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Träfflista för sökning "L773:1044 5323 OR L773:1096 3618 "

Sökning: L773:1044 5323 OR L773:1096 3618

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  • Cichocki, Frank, et al. (författare)
  • NK cell development and function - Plasticity and redundancy unleashed.
  • 2014
  • Ingår i: Seminars in Immunology. - : Elsevier BV. - 1096-3618 .- 1044-5323. ; 26:2, s. 114-126
  • Forskningsöversikt (refereegranskat)abstract
    • Bone marrow-derived natural killer (NK) cells constitute the major subset of cytotoxic lymphocytes in peripheral blood. They provide innate defense against intracellular infection or malignancy and contribute to immune homeostasis. Large numbers of NK cells are also present in tissues, including the liver and uterus, where they can mediate immunosurveillance but also play important roles in tissue remodeling and vascularization. Here, we review the pathways involved in NK cell lineage commitment and differentiation, discussing relationships to other lymphocyte populations and highlighting genetic determinants. Characterizing NK cells from distinct tissues and during infections have revealed subset specializations, reflecting inherent cellular plasticity. In this context, we discuss how different environmental and inflammatory stimuli may shape NK cells. Particular emphasis is placed on genes identified as being critical for NK cell development, differentiation, and function from studies of model organisms or associations with disease. Such studies are also revealing important cellular redundancies. Here, we provide a view of the genetic framework constraining NK cell development and function, pinpointing molecules required for these processes but also underscoring plasticity and redundancy that may underlie robust immunological function. With this view, built in redundancy may highlight the importance of NK cells to immunity.
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  • Ekdahl, Kristina N., et al. (författare)
  • Complement inhibition in biomaterial- and biosurface-induced thromboinflammation
  • 2016
  • Ingår i: Seminars in Immunology. - : Elsevier BV. - 1044-5323 .- 1096-3618. ; 28:3, s. 268-277
  • Tidskriftsartikel (refereegranskat)abstract
    • Therapeutic medicine today includes a vast number of procedures involving the use of biomaterials, transplantation of therapeutic cells or cell clusters, as well as of solid organs. These treatment modalities are obviously of great benefit to the patient, but also present a great challenge to the innate immune system, since they involve direct exposure of non-biological materials, cells of non-hematological origin as well as endothelial cells, damaged by ischemia-perfusion in solid organs to proteins and cells in the blood. The result of such an exposure may be an inappropriate activation of the complement and contact/kallikrein systems, which produce mediators capable of triggering the platelets and PMNs and monocytes, which can ultimately result in thrombotic and inflammatory (i.e., a thrombo-inflammatory) response to the treatment modality. In this concept review, we give an overview of the mechanisms of recognition within the innate immunity system, with the aim to identify suitable points for intervention. Finally, we discuss emerging and promising techniques for surface modification of biomaterials and cells with specific inhibitors in order to diminish thromboinflammation and improve clinical outcome.
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  • Gerold, Gisa, 1979-, et al. (författare)
  • What is the role of Toll-like receptors in bacterial infections?
  • 2007
  • Ingår i: Seminars in Immunology. - : Elsevier BV. - 1044-5323 .- 1096-3618. ; 19:1, s. 41-7
  • Tidskriftsartikel (refereegranskat)abstract
    • Innate immunity relies on signalling by Toll-like receptors (TLRs) to alert the immune system of the presence of invading bacteria. TLR activation leads to the release of cytokines that allow for effective innate and adaptive immune responses. However, the contribution of different TLRs depends on the site of the infection and the pathogen. This review will describe the involvement of TLRs in the development of three different bacterial infections as well as our current understanding of the role of TLRs during microbial pathogenesis.
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  • Gul, Ersin, et al. (författare)
  • Epithelial inflammasomes, gasdermins, and mucosal inflammation - Lessons from Salmonella and Shigella infected mice
  • 2023
  • Ingår i: Seminars in Immunology. - : ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD. - 1044-5323 .- 1096-3618. ; 70
  • Forskningsöversikt (refereegranskat)abstract
    • Besides its crucial function in nutrient absorbance and as barrier against the microbiota, the gut epithelium is essential for sensing pathogenic insults and mounting of an appropriate early immune response. In mice, the activation of the canonical NAIP/NLRC4 inflammasome is critical for the defense against enterobacterial infections. Activation of the NAIP/NLRC4 inflammasome triggers the extrusion of infected intestinal epithelial cells (IEC) into the gut lumen, concomitant with inflammasome-mediated lytic cell death. The membrane permeabilization, a hallmark of pyroptosis, is caused by the pore-forming proteins called gasdermins (GSDMs). Recent work has revealed that NAIP/NLRC4-dependent extrusion of infected IECs can, however, also be executed in the absence of GSDMD. In fact, several reports highlighted that various cell death pathways (e.g., pyroptosis or apoptosis) and unique mechanisms specific to particular infection models and stages of gut infection are in action during epithelial inflammasome defense against intestinal pathogens. Here, we summarize the current knowledge regarding the underlying mechanisms and speculate on the putative functions of the epithelial inflammasome activation and cell death, with a particular emphasis on mouse infection models for two prominent enterobacterial pathogens, Salmonella Typhimurium and Shigella flexneri.
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  • Holmes, TD, et al. (författare)
  • Natural killer cell memory in context
  • 2016
  • Ingår i: Seminars in immunology. - : Elsevier BV. - 1096-3618 .- 1044-5323. ; 28:4, s. 368-376
  • Tidskriftsartikel (refereegranskat)
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