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  • 1.
    Chen, Yunying
    et al.
    Karolinska Institutet.
    Wermeling, Fredrik
    Karolinska Institutet.
    Sundqvist, Johanna
    Karolinska Institutet.
    Jonsson, Ann-Beth
    Stockholm University, Faculty of Science, Department of Genetics, Microbiology and Toxicology.
    Tryggvason, Karl
    Karolinska Institutet.
    Pikkarainen, Timo
    Karolinska Institutet.
    Karlsson, Mikael C I
    Karolinska Institutet.
    A regulatory role for macrophage class A scavenger receptors in TLR4-mediated LPS responses.2010In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 40, no 5, p. 1451-60Article in journal (Refereed)
    Abstract [en]

    Recognition of microbial components by TLR, key sensors of infection, leads to induction of inflammatory responses. We found that, in vivo, TLR4 engagement by LPS induces up-regulation of the class A scavenger receptors (SR) macrophage receptor with a collagenous structure (MARCO) and SR-A, which occurs, at least in the case of MARCO, via both MyD88-dependent and -independent pathways. When challenging mice with a low dose of LPS followed by a high dose, class A SR-deficient mice showed a higher survival rate than WT mice. This was paired with increased production of IL-10 and anti-LPS Ab, as well as increased activation status of marginal zone B cells. However, the receptors were not crucial for survival when challenging mice i.p. with Neisseria meningitidis or Listeria monocytogenes, but they were found to contribute to microbial capture and clearance. This indicates physiological significance for the up-regulation of class A SR during early stages of bacterial infection. Thus, we believe that we have revealed a mechanism where SR regulate the activation status of the immune system and are involved in balancing a proper immune response to infection. This regulation could also be important in maintaining tolerance since these receptors have been shown to be involved in regulation of self-reactivity.

  • 2. Palma, Carla
    et al.
    Schiavoni, Giovanna
    Abalsamo, Laura
    Mattei, Fabrizio
    Piccaro, Giovanni
    Sanchez, Massimo
    Fernandez, Carmen
    Stockholm University, Faculty of Science, The Wenner-Gren Institute, Immunology.
    Singh, Mahavir
    Gabriele, Lucia
    Mycobacterium tuberculosis PstS1 amplifies IFN-gamma and induces IL-17/IL-22 responses by unrelated memory CD4(+) T cells via dendritic cell activation2013In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 43, no 9, p. 2386-2397Article in journal (Refereed)
    Abstract [en]

    The immunological mechanisms that modulate protection during Mycobacterium tuberculosis (Mtb) infection or vaccination are not fully understood. Secretion of IFN- and, to a lesser extent, of IL-17 by CD4(+) T cells plays a major role both in protection and immunopathology. Few MtbAgs interacting with DCs affect priming, activation, and regulation of Ag-unrelated CD4(+) T-cell responses. Here we demonstrate that PstS1, a 38 kDa-lipoprotein of Mtb, promotes Ag-independent activation of memory T lymphocytes specific for Ag85B or Ag85A, two immunodominant protective Ags of Mtb. PstS1 expands CD4(+) and CD8(+) memory T cells, amplifies secretion of IFN- and IL-22 and induces IL-17 production by effector memory cells in an Ag-unrelated manner in vitro and in vivo. These effects were mediated through the stimulation of DCs, particularly of the CD8(-) subtype, which respond to PstS1 by undergoing phenotypic maturation and by secreting IL-6, IL-1 and, to a lower extent, IL-23. IL-6 secretion by PstS1-stimulated DCs was required for IFN-, and to a lesser extent for IL-22 responses by Ag85B-specific memory T cells. These results may open new perspectives for immunotherapeutic strategies to control Th1/Th17 immune responses in Mtb infections and in vaccinations against tuberculosis.

  • 3.
    Wang, Xiao
    et al.
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Zhang, Ding
    Sjölinder, Mikael
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Wan, Yi
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Sjölinder, Hong
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. Mälar Hospital, Sweden.
    CD46 accelerates macrophage-mediated host susceptibility to meningococcal sepsis in a murine model2017In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 47, no 1, p. 119-130Article in journal (Refereed)
    Abstract [en]

    CD46, a membrane cofactor expressed on all nucleated human cells, plays an essential role in suppressing autoimmune reactions and protecting host cells from complement-mediated attack. Human transgenic CD46 homozygousmice (CD46(+/+)) are prone to lethal sepsis upon infection with Neisseria meningitidis (N. meningitidis). However, the underlying mechanisms are poorly understood. Here, we determined thatCD46(+/+) mice produce large numbers of M1 type macrophages with enhanced surface expression of MHC II and production of pro-inflammatory mediators such as IL-6, TNF, IL-12, and IL-1 beta In the presence of M-CSF or GM-CSF, CD46 signaling enhances monocyte-macrophage differentiation. Additionally, CD46(+/+) macrophages rapidly undergo apoptosis upon LPS challenge or meningococcal infection, which could contribute to uncontrolled bacterial dissemination in vivo. Adoptive transfer of CD46(+/+) peritoneal macrophages aggravated septic responses in wild-type mice, but the depletion of macrophages partially alleviated septic reactions in CD46(+/+) mice after N. meningitidis infection. Our findings reveal a novel role of CD46 in accelerating inflammatory responses upon meningococcal infection or LPS stimulation by regulating the functional polarization and survival of macrophages.

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