Kim, Min Gab, Woe Yeon Kim, Jung Ro Lee, Sun Yong Lee, Young Jun Jung, and Sang Yeol Lee. "Host immunity-suppressive molecular weapons of phytopathogenic bacteria." Journal of Plant Biology 51, no. 4 (July 2008): 233–39. http://dx.doi.org/10.1007/bf03036121.

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46

Nussenzweig, Philip M., and Luciano A. Marraffini. "Molecular Mechanisms of CRISPR-Cas Immunity in Bacteria." Annual Review of Genetics 54, no. 1 (November 23, 2020): 93–120. http://dx.doi.org/10.1146/annurev-genet-022120-112523.

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Prokaryotes have developed numerous defense strategies to combat the constant threat posed by the diverse genetic parasites that endanger them. Clustered regularly interspaced short palindromic repeat (CRISPR)-Cas loci guard their hosts with an adaptive immune system against foreign nucleic acids. Protection starts with an immunization phase, in which short pieces of the invader's genome, known as spacers, are captured and integrated into the CRISPR locus after infection. Next, during the targeting phase, spacers are transcribed into CRISPR RNAs (crRNAs) that guide CRISPR-associated (Cas) nucleases to destroy the invader's DNA or RNA. Here we describe the many different molecular mechanisms of CRISPR targeting and how they are interconnected with the immunization phase through a third phase of the CRISPR-Cas immune response: primed spacer acquisition. In this phase, Cas proteins direct the crRNA-guided acquisition of additional spacers to achieve a more rapid and robust immunization of the population.

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47

Bittel, Pascal, and Silke Robatzek. "Microbe-associated molecular patterns (MAMPs) probe plant immunity." Current Opinion in Plant Biology 10, no. 4 (August 2007): 335–41. http://dx.doi.org/10.1016/j.pbi.2007.04.021.

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48

Dodd, H. M., N. Horn, W. C. Chan, C. J. Giffard, B. W. Bycroft, G. C. K. Roberts, and M. J. Gasson. "Molecular analysis of the regulation of nisin immunity." Microbiology 142, no. 9 (September 1, 1996): 2385–92. http://dx.doi.org/10.1099/00221287-142-9-2385.

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Burel, Julie G., Simon H. Apte, and Denise L. Doolan. "Systems Approaches towards Molecular Profiling of Human Immunity." Trends in Immunology 37, no. 1 (January 2016): 53–67. http://dx.doi.org/10.1016/j.it.2015.11.006.

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Weinmann, Amy S., Ben A. Youngblood, Stephen T. Smale, Robert Brink, David G. Schatz, and Michael McHeyzer-Williams. "A Future Outlook on Molecular Mechanisms of Immunity." Trends in Immunology 41, no. 7 (July 2020): 549–55. http://dx.doi.org/10.1016/j.it.2020.05.005.

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Journal articles on the topic 'Molecular immunity'

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