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  • 1.
    Bulfone-Paus, Silvia
    et al.
    Univ Manchester, Div Musculoskeletal & Dermatol Sci, Fac Biol Med & Hlth, Manchester, Lancs, England..
    Nilsson, Gunnar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology. Karolinska Inst, Dept Med, Immunol & Allergy Unit, Stockholm, Sweden.;Karolinska Univ Hosp, Stockholm, Sweden.
    Draber, Petr
    Acad Sci Czech Republ, Inst Mol Genet, Dept Signal Transduct, Prague, Czech Republic..
    Blank, Ulrich
    INSERM, U1149, Ctr Rech Inflammat, Paris, France.;CNRS, ERL8252, Paris, France.;Univ Paris Diderot, Sorbonne Paris Cite, Fac Med, Site Xavier Bichat,Inflamex Lab Excellence, Paris, France..
    Levi-Schaffer, Francesca
    Hebrew Univ Jerusalem, Inst Drug Res, Sch Pharm, Fac Med,Pharmacol & Expt Therapeut Unit, Jerusalem, Israel..
    Positive and Negative Signals in Mast Cell Activation2017In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 38, no 9, p. 657-667Article, review/survey (Refereed)
    Abstract [en]

    Mast cells are powerful immune modulators of the tissue microenvironment. Within seconds of activation, these cells release a variety of preformed biologically active products, followed by a wave of mediator synthesis and secretion. Increasing evidence suggests that an intricate network of inhibitory and activating receptors, specific signaling pathways, and adaptor proteins governs mast cell responsiveness to stimuli. Here, we discuss the biological and clinical relevance of negative and positive signaling modalities that control mast cell activation, with an emphasis on novel Fc epsilon RI regulators, immunoglobulin E (IgE)-independent pathways [e.g., Mas-related G protein-coupled receptor X2 (MRGPRX2)], tetraspanins, and the CD300 family of inhibitory and activating receptors.

  • 2.
    Cerenius, Lage
    et al.
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Comparative Physiology.
    Lee, Bok Luel
    Söderhäll, Kenneth
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Comparative Physiology.
    The proPO-system: pros and cons for its role in invertebrate immunity2008In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 29, no 6, p. 263-271Article, review/survey (Refereed)
    Abstract [en]

    Melanisation is an important immune response in many invertebrates. Recent evidence also strongly implies that the melanisation (prophenoloxidase activating) cascade is intimately associated with the appearance of factors stimulating cellular defence by aiding phagocytosis and encapsulation reactions. However, some controversy exists in the field, and at least in flies and mosquitoes, the successful combat of some pathogens does not seem to be dependent on phenoloxidase activity. This may be because of redundancy among separate immune mechanisms, inappropriate testing, species differences or a combination thereof. Recently, by using RNA interference against phenoloxidase or in specific host-pathogen interactions where the pathogen prevents melanin production by the host, convincing data have confirmed the importance of this cascade in invertebrate innate immunity.

  • 3.
    Christoffersson, Gustaf
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
    von Herrath, Matthias
    La Jolla Inst Allergy & Immunol, Type Diabet Ctr 1, La Jolla, CA 92037 USA;Novo Nordisk Res Ctr, Seattle, WA 98109 USA.
    Regulatory Immune Mechanisms beyond Regulatory T Cells2019In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 40, no 6, p. 482-491Article, review/survey (Refereed)
    Abstract [en]

    In autoimmunity, aggressive immune responses are counteracted by suppressive rejoinders. For instance, FOXP3-expressing regulatory T cells (Tregs), have shown remarkable effects in limiting autoimmunity in preclinical models. However, early results from human Treg trials have not been as positive. Here, we highlight questions surrounding Treg transfers as putative treatments for autoimmunity. We discuss whether lack of antigenic recognition might be key to shifting cells from contributing to an aggressive autoresponse, to being part of a regulatory network. Moreover, we argue that identifying the physiological range of immunosuppression of Tregs might help potentiate their efficacy. We propose widening the view on immunoregulation by considering the participation of CD8(+) Tregs in this process, which could have major implications in autoimmunity.

  • 4. Markiewski, Maciej M.
    et al.
    Nilsson, Bo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Clinical Immunology.
    Ekdahl, Kristina Nilsson
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Clinical Immunology.
    Mollnes, Tom Eirik
    Lambris, John D.
    Complement and coagulation: strangers or partners in crime?2007In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 28, no 4, p. 184-192Article, review/survey (Refereed)
    Abstract [en]

    The convergence between complement and the clotting system extends far beyond the chemical nature of the complement and coagulation components, both of which form proteolytic cascades. Complement effectors directly enhance coagulation. These effects are supplemented by the interactions of complement with other inflammatory mediators that can increase the thrombogenicity of blood. In addition, complement inhibits anticoagulant factors. The crosstalk between complement and coagulation is also well illustrated by the ability of certain coagulation enzymes to activate complement components. Understanding the interplay between complement and coagulation has fundamental clinical implications in the context of diseases with an inflammatory pathogenesis, in which complement-coagulation interactions contribute to the development of life-threatening complications. Here, we review the interactions of the complement system with hemostasis and their roles in various diseases.

  • 5.
    Nilsson, Bo
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Clinical Immunology.
    Korsgren, Olle
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Clinical Immunology.
    Lambris, John D.
    Ekdahl, Kristina Nilsson
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Clinical Immunology.
    Can cells and biomaterials in therapeutic medicine be shielded from innate immune recognition?2010In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 31, no 1, p. 32-38Article, review/survey (Refereed)
    Abstract [en]

    Biomaterials (e.g. polymers, metals, or ceramics), cell and cell cluster (e.g. pancreatic islets) transplantation are beginning to offer novel treatment modalities for some otherwise intractable diseases. The innate immune system is involved in incompatibility reactions that occur when biomaterials or cells are introduced into the blood circulation. In particular, the complement, coagulation and contact systems are involved in the recognition of biomaterials and cells, eliciting activation of platelets and leukocytes. Such treatments are associated with anaphylactoid and thrombotic reactions, inflammation, and rejection of biomaterials and cells, leading to treatment failures and adverse reactions. We discuss here the new technologies that are being developed to shield the biomaterial and cell surfaces from recognition by the innate immune system.

  • 6. Pejler, Gunnar
    et al.
    Knight, Stefan D.
    Swedish University of Agricultural Sciences, Dept of Molecular Biology, Uppsala, Sweden.
    Henningson, Frida
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Wernersson, Sara
    Novel insights into the biological function of mast cell carboxypeptidase A2009In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 30, no 8, p. 401-408Article, review/survey (Refereed)
    Abstract [en]

    When mast cells are activated they can respond by releasing their secretory granule compounds, including mast cell-specific proteases of chymase, tryptase and carboxypeptidase A (MC-CPA) type. MC-CPA is a dominant protein component of the mast cell granule and the MC-CPA gene is extremely highly expressed. Despite this, relatively little has been known of its biological function. However, the recent generation of mouse strains lacking MC-CPA has opened up new possibilities for investigations related to this protease. This recent development has revealed a role for MC-CPA in regulating innate immunity responses, including the degradation of harmful substances such as the vasoconstrictive factor endothelin 1 and snake venom toxins. Here, we summarize the current knowledge of MC-CPA.

  • 7.
    Phillipson, Mia
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
    Kubes, Paul
    Univ Calgary, Snyder Inst Infect Immun & Inflammat, Calgary, AB T2N 4N1, Canada;Univ Calgary, Dept Physiol & Pharmacol, Calgary, AB T2N 4N1, Canada.
    The Healing Power of Neutrophils2019In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 40, no 7, p. 635-647Article, review/survey (Refereed)
    Abstract [en]

    Neutrophils promptly accumulate in large numbers at sites of tissue injury. Injuries to the skin or mucosae disrupt barriers against the external environment, and the bactericidal actions of neutrophils are important in preventing microbial invasion. Neutrophils have also been associated with exacerbated inflammation, for example in non-healing wounds or in conditions such as inflammatory bowel disease (IBD). However, additional neutrophil functions important for angiogenesis and tissue restoration have been uncovered in models of sterile and ischemic injury, as well as in tumors. These functions are also relevant in healing skin and mucosal wounds, and can be impaired in conditions associated with non-healing wounds, such as diabetes. Here, we discuss our current understanding of neutrophil contributions to healing, and how the latter can be compromised in disease.

  • 8.
    Sellin, Mikael E.
    et al.
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Maslowski, Kendle M.
    Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences, Yokohama 230-0045, Japan.
    Maloy, Kevin J.
    Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK.
    Wolf-Dietrich, Hardt
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Inflammasomes of the intestinal epithelium2015In: Trends in immunology, ISSN 1471-4906, E-ISSN 1471-4981, Vol. 36, no 8, p. 442-450Article in journal (Refereed)
    Abstract [en]

    While the functional importance of inflammasomes in blood-derived cell types is well established, it remains poorly understood how inflammasomes in nonhematopoietic cells contribute to mucosal immunity. Recent studies have revealed functional roles of inflammasomes - particularly NAIP/NLRC4, NLRP6, and noncanonical caspase-4 (caspase-11) - within epithelial cells of the gut in mucosal immune defense, inflammation, and tumorigenesis. Here, we review and discuss these findings in the broader context of tissue compartment-specific mucosal immunity. We propose several models whereby activities of the intestinal epithelial inflammasomes converge on mechanisms to remove compromised epithelial cells, maintain host-microbiota mutualism, and communicate with immune cells of the underlying lamina propria.

1 - 8 of 8
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