Journal articles: 'Triggering receptor'

1

Weiss, R. "Allergy-Triggering Receptor Made en masse." Science News 135, no. 16 (April 22, 1989): 246. http://dx.doi.org/10.2307/3973558.

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Ma, Zhengyu, and Terri H. Finkel. "T cell receptor triggering by force." Trends in Immunology 31, no. 1 (January 2010): 1–6. http://dx.doi.org/10.1016/j.it.2009.09.008.

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van der Merwe, P. Anton, and Omer Dushek. "Mechanisms for T cell receptor triggering." Nature Reviews Immunology 11, no. 1 (December 3, 2010): 47–55. http://dx.doi.org/10.1038/nri2887.

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Zhai, Qian, Feng Li, Xiyao Chen, Ji Jia, Sisi Sun, Dandan Zhou, Lei Ma, et al. "Triggering Receptor Expressed on Myeloid Cells 2, a Novel Regulator of Immunocyte Phenotypes, Confers Neuroprotection by Relieving Neuroinflammation." Anesthesiology 127, no. 1 (July 1, 2017): 98–110. http://dx.doi.org/10.1097/aln.0000000000001628.

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Abstract Background Microglia can not only detrimentally augment secondary injury but also potentially promote recovery. However, the mechanism underlying the regulation of microglial phenotypes after stroke remains unclear. Methods Mice were subjected to middle cerebral artery occlusion for 60 min. At 3 days after reperfusion, the effects of activation and suppression of triggering receptor expressed on myeloid cells 2 on immunocyte phenotypes (n = 5), neurobehavioral scores (n = 7), infarct volumes (n = 8), and neuronal apoptosis (n = 7) were analyzed. In vitro, cultured microglia were exposed to oxygen–glucose deprivation for 4 h. Inflammatory cytokines, cellular viability (n = 8), neuronal apoptosis (n = 7), and triggering receptor expressed on myeloid cells 2 expression (n = 5) were evaluated in the presence or absence of triggering receptor expressed on myeloid cell-specific small interfering RNA or triggering receptor expressed on myeloid cells 2 overexpression lentivirus. Results Triggering receptor expressed on myeloid cells 2 expression in the ischemic penumbra peaked at 3 days after ischemia–reperfusion injury (4.4 ± 0.1-fold, P = 0.0004) and was enhanced in interleukin-4/interleukin-13–treated microglia in vitro (1.7 ± 0.2-fold, P = 0.0119). After oxygen–glucose deprivation, triggering receptor expressed on myeloid cells 2 conferred neuroprotection by regulating the phenotypic conversion of microglia and inflammatory cytokine release. Intraperitoneal administration of triggering receptor expressed on myeloid cells 2 agonist heat shock protein 60 or unilateral delivery of a recombinant triggering receptor expressed on myeloid cells 2 lentivirus into the cerebral ventricle induced a significant neuroprotective effect in mice (apoptotic neurons decreased to 31.3 ± 7.6%; infarct volume decreased to 44.9 ± 5.3%). All values are presented as the mean ± SD. Conclusions Activation or up-regulation of triggering receptor expressed on myeloid cells 2 promoted the phenotypic conversion of microglia and decreased the number of apoptotic neurons. Our study suggests that triggering receptor expressed on myeloid cells 2 is a novel regulator of microglial phenotypes and may be a potential therapeutic target for stroke.

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Menon, A. K., D. Holowka, W. W. Webb, and B. Baird. "Clustering, mobility, and triggering activity of small oligomers of immunoglobulin E on rat basophilic leukemia cells." Journal of Cell Biology 102, no. 2 (February 1, 1986): 534–40. http://dx.doi.org/10.1083/jcb.102.2.534.

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We have recently shown that small oligomers of IgE bound to univalent receptors for IgE on the surface of rat basophilic leukemia cells induce extensive aggregation of the receptors at 4 degrees C into patches resolvable by fluorescence microscopy and that this does not occur with monomeric IgE (Menon, A. K., D. Holowka, and B. Baird, 1984, J. Cell Biol. 98:577-583). Here we use fluorescence photobleaching recovery measurements to show that receptor oligomerization by this means is accompanied by a dramatic reduction of receptor lateral mobility, and that this immobilization occurs even when the clustering is not microscopically detectable. Furthermore, the degree of immobility induced by a particular oligomer fraction from a gel filtration column correlates positively with its ability to trigger cellular degranulation, whereas receptors labeled with monomeric IgE have no triggering activity and exhibit typical membrane protein mobility. The slow, large-scale oligomer-induced clustering appears to be a long term consequence of earlier selective interactions that result in receptor immobilization, and this highly clustered state provides a competent, noninhibitory triggering signal resulting in cellular degranulation upon warming to 37 degrees C. We conclude that even limited clustering of IgE receptors on rat basophilic leukemia cells induces interactions with other cellular components that constrain receptor mobility and eventually cause massive coalescence of the clusters. These primary selective interactions occurring at the level of receptor oligomers or small clusters of oligomers that result in immobilization may play a role in triggering cellular degranulation.

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Dalpke, Alexander, and Klaus Heeg. "Signal Integration Following Toll-like Receptor Triggering." Critical Reviews™ in Immunology 22, no. 3 (2002): 34. http://dx.doi.org/10.1615/critrevimmunol.v22.i3.40.

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Xu, Xinyi, Hua Li, and Chenqi Xu. "Structural understanding of T cell receptor triggering." Cellular & Molecular Immunology 17, no. 3 (February 11, 2020): 193–202. http://dx.doi.org/10.1038/s41423-020-0367-1.

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Davis, Simon J., and P. Anton van der Merwe. "TCR triggering: co-receptor-dependent or -independent?" Trends in Immunology 24, no. 12 (December 2003): 624–26. http://dx.doi.org/10.1016/j.it.2003.10.009.

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Pazin, Michael J., and Lewis T. Williams. "Triggering signaling cascades by receptor tyrosine kinases." Trends in Biochemical Sciences 17, no. 10 (October 1992): 374–78. http://dx.doi.org/10.1016/0968-0004(92)90003-r.

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Ma, Zhengyu, Paul A. Janmey, and Terri H. Finkel. "The receptor deformation model of TCR triggering." FASEB Journal 22, no. 4 (November 5, 2007): 1002–8. http://dx.doi.org/10.1096/fj.07-9331hyp.

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Barraud, Damien, and Sébastien Gibot. "Triggering Receptor Expressed on Myeloid Cell 1." Critical Care Clinics 27, no. 2 (April 2011): 265–79. http://dx.doi.org/10.1016/j.ccc.2010.12.006.

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12

Felce, James H., Erdinc Sezgin, Madina Wane, Heather Brouwer, Michael L. Dustin, Christian Eggeling, and Simon J. Davis. "CD45 exclusion– and cross-linking–based receptor signaling together broaden FcεRI reactivity." Science Signaling 11, no. 561 (December 18, 2018): eaat0756. http://dx.doi.org/10.1126/scisignal.aat0756.

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For many years, the high-affinity receptor for immunoglobulin E (IgE) FcεRI, which is expressed by mast cells and basophils, has been widely held to be the exemplar of cross-linking (that is, aggregation dependent) signaling receptors. We found, however, that FcεRI signaling could occur in the presence or absence of receptor cross-linking. Using both cell and cell-free systems, we showed that FcεRI signaling was stimulated by surface-associated monovalent ligands through the passive, size-dependent exclusion of the receptor-type tyrosine phosphatase CD45 from plasma membrane regions of FcεRI-ligand engagement. Similarly to the T cell receptor, FcεRI signaling could also be initiated in a ligand-independent manner. These data suggest that a simple mechanism of CD45 exclusion–based receptor triggering could function together with cross-linking–based FcεRI signaling, broadening mast cell and basophil reactivity by enabling these cells to respond to both multivalent and surface-presented monovalent antigens. These findings also strengthen the case that a size-dependent, phosphatase exclusion–based receptor triggering mechanism might serve generally to facilitate signaling by noncatalytic immune receptors.

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Cordoba, Shaun-Paul, Kaushik Choudhuri, Hao Zhang, Marcus Bridge, Alp Bugra Basat, Michael L. Dustin, and P. Anton van der Merwe. "The large ectodomains of CD45 and CD148 regulate their segregation from and inhibition of ligated T-cell receptor." Blood 121, no. 21 (May 23, 2013): 4295–302. http://dx.doi.org/10.1182/blood-2012-07-442251.

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Key Points The large extracellular domains of the tyrosine phosphatases CD45 and CD148 prevent them from inhibiting T-cell receptor triggering. These domains are required for optimal segregation from the engaged T-cell receptor, supporting the kinetic-segregation model of triggering.

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Radoja, Sasa, Alan B. Frey, and Stanislav Vukmanovic. "T-Cell Receptor Signaling Events Triggering Granule Exocytosis." Critical Reviews™ in Immunology 26, no. 3 (2006): 265–90. http://dx.doi.org/10.1615/critrevimmunol.v26.i3.40.

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Choudhuri, Kaushik, and P. Anton van der Merwe. "Molecular mechanisms involved in T cell receptor triggering." Seminars in Immunology 19, no. 4 (August 2007): 255–61. http://dx.doi.org/10.1016/j.smim.2007.04.005.

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Lemarié, Jérémie, and Sébastien Gibot. "Soluble Triggering Receptor Expressed on Myeloid Cells-1." Critical Care Clinics 36, no. 1 (January 2020): 41–54. http://dx.doi.org/10.1016/j.ccc.2019.08.004.

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17

Menon, A. K., D. Holowka, W. W. Webb, and B. Baird. "Cross-linking of receptor-bound IgE to aggregates larger than dimers leads to rapid immobilization." Journal of Cell Biology 102, no. 2 (February 1, 1986): 541–50. http://dx.doi.org/10.1083/jcb.102.2.541.

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Controlled cross-linking of IgE-receptor complexes on the surface of rat basophilic leukemia cells and mast cells has allowed a comparison of the lateral mobility and cell triggering activity of monomers, dimers, and higher oligomers of receptors. Addition of a monoclonal anti-IgE(Fc) antibody to IgE-sensitized cells in stoichiometric amounts relative to IgE produces IgE-receptor dimers with high efficiency. These dimers are nearly as mobile as IgE-receptor monomers and trigger cellular degranulation poorly, but in the presence of 30% D2O, substantial immobilization of the dimers is seen and degranulation activity doubles. Addition of this monoclonal antibody in larger amounts results in the formation of larger oligomeric receptor clusters which are immobile and effectively trigger the cells. Thus, small receptor clusters that are active in stimulating degranulation are immobilized in a process that is not anticipated by simple hydrodynamic theories. Further experiments involving cross-linking of receptor-bound IgE by multivalent antigen demonstrate that immobilization of receptors occurs rapidly (less than 2 min) upon cross-linking and is fully and rapidly reversible by the addition of excess monovalent hapten. The rapidity and reversibility of the immobilization process are entirely consistent with the possibility that immobilization represents a recognition event between clustered receptors and cytoskeleton-associated components that plays an important role early in the cell triggering mechanism.

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Cronstein, B. N., and K. A. Haines. "Stimulus-response uncoupling in the neutrophil. Adenosine A2-receptor occupancy inhibits the sustained, but not the early, events of stimulus transduction in human neutrophils by a mechanism independent of actin-filament formation." Biochemical Journal 281, no. 3 (February 1, 1992): 631–35. http://dx.doi.org/10.1042/bj2810631.

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Generation of superoxide anion (O2-) in response to occupancy of neutrophil chemoattractant receptors requires both early events (‘triggering’) and sustained signals (‘activation’). We have previously demonstrated that occupancy of adenosine A2 receptors inhibits O2- generation by neutrophils. In parallel, adenosine-receptor occupancy promotes association of bound N-formylmethionyl-leucyl-phenylalanine (fMLP) receptors with the cytoskeleton, a process associated with termination of neutrophil activation (stimulus-response uncoupling). We undertook this study to determine whether inhibition of neutrophil function by adenosine-receptor occupancy requires intact actin filaments and to examine the effect of adenosine-receptor occupancy on the stimulated generation of intracellular signals involved in neutrophil triggering and activation. Occupancy of adenosine A2 receptors by 5′-N-ethylcarboxamidoadenosine (NECA, 1 microM) significantly increased (130 +/- 1% of control, P less than 0.001, n = 3) association of [3H]fMLP with cytoskeletal preparations. Cytochalasin B (5 micrograms/ml), an agent which disrupts actin filaments, completely blocked association of [3H]fMLP with cytoskeletal preparations, as previously reported. However, NECA markedly increased association of [3H]fMLP with the cytoskeleton even in the presence of cytochalasin B (P less than 0.0002). Moreover, NECA did not significantly affect either the early (30s) or the late (5 min) formation of actin filaments after stimulation by chemoattractant (fMLP, 0.1-100 nM). Cytochalasin B markedly inhibited actin-filament formation by stimulated neutrophils, and NECA did not reverse the effect of cytochalasin B on actin-filament formation. Adenosine-receptor occupancy did not affect the rapid peak in diacylglycerol generation (less than or equal to 15 s) from either [3H]arachidonate- or [14C]glycerol-labelled phospholipid pools. However, as would be predicted if occupancy of the adenosine receptor was a signal for early termination of cell activation, NECA (1 microM) markedly diminished the slow sustained generation of diacylglycerol. These results suggest that adenosine-A2-receptor occupancy does not affect triggering of the neutrophil, but that occupancy of adenosine receptors is an early signal for the termination of neutrophil activation, i.e. the ‘premature’ finish of signal transduction. Moreover, these data indicate that at least two pathways are available for increasing the association of ligated chemoattractant receptors with the cytoskeleton of neutrophils: F-actin-dependent and -independent.

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Speiser, Daniel E., Mikaël J. Pittet, Danila Valmori, Rod Dunbar, Donata Rimoldi, Danielle Liénard, H. Robson MacDonald, Jean-Charles Cerottini, Vincenzo Cerundolo, and Pedro Romero. "In Vivo Expression of Natural Killer Cell Inhibitory Receptors by Human Melanoma–Specific Cytolytic T Lymphocytes." Journal of Experimental Medicine 190, no. 6 (September 20, 1999): 775–82. http://dx.doi.org/10.1084/jem.190.6.775.

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Natural killer (NK) receptor signaling can lead to reduced cytotoxicity by NK cells and cytolytic T lymphocytes (CTLs) in vitro. Whether T cells are inhibited in vivo remains unknown, since peptide antigen–specific CD8+ T cells have so far not been found to express NK receptors in vivo. Here we demonstrate that melanoma patients may bear tumor-specific CTLs expressing NK receptors. The lysis of melanoma cells by patient-derived CTLs was inhibited by the NK receptor CD94/NKG2A. Thus, tumor-specific CTL activity may be decreased through NK receptor triggering in vivo.

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Pelham, Christopher J., Amit N. Pandya, and Devendra K. Agrawal. "Triggering receptor expressed on myeloid cells receptor family modulators: a patent review." Expert Opinion on Therapeutic Patents 24, no. 12 (November 2014): 1383–95. http://dx.doi.org/10.1517/13543776.2014.977865.

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Zipperle, Ljerka, Johannes P. M. Langedijk, Claes Örvell, Marc Vandevelde, Andreas Zurbriggen, and Philippe Plattet. "Identification of Key Residues in Virulent Canine Distemper Virus Hemagglutinin That Control CD150/SLAM-Binding Activity." Journal of Virology 84, no. 18 (July 14, 2010): 9618–24. http://dx.doi.org/10.1128/jvi.01077-10.

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ABSTRACT Morbillivirus cell entry is controlled by hemagglutinin (H), an envelope-anchored viral glycoprotein determining interaction with multiple host cell surface receptors. Subsequent to virus-receptor attachment, H is thought to transduce a signal triggering the viral fusion glycoprotein, which in turn drives virus-cell fusion activity. Cell entry through the universal morbillivirus receptor CD150/SLAM was reported to depend on two nearby microdomains located within the hemagglutinin. Here, we provide evidence that three key residues in the virulent canine distemper virus A75/17 H protein (Y525, D526, and R529), clustering at the rim of a large recessed groove created by β-propeller blades 4 and 5, control SLAM-binding activity without drastically modulating protein surface expression or SLAM-independent F triggering.

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Hernández-Caselles, Trinidad, Rubén Corral-San Miguel, Antonio José Ruiz-Alcaraz, and Pilar García-Peñarrubia. "CD33 (Siglec-3) Inhibitory Function: Role in the NKG2D/DAP10 Activating Pathway." Journal of Immunology Research 2019 (April 15, 2019): 1–15. http://dx.doi.org/10.1155/2019/6032141.

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CD33 (siglec-3), a well-known target in leukemia therapy, is an inhibitory sialoadhesin expressed in human leukocytes of the myeloid lineage and some lymphoid subsets, including NK cells. It may constitute a control mechanism of the innate immune system; nevertheless, its role as an inhibitory receptor remains elusive. Using human NK cells as a cellular model, we analyzed CD33 inhibitory function upon different activating receptors. In high-cytotoxicity NKL cells, CD33 displayed a prominent inhibition on cytotoxicity triggered by the activating receptors NKG2D and, in a lower extent, 2B4, whereas it did not inhibit NKp46-induced cytotoxicity. NKp46 was partially inhibited by CD33 only when low-cytotoxicity NKL cells were tested. CD33 triggering did not inhibit IFN-γsecretion, contrasting with ILT-2 and CD94/NKG2A inhibitory receptors that inhibited cytotoxicity and IFN-γsecretion induced by all activating receptors tested. CD33-mediated inhibition of NKG2D-induced triggering involved Vav1 dephosphorylation. Our results support the role of CD33 as an inhibitory receptor preferentially regulating the NKG2D/DAP10 cytotoxic signaling pathway, which could be involved in self-tolerance and tumor and infected cell recognition.

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Liu, Qian, Birgit Bradel-Tretheway, Abrrey I. Monreal, Jonel P. Saludes, Xiaonan Lu, Anthony V. Nicola, and Hector C. Aguilar. "Nipah Virus Attachment Glycoprotein Stalk C-Terminal Region Links Receptor Binding to Fusion Triggering." Journal of Virology 89, no. 3 (November 26, 2014): 1838–50. http://dx.doi.org/10.1128/jvi.02277-14.

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ABSTRACTMembrane fusion is essential for paramyxovirus entry into target cells and for the cell-cell fusion (syncytia) that results from many paramyxoviral infections. The concerted efforts of two membrane-integral viral proteins, the attachment (HN, H, or G) and fusion (F) glycoproteins, mediate membrane fusion. The emergent Nipah virus (NiV) is a highly pathogenic and deadly zoonotic paramyxovirus. We recently reported that upon cell receptor ephrinB2 or ephrinB3 binding, at least two conformational changes occur in the NiV-G head, followed by one in the NiV-G stalk, that subsequently result in F triggering and F execution of membrane fusion. However, the domains and residues in NiV-G that trigger F and the specific events that link receptor binding to F triggering are unknown. In the present study, we identified a NiV-G stalk C-terminal region (amino acids 159 to 163) that is important for multiple G functions, including G tetramerization, conformational integrity, G-F interactions, receptor-induced conformational changes in G, and F triggering. On the basis of these results, we propose that this NiV-G region serves as an important structural and functional linker between the NiV-G head and the rest of the stalk and is critical in propagating the F-triggering signal via specific conformational changes that open a concealed F-triggering domain(s) in the G stalk. These findings broaden our understanding of the mechanism(s) of receptor-induced paramyxovirus F triggering during viral entry and cell-cell fusion.IMPORTANCEThe emergent deadly viruses Nipah virus (NiV) and Hendra virus belong to theHenipavirusgenus in theParamyxoviridaefamily. NiV infections target endothelial cells and neurons and, in humans, result in 40 to 75% mortality rates. The broad tropism of the henipaviruses and the unavailability of therapeutics threaten the health of humans and livestock. Viral entry into host cells is the first step of henipavirus infections, which ultimately cause syncytium formation. After attaching to the host cell receptor, henipaviruses enter the target cell via direct viral-cell membrane fusion mediated by two membrane glycoproteins: the attachment protein (G) and the fusion protein (F). In this study, we identified and characterized a region in the NiV-G stalk C-terminal domain that links receptor binding to fusion triggering via several important glycoprotein functions. These findings advance our understanding of the membrane fusion-triggering mechanism(s) of the henipaviruses and the paramyxoviruses.

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Porotto, Matteo, Matthew Murrell, Olga Greengard, Lynne Doctor, and Anne Moscona. "Influence of the Human Parainfluenza Virus 3 Attachment Protein's Neuraminidase Activity on Its Capacity To Activate the Fusion Protein." Journal of Virology 79, no. 4 (February 15, 2005): 2383–92. http://dx.doi.org/10.1128/jvi.79.4.2383-2392.2005.

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ABSTRACT In order to examine functions of the hemagglutinin-neuraminidase (HN) protein that quantitatively influence fusion promotion, human parainfluenza virus 3 (HPIV3) variants with alterations in HN were studied. The variant HNs have mutations that affect either receptor binding avidity, neuraminidase activity, or fusion protein (F) activation. Neuraminidase activity was regulated by manipulation of temperature and pH. F activation was assessed by quantitating the irreversible binding of target erythrocytes (RBC) to HN/F-coexpressing cells in the presence of 4-GU-DANA (zanamivir) to release target cells bound only by HN-receptor interactions; the remaining, irreversibly bound target cells are retained via the fusion protein. In cells coexpressing wild-type (wt) or variant HNs with wt F, the fusion promotion capacity of HN was distinguished from target cell binding by measuring changes with time in the amounts of target RBC that were (i) reversibly bound by HN-receptor interaction (released only upon the addition of 4-GU-DANA), (ii) released by HN′s neuraminidase, and (iii) irreversibly bound by F-insertion or fusion (F triggered). For wt HN, lowering the pH (to approach the optimum for HPIV3 neuraminidase) decreased F triggering via release of HN from its receptor. An HN variant with increased receptor binding avidity had F-triggering efficiency like that of wt HN at pH 8.0, but this efficiency was not decreased by lowering the pH to 5.7, which suggested that the variant HN′s higher receptor binding activity counterbalanced the receptor dissociation promoted by increased neuraminidase activity. To dissect the specific contribution of neuraminidase to triggering, two variant HNs that are triggering-defective due to a mutation in the HN stalk were evaluated. One of these variants has, in addition, a mutation in the globular head that renders it neuraminidase dead, while the HN with the stalk mutation alone has 30% of wt neuraminidase. While the variant without neuraminidase activity triggered F effectively at 37°C irrespective of pH, the variant possessing effective neuraminidase activity completely failed to activate F at pH 5.7 and was capable of only minimal triggering activity even at pH 8.0. These results demonstrate that neuraminidase activity impacts the extent of HPIV3-mediated fusion by releasing HN from contact with receptor. Any particular HN′s competence to promote F-mediated fusion depends on the balance between its inherent F-triggering efficacy and its receptor-attachment regulatory functions (binding and receptor cleavage).

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Porotto, Matteo, Micaela Fornabaio, Glen E. Kellogg, and Anne Moscona. "A Second Receptor Binding Site on Human Parainfluenza Virus Type 3 Hemagglutinin-Neuraminidase Contributes to Activation of the FusionMechanism." Journal of Virology 81, no. 7 (January 17, 2007): 3216–28. http://dx.doi.org/10.1128/jvi.02617-06.

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ABSTRACT The hemagglutinin-neuraminidase (HN) protein of paramyxoviruses carries out three discrete activities that each affect the ability of HN to promote viral fusion and entry: receptor binding, receptor cleaving (neuraminidase), and triggering of the fusion protein. The interrelationship between the receptor binding and fusion-triggering functions of HN has not been clear. For human parainfluenza type 3 (HPIV3), one bifunctional site on HN can carry out both receptor binding and neuraminidase activities, and this site's receptor binding can be inhibited by the small receptor analog zanamivir. We now report experimental evidence, complemented by computational data, for a second receptor binding site near the HPIV3 HN dimer interface. This second binding site can mediate receptor binding even in the presence of zanamivir, and it differs from the second receptor binding site of the paramyxovirus Newcastle disease virus in its function and its relationship to the primary binding site. This second binding site of HPIV3 HN is involved in triggering F. We suggest that the two receptor binding sites on HPIV3 HN each contribute in distinct ways to virus-cell interaction; one is the multifunctional site that contains both binding and neuraminidase activities, and the other contains binding activity and also is involved in fusion promotion.

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Vitale, Massimo, Jacques Zimmer, Roberta Castriconi, Daniel Hanau, Lionel Donato, Cristina Bottino, Lorenzo Moretta, Henri de la Salle, and Alessandro Moretta. "Analysis of natural killer cells in TAP2-deficient patients: expression of functional triggering receptors and evidence for the existence of inhibitory receptor(s) that prevent lysis of normal autologous cells." Blood 99, no. 5 (March 1, 2002): 1723–29. http://dx.doi.org/10.1182/blood.v99.5.1723.

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Natural killer (NK) cells are characterized by the ability to kill cells that lack HLA class I molecules while sparing autologous normal (HLA class I+) cells. However, patients with transporter-associated antigen processing (TAP) deficiency, though displaying strong reductions of HLA class I surface expression, in most instances do not experience NK-mediated autoimmune phenomena. A possible mechanism by which TAP−/− NK cells avoid autoreactivity against autologous HLA class I–deficient cells could be based on either quantitative or qualitative defects of surface receptors involved in NK cell triggering. In this study we show that NK cells derived from 2 patients with TAP2−/− express normal levels of all known triggering receptors. As revealed by the analysis of polyclonal and clonal NK cells, these receptors display normal functional capabilities and allow the killing of a panel of NK-susceptible targets, including autologous B-LCLs. On the other hand, TAP2−/− NK cells were unable to kill either allogeneic (HLA class I+) or autologous (HLA class I− ) phytohemagglutinin (PHA) blasts even in the presence of anti-HLA class I monoclonal antibody. These data suggest that TAP2−/− NK cells express still unknown inhibitory receptor(s) capable of down-regulating the NK cell cytotoxicity on binding to surface ligand(s) expressed by T cell blasts. Functional analyses, both at the polyclonal and at the clonal level, are consistent with the concept that the putative inhibitory receptor is expressed by virtually all TAP2−/− NK cells, whereas it is present only in rare NK cells from healthy persons. Another possibility would be that TAP2−/− NK cells are missing a still unidentified triggering receptor involved in NK cell-mediated killing of PHA blasts.

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Park, Yoonseong, Young-Joon Kim, Vincent Dupriez, and Michael E. Adams. "Two Subtypes of Ecdysis-triggering Hormone Receptor inDrosophila melanogaster." Journal of Biological Chemistry 278, no. 20 (February 13, 2003): 17710–15. http://dx.doi.org/10.1074/jbc.m301119200.

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Nguyen, Austin Huy, Carleigh Koenck, Shannon K. Quirk, Victoria M. Lim, Mario V. Mitkov, Ryan M. Trowbridge, William J. Hunter, and Devendra K. Agrawal. "Triggering Receptor Expressed on Myeloid Cells in Cutaneous Melanoma." Clinical and Translational Science 8, no. 5 (July 16, 2015): 441–44. http://dx.doi.org/10.1111/cts.12308.

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Rui, H., J. Y. Djeu, G. A. Evans, P. A. Kelly, and W. L. Farrar. "Prolactin receptor triggering. Evidence for rapid tyrosine kinase activation." Journal of Biological Chemistry 267, no. 33 (November 1992): 24076–81. http://dx.doi.org/10.1016/s0021-9258(18)35948-9.

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Hasegawa, Kosei, Chunling Hu, Takafumi Nakamura, James D. Marks, Stephen J. Russell, and Kah-Whye Peng. "Affinity Thresholds for Membrane Fusion Triggering by Viral Glycoproteins." Journal of Virology 81, no. 23 (September 5, 2007): 13149–57. http://dx.doi.org/10.1128/jvi.01415-07.

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ABSTRACT Enveloped viruses trigger membrane fusion to gain entry into cells. The receptor affinities of their attachment proteins vary greatly, from 10−4 M to 10−9 M, but the significance of this is unknown. Using six retargeted measles viruses that bind to Her-2/neu with a 5-log range in affinity, we show that receptor affinity has little impact on viral attachment but is nevertheless a key determinant of infectivity and intercellular fusion. For a given cell surface receptor density, there is an affinity threshold above which cell-cell fusion proceeds efficiently. Suprathreshold affinities do not further enhance the efficiency of membrane fusion.

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Derive, Marc, Amir Boufenzer, and Sébastien Gibot. "Attenuation of Responses to Endotoxin by the Triggering Receptor Expressed on Myeloid Cells-1 Inhibitor LR12 in Nonhuman Primate." Anesthesiology 120, no. 4 (April 1, 2014): 935–42. http://dx.doi.org/10.1097/aln.0000000000000078.

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Abstract Background: The triggering receptor expressed on myeloid cells-1 is an immunoreceptor that amplifies the inflammatory response mediated by toll-like receptors engagement. Triggering receptor expressed on myeloid cells-1 inhibitory peptides such LR12 have been shown to prevent hyperresponsiveness and death in several experimental models of septic shock. Methods: Twelve adult male Cynomolgus (Macaca fascicularis) monkeys exposed to an intravenous bolus of endotoxin (10 μg/kg) were randomized to receive LR12 or placebo (n = 6 per group) as an initial intravenous bolus followed by an 8-h continuous intravenous infusion. An additional group of four only received vehicle infusion. Vital signs were monitored for 8 h. Blood was sampled at H0, 1, 2, 4, and 8 for analysis of clinical chemistries, leukocyte count, coagulation parameters, and cytokine plasma concentration. Results: LR12 showed no effect on heart rate and body temperature. By contrast to the placebo group, which experienced a 25 to 40% blood pressure decrease after endotoxin administration, LR12-treated monkeys remained normotensive. Endotoxin induced leukopenia at 2 h (mean leukocyte count, 7.62 g/l vs. 21.1 at H0), which was attenuated by LR12. LR12 also attenuated cytokine production. Conclusions: The triggering receptor expressed on myeloid cells-1 inhibitor LR12 is able to mitigate endotoxin-associated clinical and biological alterations, with no obvious side effects. This study paves the way for future phases Ia and Ib trials in humans.

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Fernandes, Ricardo A., Kristina A. Ganzinger, Justin C. Tzou, Peter Jönsson, Steven F. Lee, Matthieu Palayret, Ana Mafalda Santos, et al. "A cell topography-based mechanism for ligand discrimination by the T cell receptor." Proceedings of the National Academy of Sciences 116, no. 28 (June 20, 2019): 14002–10. http://dx.doi.org/10.1073/pnas.1817255116.

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The T cell receptor (TCR) initiates the elimination of pathogens and tumors by T cells. To avoid damage to the host, the receptor must be capable of discriminating between wild-type and mutated self and nonself peptide ligands presented by host cells. Exactly how the TCR does this is unknown. In resting T cells, the TCR is largely unphosphorylated due to the dominance of phosphatases over the kinases expressed at the cell surface. However, when agonist peptides are presented to the TCR by major histocompatibility complex proteins expressed by antigen-presenting cells (APCs), very fast receptor triggering, i.e., TCR phosphorylation, occurs. Recent work suggests that this depends on the local exclusion of the phosphatases from regions of contact of the T cells with the APCs. Here, we developed and tested a quantitative treatment of receptor triggering reliant only on TCR dwell time in phosphatase-depleted cell contacts constrained in area by cell topography. Using the model and experimentally derived parameters, we found that ligand discrimination likely depends crucially on individual contacts being ∼200 nm in radius, matching the dimensions of the surface protrusions used by T cells to interrogate their targets. The model not only correctly predicted the relative signaling potencies of known agonists and nonagonists but also achieved this in the absence of kinetic proofreading. Our work provides a simple, quantitative, and predictive molecular framework for understanding why TCR triggering is so selective and fast and reveals that, for some receptors, cell topography likely influences signaling outcomes.

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Meyer-Wentrup, Friederike, Daniel Benitez-Ribas, Paul J. Tacken, Cornelis J. A. Punt, Carl G. Figdor, I. Jolanda M. de Vries, and Gosse J. Adema. "Targeting DCIR on human plasmacytoid dendritic cells results in antigen presentation and inhibits IFN-α production." Blood 111, no. 8 (April 15, 2008): 4245–53. http://dx.doi.org/10.1182/blood-2007-03-081398.

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Abstract C-type lectin receptors (CLRs) fulfill multiple functions within the immune system by recognition of carbohydrate moieties on foreign or (altered) self-structures. CLRs on myeloid dendritic cells (DCs) have been well characterized as pattern-recognition receptors (PRRs) combining ligand internalization with complex signaling events. Much less is known about CLR expression and function in human plasmacytoid DCs (pDCs), the major type I interferon (IFN) producers. In this study, we demonstrate that, next to the CLR BDCA-2, human pDCs express DC immunoreceptor (DCIR), a CLR with putative immune-inhibitory function, but not dectin-1, mannose receptor, or DC-specific ICAM-3–grabbing nonintegrin. DCIR surface levels are reduced on pDC maturation after TLR9 triggering. Interestingly, DCIR triggering inhibits TLR9-induced IFN-α production while leaving up-regulation of costimulatory molecule expression unaffected. Furthermore, DCIR is readily internalized into pDCs after receptor triggering. We show that DCIR internalization is clathrin-dependent because it can be inhibited by hypertonic shock and dominant-negative dynamin. Importantly, antigens targeted to pDCs via DCIR are presented to T cells. These findings indicate that targeting DCIR on pDCs not only results in efficient antigen presentation but also affects TLR9-induced IFN-α production. Collectively, the data show that targeting of DCIR can modulate human pDC function and may be applied in disease preven-tion and treatment.

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Schrezenmeier, H., G. Ahnert-Hilger, and B. Fleischer. "Inactivation of a T cell receptor-associated GTP-binding protein by antibody-induced modulation of the T cell receptor/CD3 complex." Journal of Experimental Medicine 168, no. 2 (August 1, 1988): 817–22. http://dx.doi.org/10.1084/jem.168.2.817.

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TCR modulation induced by anti-TCR or anti-CD3 mAbs leads to a transient state of refractoriness of the T cell to all signals given via cell surface structures. To investigate the underlying mechanisms, we have used human CTL permeabilized with the alpha toxin of S. aureus. This method of permeabilization allows manipulation of the interior milieu of the cell, but maintains its functional and structural integrity. Introduction of the G protein activator GTP gamma S into permeabilized CTL leads to triggering of granule exocytosis. The G protein inactivator GDP beta S inhibited exocytosis induced by TCR triggering but not that induced by activation of protein kinase C. This indicates that the G protein that triggers exocytosis is localized after CD3 triggering but before formation of the polyphosphoinositol breakdown product diacylglycerol. In TCR-modulated CTL, GTP gamma S is no longer able to activate exocytosis. Such CTL, however, still respond to PKC activators. This demonstrates that a TCR-associated G protein has been functionally inactivated by TCR modulation.

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Pende, Daniela, Silvia Parolini, Anna Pessino, Simona Sivori, Raffaella Augugliaro, Luigia Morelli, Emanuela Marcenaro, et al. "Identification and Molecular Characterization of Nkp30, a Novel Triggering Receptor Involved in Natural Cytotoxicity Mediated by Human Natural Killer Cells." Journal of Experimental Medicine 190, no. 10 (November 15, 1999): 1505–16. http://dx.doi.org/10.1084/jem.190.10.1505.

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Two major receptors involved in human natural cytotoxicity, NKp46 and NKp44, have recently been identified. However, experimental evidence suggested the existence of additional such receptor(s). In this study, by the generation of monoclonal antibodies (mAbs), we identified NKp30, a novel 30-kD triggering receptor selectively expressed by all resting and activated human natural killer (NK) cells. Although mAb-mediated cross-linking of NKp30 induces strong NK cell activation, mAb-mediated masking inhibits the NK cytotoxicity against normal or tumor target cells. NKp30 cooperates with NKp46 and/or NKp44 in the induction of NK-mediated cytotoxicity against the majority of target cells, whereas it represents the major triggering receptor in the killing of certain tumors. This novel receptor is associated with CD3ζ chains that become tyrosine phosphorylated upon sodium pervanadate treatment of NK cells. Molecular cloning of NKp30 cDNA revealed a member of the immunoglobulin superfamily, characterized by a single V-type domain and a charged residue in the transmembrane portion. Moreover, we show that NKp30 is encoded by the previously identified 1C7 gene, for which the function and the cellular distribution of the putative product were not identified in previous studies.

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Costa, Blaise M. "NMDA receptor modulation and severe acute respiratory syndrome treatment." F1000Research 10 (October 18, 2021): 1060. http://dx.doi.org/10.12688/f1000research.73897.1.

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N-Methyl-D-aspartate (NMDA) subtype of glutamate receptors is expressed in the human lungs and central nervous system. NMDA receptor potentiation could increase calcium ion influx and promote downstream signaling mechanisms associated with cellular contractions that are disrupted in severe acute respiratory syndrome. Pharmacological effects generated by triggering glutamate receptor function in the brain, coupled with concurrent stimulation of the respiratory tract, may produce a synergetic effect, improving the airway smooth muscle function. A novel multipronged intervention to simultaneously potentiate NMDA receptors expressed both in the central nervous system and airway muscles would be helpful for the treatment of severe acute respiratory syndrome that deteriorates peripheral and central nervous system function before causing death in humans.

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Tursun, Serkan, Ayşegül Alpcan, Metin Özsoy, Nermin Dindar Badem, Yaşar Kandur, and Banu Çelikel Acar. "Diagnostic Value of Plasma Soluble Triggering Receptor Expressed on Myeloid Cells-1 in Children with Urinary Tract Infections." Journal of Pediatric Infectious Diseases 16, no. 03 (February 25, 2021): 129–33. http://dx.doi.org/10.1055/s-0041-1724024.

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Abstract Objective The aim of the present study was to evaluate the diagnostic value of soluble triggering receptor on myeloid cells-1 as a novel marker for diagnosis of childhood urinary tract infections (UTI). Methods This study enrolled 30 pediatric patients diagnosed with acute febrile UTIs; 30 healthy children were included as the control group. The blood samples from the patients and healthy controls were collected for a soluble triggering receptor on myeloid cells-1 (sTREM-1) test. Results The study group was composed of 9 males and 21 females, and the mean age of the study population was 6.6 ± 3.2 (range = 1–14) years. sTREM-1 levels were significantly higher in UTI patients than in the controls (592 ± 323 vs. 490 ± 299 pg/mL, p = 0.04). The receiver operating curve analysis revealed a cut-off value of soluble triggering receptor expressed on myeloid cells-1 of 514 ng/mL (area under the curve = 0.562). When the cut-off value was taken 514 pg/mL, soluble triggering receptor expressed on myeloid cells-1 had a sensitivity of 57% and a specificity of 50% for the diagnosis of UTI. Conclusion The present study revealed that plasma sTREM-1 level may be elevated in UTI and may therefore serve as a useful predictive tool for the diagnosis of UTI.

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Brattsand, G., D. A. Cantrell, S. Ward, F. Ivars, and M. Gullberg. "Signal transduction through the T cell receptor-CD3 complex. Evidence for heterogeneity in receptor coupling." Journal of Immunology 144, no. 10 (May 15, 1990): 3651–58. http://dx.doi.org/10.4049/jimmunol.144.10.3651.

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Abstract T cell receptor-CD3 complex (TCR-CD3)-mediated signal transduction was analyzed in HPB-ALL and Jurkat T cell lines. Both cell lines express high levels of TCR-CD3 complex on the cell surface, but provide different model systems for TCR-CD3 signaling in T cells. Jurkat responds with both inositol phosphate generation and intracellular Ca2+ mobilization after triggering of TCR-CD3, whereas TCR-CD3 triggering of HPB-ALL induces Ca2+ mobilization without detectable inositol phosphate generation. By employing a permeabilized cell system, we show that the HPB-ALL line expressed normal levels of Ca2(+)-induced phospholipase C activity. However, the TCR-CD3 on this cell line seems to be uncoupled from phospholipase C activation. In agreement with this result we also show, by analysis of protein kinase C-dependent phosphorylation of three distinct substrates, that TCR-CD3 in HPB-ALL is apparently uncoupled from protein kinase C activation. These findings may have implications for understanding signal-transducing pathways in T cells at various stages of differentiation.

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Hollenberg, Morley D. "Receptor triggering and receptor regulation: structure-activity relationships from the receptor's point of view." Journal of Medicinal Chemistry 33, no. 5 (May 1990): 1275–81. http://dx.doi.org/10.1021/jm00167a001.

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Washington, A. Valance, Laura Quigley, and Daniel W. McVicar. "Initial characterization of TREM-like transcript (TLT)–1: a putative inhibitory receptor within the TREM cluster." Blood 100, no. 10 (November 15, 2002): 3822–24. http://dx.doi.org/10.1182/blood-2002-02-0523.

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The TREMs (triggering receptors expressed on myeloid cells) represent a family of 5 receptors clustered on murine chromosome 17. TREMs 1 and 2 affect various aspects of myeloid cell activation and development, including responsiveness to lipopolysaccharide and regulation of dendritic cell maturation, yet no inhibitory receptor has been demonstrated within this cluster. Here we characterize TLT-1 (TREM-like transcript-1), a putative inhibitory receptor within the TREM cluster that contains an extracellular V-set Ig domain, a proline-rich region, and an immune receptor tyrosine-based inhibitory motif (ITIM) in its cytoplasmic tail. To our knowledge, TLT-1 is the first ITIM-containing receptor carrying a potential Src homology 3 domain ligand. TLT-1 transcripts are abundant in bone marrow cells, but not in lymphocytes, and phosphorylated TLT-1 associates with SHP-1, suggesting that it is indeed an inhibitory receptor. Based on these characteristics, it is likely that TLT-1 regulates the signaling of the TREM family receptors.

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Rubic, Tina, Günther Lametschwandtner, Sandra Jost, Sonja Hinteregger, Julia Kund, Nicole Carballido-Perrig, Christoph Schwärzler, et al. "Triggering the succinate receptor GPR91 on dendritic cells enhances immunity." Nature Immunology 9, no. 11 (September 28, 2008): 1261–69. http://dx.doi.org/10.1038/ni.1657.

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Matadeen, Rishi, Wai-Ching Hon, John K. Heath, E. Yvonne Jones, and Stephen Fuller. "The Dynamics of Signal Triggering in a gp130-Receptor Complex." Structure 15, no. 4 (April 2007): 441–48. http://dx.doi.org/10.1016/j.str.2007.02.006.

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Yang, Jianying, and Michael Reth. "The dissociation activation model of B cell antigen receptor triggering." FEBS Letters 584, no. 24 (October 2, 2010): 4872–77. http://dx.doi.org/10.1016/j.febslet.2010.09.045.

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Berk, Lieke C. J. van den, Bastiaan J. H. Jansen, Kim G. C. Siebers-Vermeulen, Mihai G. Netea, Talia Latuhihin, Saskia Bergevoet, Reinier A. Raymakers, et al. "Toll-like receptor triggering in cord blood mesenchymal stem cells." Journal of Cellular and Molecular Medicine 13, no. 9b (January 29, 2010): 3415–26. http://dx.doi.org/10.1111/j.1582-4934.2008.00653.x.

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Berk, Lieke C. J. van den, Bastiaan J. H. Jansen, Kim G. C. Siebers-Vermeulen, Mihai G. Netea, Talia Latuhihin, Saskia Bergevoet, Reinier A. Raymakers, et al. "Toll-like receptor triggering in cord blood mesenchymal stem cells." Journal of Cellular and Molecular Medicine 13, no. 9b (September 2009): 3415–26. http://dx.doi.org/10.1111/j.1582-4934.2009.00653.x.

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Ponassi, Marco, Claudia Cantoni, Roberto Biassoni, Romana Conte, Andrea Spallarossa, Alessandra Pesce, Alessandro Moretta, Lorenzo Moretta, Martino Bolognesi, and Domenico Bordo. "Structure of the human NK cell triggering receptor NKp46 ectodomain." Biochemical and Biophysical Research Communications 309, no. 2 (September 2003): 317–23. http://dx.doi.org/10.1016/j.bbrc.2003.08.007.

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Bittner, Sebastian, and Martin Ehrenschwender. "Multifaceted death receptor 3 signaling-promoting survival and triggering death." FEBS Letters 591, no. 17 (July 20, 2017): 2543–55. http://dx.doi.org/10.1002/1873-3468.12747.

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N'Diaye, Elsa-Noah, Catherine S. Branda, Steven S. Branda, Lisette Nevarez, Marco Colonna, Clifford Lowell, Jessica A. Hamerman, and William E. Seaman. "TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria." Journal of Cell Biology 184, no. 2 (January 26, 2009): 215–23. http://dx.doi.org/10.1083/jcb.200808080.

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Phagocytosis, which is essential for the immune response to pathogens, is initiated by specific interactions between pathogens and cell surface receptors expressed by phagocytes. This study identifies triggering receptor expressed on myeloid cells 2 (TREM-2) and its signaling counterpart DAP12 as a molecular complex that promotes phagocytosis of bacteria. Expression of TREM-2–DAP12 enables nonphagocytic Chinese hamster ovary cells to internalize bacteria. This function depends on actin cytoskeleton dynamics and the activity of the small guanosine triphosphatases Rac and Cdc42. Internalization also requires src kinase activity and tyrosine phosphorylation. In bone marrow–derived macrophages, phagocytosis is decreased in the absence of DAP12 and can be restored by expression of TREM-2–DAP12. Depletion of TREM-2 inhibits both binding and uptake of bacteria. Finally, TREM-2–dependent phagocytosis is impaired in Syk-deficient macrophages. This study highlights a novel role for TREM-2–DAP12 in the immune response to bacterial pathogens.

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Zheng, Honghua, Chia-Chen Liu, Yuka Atagi, Xiao-Fen Chen, Lin Jia, Longyu Yang, Wencan He, et al. "Opposing roles of the triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells-like transcript 2 in microglia activation." Neurobiology of Aging 42 (June 2016): 132–41. http://dx.doi.org/10.1016/j.neurobiolaging.2016.03.004.

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Albert, F., C. Hua, A. Truneh, M. Pierres, and A. M. Schmitt-Verhulst. "Distinction between antigen receptor and IL 2 receptor triggering events in the activation of alloreactive T cell clones with calcium ionophore and phorbol ester." Journal of Immunology 134, no. 6 (June 1, 1985): 3649–55. http://dx.doi.org/10.4049/jimmunol.134.6.3649.

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Abstract A previous study indicated that Ca++ ionophores in conjunction with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) could induce normal T lymphocytes to express receptors for the T cell growth factor, interleukin 2 (IL 2), to secrete IL 2, and to proliferate (1). Here we used long-term alloreactive Lyt-2+ cytotoxic or T4+ "helper" T cell clones. In response to their specific alloantigen, all of the clones secreted IFN-gamma but only the T4+ clone secreted IL 2 and proliferated in response to the appropriate alloantigen in the absence of exogenous IL 2. The Ca++ ionophore ionomycin and TPA, used in conjunction, mimicked the effect of specific alloantigen on these T cell clones, i.e., they induced the secretion of IFN-gamma in all clones and the secretion of IL 2 in the T4+ clone. In the absence of exogenous IL 2, a proliferative response was induced only for the IL 2 secreting clone. Increased sensitivity to exogenous IL 2 for some T cell clones was also observed after either alloantigen or ionomycin and TPA treatment; this could be correlated with an increase in the expression of IL 2 receptors 6 hr after a pulse with ionomycin and TPA. These results suggest that, for a given T cell clone, activation of the Ca++ -dependent protein kinase c can replace the antigen-receptor triggering events leading to interleukin secretion and increased expression of IL 2 receptors but cannot substitute for the IL 2 dependent triggering of the IL 2 receptor.

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Journal articles on the topic 'Triggering receptor'

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