Bibliografías temáticas / C-type lectin receptors

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Literatura académica sobre el tema "C-type lectin receptors"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 20 de febrero de 2023

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Artículos de revistas sobre el tema "C-type lectin receptors"

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SUZUKI-INOUE, Katsue. "C-type lectin receptors". Japanese Journal of Thrombosis and Hemostasis 26, n.º 1 (2015): 29–34. http://dx.doi.org/10.2491/jjsth.26.29.

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Jégouzo, Sabine A. F., Conor Nelson, Thomas Hardwick, S. T. Angel Wong, Noel Kuan Kiat Lau, Gaik Kin Emily Neoh, Rocío Castellanos-Rueda et al. "Mammalian lectin arrays for screening host–microbe interactions". Journal of Biological Chemistry 295, n.º 14 (24 de febrero de 2020): 4541–55. http://dx.doi.org/10.1074/jbc.ra120.012783.

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Many members of the C-type lectin family of glycan-binding receptors have been ascribed roles in the recognition of microorganisms and serve as key receptors in the innate immune response to pathogens. Other mammalian receptors have become targets through which pathogens enter target cells. These receptor roles have often been documented with binding studies involving individual pairs of receptors and microorganisms. To provide a systematic overview of interactions between microbes and the large complement of C-type lectins, here we developed a lectin array and suitable protocols for labeling of microbes that could be used to probe this array. The array contains C-type lectins from cow, chosen as a model organism of agricultural interest for which the relevant pathogen–receptor interactions have not been previously investigated in detail. Screening with yeast cells and various strains of both Gram-positive and -negative bacteria revealed distinct binding patterns, which in some cases could be explained by binding to lipopolysaccharides or capsular polysaccharides, but in other cases they suggested the presence of novel glycan targets on many of the microorganisms. These results are consistent with interactions previously ascribed to the receptors, but they also highlight binding to additional sugar targets that have not previously been recognized. Our findings indicate that mammalian lectin arrays represent unique discovery tools for identifying both novel ligands and new receptor functions.
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Mischenko, A. A. "Transmembrane C-type lectin receptors in immunity". Вестник Сыктывкарского университета. Серия 2: Биология. Геология. Химия. Экология, n.º 4 (2021): 8–21. http://dx.doi.org/10.34130/2306-6229-2021-4-8.

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Wevers, Brigitte A., Teunis BH Geijtenbeek y Sonja I. Gringhuis. "C-type lectin receptors orchestrate antifungal immunity". Future Microbiology 8, n.º 7 (julio de 2013): 839–54. http://dx.doi.org/10.2217/fmb.13.56.

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Willment, Janet A. y Gordon D. Brown. "C-type lectin receptors in antifungal immunity". Trends in Microbiology 16, n.º 1 (enero de 2008): 27–32. http://dx.doi.org/10.1016/j.tim.2007.10.012.

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Hardison, Sarah E. y Gordon D. Brown. "C-type lectin receptors orchestrate antifungal immunity". Nature Immunology 13, n.º 9 (21 de agosto de 2012): 817–22. http://dx.doi.org/10.1038/ni.2369.

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Upham, Jacqueline P., Danielle Pickett, Tatsuro Irimura, E. Margot Anders y Patrick C. Reading. "Macrophage Receptors for Influenza A Virus: Role of the Macrophage Galactose-Type Lectin and Mannose Receptor in Viral Entry". Journal of Virology 84, n.º 8 (27 de enero de 2010): 3730–37. http://dx.doi.org/10.1128/jvi.02148-09.

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ABSTRACT Although sialic acid has long been recognized as the primary receptor determinant for attachment of influenza virus to host cells, the specific receptor molecules that mediate viral entry are not known for any cell type. For the infection of murine macrophages by influenza virus, our earlier study indicated involvement of a C-type lectin, the macrophage mannose receptor (MMR), in this process. Here, we have used direct binding techniques to confirm and characterize the interaction of influenza virus with the MMR and to seek additional macrophage surface molecules that may have potential as receptors for viral entry. We identified the macrophage galactose-type lectin (MGL) as a second macrophage membrane C-type lectin that binds influenza virus and is known to be endocytic. Binding of influenza virus to MMR and MGL occurred independently of sialic acid through Ca2+-dependent recognition of viral glycans by the carbohydrate recognition domains of the two lectins; influenza virus also bound to the sialic acid on the MMR. Multivalent ligands of the MMR and MGL inhibited influenza virus infection of macrophages in a manner that correlated with expression of these receptors on different macrophage populations. Influenza virus strain A/PR/8/34, which is poorly glycosylated and infects macrophages poorly, was not recognized by the C-type lectin activity of either the MMR or the MGL. We conclude that lectin-mediated interactions of influenza virus with the MMR or the MGL are required for the endocytic uptake of the virus into macrophages, and these lectins can thus be considered secondary or coreceptors with sialic acid for infection of this cell type.
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Marakalala, Mohlopheni J. y Hlumani Ndlovu. "Signaling C-type lectin receptors in antimycobacterial immunity". PLOS Pathogens 13, n.º 6 (22 de junio de 2017): e1006333. http://dx.doi.org/10.1371/journal.ppat.1006333.

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Shiokawa, Moe, Sho Yamasaki y Shinobu Saijo. "C-type lectin receptors in anti-fungal immunity". Current Opinion in Microbiology 40 (diciembre de 2017): 123–30. http://dx.doi.org/10.1016/j.mib.2017.11.004.

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Redelinghuys, Pierre y Gordon D. Brown. "Inhibitory C-type lectin receptors in myeloid cells". Immunology Letters 136, n.º 1 (abril de 2011): 1–12. http://dx.doi.org/10.1016/j.imlet.2010.10.005.

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Tesis sobre el tema "C-type lectin receptors"

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Christou, Charita. "C-type lectin-like receptors and their interactions". Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509908.

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Kerscher, Berhard Gerhard Richard. "Characterisation of the C-type lectin receptor Clecsf8". Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230779.

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C-type lectin-like receptors (CTLRs) play critical roles in immunity and homeostasis by recognising a variety of microbial or endogenous ligands. Clecsf8 is a member of the Dectin-2 family of CTLRs. Clecsf8 shares important similarities with its relatives Mincle and Dectin-2, such as the lack of an integral signalling motif and a single, calcium dependent ligand binding domain. They were shown to associate with the FcRγ adaptor, which is essential for receptor surface expression and downstream signalling. Recent publications revealed an important role for Clecsf8 in anti-mycobacterial immunity. It was reported to recognise the mycobacterial cord factor (TDM), similar to the related CTLR Mincle, as well as a possible role in candidiasis. In this study, we characterised the underlying mechanism of Clecsf8 expression in a context of mycobacterial disease. The generation of novel anti-Clecsf8 monoclonal antibodies allowed us to characterise the expression of Clecsf8 in detail in homeostasis and inflammation in murine models in vivo and culture systems in vitro. We found Clecsf8 to be predominantly expressed on monocytes/macrophages and neutrophils within e. g. the peritoneal cavity, blood and bone marrow. Notably, Clecsf8 was expressed only weakly in the lung, but strongly upregulated in a pulmonary mycobacterial infection model. In vitro, Clecsf8 expression on elicited macrophages was strongly induced upon treatment with microbial stimuli in a Myd88- and Mincle dependent manner. Interestingly, surface expression of Clecsf8 in a murine fibroblast cell line was greatly enhanced by co-transfection of Mincle, but not another related CTLR, Dectin-2. Notably, we confirmed mycobacteria as a ligand of CLECSF8, but found no role for the receptor in Candida immunity. In conclusion, Clecsf8 is a myeloid expressed, mycobacterial receptor, showing significant interdependence with Mincle and is regulated through the Myd88 pathway.
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Clark, Alexandra Elsie. "Characterisation of the C-type lectin-like receptor 1 (CLEC-1)". Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=210080.

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Mayer-Lambertz, Sabine [Verfasser]. "Role of C-type lectin receptors in bacterial recognition / Sabine Mayer-Lambertz". Hannover : Stiftung Tierärztliche Hochschule Hannover, 2019. http://d-nb.info/1192752465/34.

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Drummond, Rebcca Anne. "The role of C-type lectin receptors in Candida albicans specific immunity". Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=211412.

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Candida albicans is a human fungal pathogen responsible for superficial mucosal infections and life-threatening systemic disease. Despite the availability of potent antifungal drugs, mortality rates of systemic candidiasis remain high. Alternative therapies and vaccines are therefore desirable; however their generation depends on a comprehensive understanding of antifungal immunity. Innate recognition of fungi by the immune system is primarily mediated by a class of myeloid-expressed molecules termed the C-type lectin receptors (CLRs). CLRs mediate a variety of functions including phagocytosis, fungal killing, initiation of inflammation, and the generation of adaptive immunity. Adaptive responses are required for long-term memory and are shaped by the initial innate immune response controlled by CLR-expressing myeloid cells, yet the influence of CLRs on fungal-specific adaptive immunity is not well understood. In this thesis, the generation of C. albicans-specific T-cell immunity, particularly the CD4+ T-cell response, was investigated using OT.II transgenic T-cells and an ovalbumin-expressing strain of C. albicans. Using this model system, a novel role for the CLR, Dectin-1, was found in controlling CD4+ T-cell viability and recruitment to the GI tract. No roles for Dectin-1, or the related CLR Dectin-2, were found in controlling T-cell responses in the C. albicans infected kidney. However, it was found that, surprisingly, antigen-specific CD4+ T-cells did not migrate into the kidney during infection. Artificial restoration of this defect using immunoliposomes could significantly protect against infection, thus highlighting the importance of these lymphocytes to antifungal immunity. Furthermore, this thesis also explores the generation of better tools to study C. albicans-specific T-cell responses, and the roles of uncharacterised CLRs in the generation of adaptive immunity. Collectively, this research provides new insights into the generation and regulation of antigen-specific CD4+ T-cell immunity during C. albicans infections.
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Fuchsberger, Felix Franz Robert [Verfasser]. "Quantification of C-type lectin receptors signal transduction / Felix Franz Robert Fuchsberger". Berlin : Freie Universität Berlin, 2021. http://d-nb.info/1235400352/34.

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Maglinao, Maha Fay Binudin [Verfasser]. "C-type lectin receptors in cell-specific targeting and malaria infection / Maha Maglinao". Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1042940037/34.

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Alshahrani, Mohammad. "The role of C-type lectin receptors in the recognition of Pseudiminas aeruginosa". Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/53553/.

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Cystic fibrosis patients endure serious lung infection caused by colonisation and persistent infection by a wide range of pathogens, most commonly Pseudomonas aeruginosa (PA). One of the factors that facilitates establishment of chronic lung infection is formation of biofilms which are structures resistant to antimicrobial drugs and immune attack. Biofilms are embedded within extracellular polymeric substance (EPS) that maintains the structure of biofilms. PA produces two important polysaccharides Pel and Psl, which have been implicated in promoting biofilm development and biofilm maintenance, respectively, as well as cell aggregation . To the best of our knowledge, there has not been any study showing the presence of specific immune receptors for the recognition of PA biofilms. C-type lectin receptors (CLRs) are pathogen-recognition receptors that contribute to the recognition of infectious agents through the detection of carbohydrates moieties representing a subset of pathogen-associated molecular patterns (PAMPs). We hypothesized that CLRs such as DC-SIGN (CD209) and mannose receptor (MR) (CD206) could play a crucial role in the immune recognition of PA biofilms through the binding to different carbohydrate-containing components. Investigating the CLR-PA cross-talk and the response of immune cells expressing CLRs to different PA components could lead to a novel strategy to eradicate infections. The main aim of this thesis is to determine the capability of CLRs, particularly MR and DC-SIGN, to interact with PA biofilms. We have shown that CTLD4-7, a region of MR, and DC-SIGN bind to PA biofilms with DC-SIGN binding significantly better than MR. Both lectins also recognised several independent preparations of EPS lacking Pel. Surprisingly, we found that DC-SIGN also binds to planktonic PA in the absence of Psl and Pel which indicates that DC-SIGN could recognize non-EPS carbohydrate-containing ligands in the bacteria. Further investigation unveiled that DC-SIGN requires the presence of the common polysaccharide antigen (CPA) which is shared among all PA serotypes to bind planktonic cells. These results indicate that CPA is a candidate ligand for DC-SIGN in PA. To determine the significance of these findings, assays incubating human dendritic cells with purified EPS and planktonic PA were performed but no definitive conclusion could be drawn. These findings shed light on the potential impact of PA Psl and CPA-LPS on the recognition of PA by immune cells expressing CLRs and might open new avenues for therapeutic approaches.
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Salvage-Jones, Judith. "The Macrophage Inducible C-type Lectin (Mincle) is a Receptor for the Yeast, Candida Albicans". Thesis, Griffith University, 2017. http://hdl.handle.net/10072/367510.

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The Macrophage-Inducible C-type Lectin (Mincle) belongs to the family of C-type lectin receptors some of which have been well characterised. We investigated a role for Mincle in response to systemic candidiasis both in vivo and ex vivo. Our results show that while Mincle recognises C. albicans it is not phagocytic or candicidal. It does however, recognise this yeast as measured by reduced TNF-α production in Mincle deficient bone marrow-derived macrophages. Furthermore, there was a significant reduction in the cytokines KC, IL-1β, IL-10, IL-13, GCS-F, MIP-1β and RANTES in these cells. By using a mouse model of systemic infection, we were able to investigate levels of yeast fungal burden and tissue damage inMincle-/- and isogenic control mice. Mincle deficient mice were more susceptible to C. albicans infection, demonstrated by increased fungal burden and increased tissue damage in the kidney and brain of our knock-out mice, confirming a role for Mincle in control of C. albicans infection. Mincle shares some features in common with the β-glucan receptor (Dectin-1) and its close relative Dectin-2. Dectin-1 and Dectin-2 have both been shown to recognise the yeast Candida albicans. We therefore, went on to look at the RNA and protein expression profiles of these three C-type lectins and found Mincle was consistently upregulated in response to Candida in the brain, kidney, lung and spleen. Dectin-1 showed delayed induction and Dectin-2 was significantly up-regulated in all tissues in the absence of Mincle.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
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Tomlinson, Neil David. "Regulation of C-type lectin-like receptors dectin-1 and CLEC-2 by tetraspanins". Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/826/.

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Tetraspanins are a superfamily of glycoproteins that function as ‘organisers’ of membranes by clustering with each other to form tetraspanin-enriched microdomains, into which certain other receptors and signalling proteins are recruited and regulated. Tetraspanin microdomains have been implicated in a range of biological processes including cell signalling, adhesion, intracellular trafficking, cell-cell fusion and viral entry. The tetraspanin CD37 was recently shown to negatively regulate the C-type lectin-like receptor dectin-1, which is essential for innate immune responses to fungal pathogens. The aim of this thesis was to firstly develop a cell line model system to investigate the mechanism by which tetraspanins inhibit dectin-1, and to secondly extend this work to the dectin-1-related CLEC-2, which is essential for platelet thrombus formation and stability. Using a nuclear factor of activated T-cells (NFAT) transcriptional reporter assay in the Jurkat T-cell line, transient over-expression of CD37 was found to powerfully inhibit dectin-1 signalling following stimulation with its ligand, β-glucan. Over-expression of other tetraspanins also inhibited dectin-1 signalling, but did not globally inhibit receptor signalling because the platelet collagen receptor, GPVI, was unaffected. Similar to dectin-1, CLEC-2 signalling in response to its ligand, the snake venom toxin rhodocytin, was also abrogated following tetraspanin over-expression. However, stable tetraspanin over-expression only partially reduced signalling. Moreover, knockdown of the major Jurkat cell tetraspanin, CD81, and deletion of the major platelet tetraspanin, CD9, did not affect dectin-1 and CLEC-2 signalling, respectively. In summary, the importance of transient tetraspanin over-expression for dectin-1 and CLEC-2 inhibition, and the fact that any tetraspanin can inhibit, suggests that tetraspanin microdomains are disrupted by the presence of one over-expressed tetraspanin. This leads to a failure of dectin-1 and CLEC-2 signalling by a mechanism that is not clear, but suggests that tetraspanin microdomains are important for signalling by these C-type lectin-like receptors.
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Libros sobre el tema "C-type lectin receptors"

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Yamasaki, Sho, ed. C-Type Lectin Receptors in Immunity. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9.

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Yamasaki, Sho. C-Type Lectin Receptors in Immunity. Springer, 2018.

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Yamasaki, Sho. C-Type Lectin Receptors in Immunity. Springer Japan, 2016.

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Capítulos de libros sobre el tema "C-type lectin receptors"

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Kanazawa, Nobuo. "C-Type Lectin Receptors". En Immunology of the Skin, 255–74. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55855-2_17.

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Foster, Amy J., Jessie H. Bird, Mattie S. M. Timmer y Bridget L. Stocker. "The Ligands of C-Type Lectins". En C-Type Lectin Receptors in Immunity, 191–215. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_13.

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Li, Kai y David M. Underhill. "C-Type Lectin Receptors in Phagocytosis". En Current Topics in Microbiology and Immunology, 1–18. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/82_2020_198.

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Roth, Susanne, Christina Thomas y Jürgen Ruland. "Immunobiology of C-Type Lectin Receptors". En Innate Immunity: Resistance and Disease-Promoting Principles, 11–14. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000346538.

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Furukawa, Atsushi, Shunsuke Kita, Takashi Tadokoro, Hideo Fukuhara y Katsumi Maenaka. "Structural Aspects of C-Type Lectin Receptors". En C-Type Lectin Receptors in Immunity, 179–90. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_12.

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Yabe, Rikio y Shinobu Saijo. "Dectin-2 in Antimicrobial Immunity and Homeostasis". En C-Type Lectin Receptors in Immunity, 3–13. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_1.

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Hofmann, Anja, Tatsuya Sawamura y Henning Morawietz. "LOX-1 and Immunity". En C-Type Lectin Receptors in Immunity, 151–63. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_10.

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Denda-Nagai, Kaori y Tatsuro Irimura. "MGL/CD301 as a Unique C-Type Lectin Expressed on Dendritic Cells and Macrophages". En C-Type Lectin Receptors in Immunity, 165–78. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_11.

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Nagata, Masahiro, Zakaria Omahdi y Sho Yamasaki. "Pathogen-Sensing by Mincle: Function and Molecular Aspects". En C-Type Lectin Receptors in Immunity, 15–34. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_2.

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Hsieh, Shie-Liang. "The DAP12-Associated Myeloid C-Type Lectin 5A (CLEC5A)". En C-Type Lectin Receptors in Immunity, 35–48. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_3.

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Actas de conferencias sobre el tema "C-type lectin receptors"

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Lax, Sian, Julie Rayes, David Thickett y Steve Watson. "LSC Abstract – The role of platelet-expressed C-type lectin-like receptor-2 in regulating the severity of murine lung injury". En ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa936.

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Lax, Sian, Julie Rayes, David Thickett y Steve Watson. "LSC Abstract – The role of platelet-expressed C-type lectin-like receptor-2 in regulating the severity of murine lung injury". En ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pp228.

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