Results 41 to 50 of about 2,829,847 (276)

Macrophages exposed continuously to lipopolysaccharide and other agonists that act via toll-like receptors exhibit a sustained and additive activation state [PDF]

open access: yes, 2001
Background: Macrophages sense microorganisms through activation of members of the Toll-like receptor family, which initiate signals linked to transcription of many inflammation associated genes.
Aderem, A   +17 more
core   +1 more source

CSF-1 as a regulator of macrophage activation and immune responses [PDF]

open access: yes, 2003
Macrophage activation is a key determinant of susceptibility and pathology in a variety of inflammatory diseases. The extent of macrophage activation is tightly regulated by a number of pro-inflammatory cytokines (e.g.
Sweet, MJ   +3 more
core  

Spatiotemporal and quantitative analyses of phosphoinositides – fluorescent probe—and mass spectrometry‐based approaches

open access: yesFEBS Letters, EarlyView.
Fluorescent probes allow dynamic visualization of phosphoinositides in living cells (left), whereas mass spectrometry provides high‐sensitivity, isomer‐resolved quantitation (right). Their synergistic use captures complementary aspects of lipid signaling. This review illustrates how these approaches reveal the spatiotemporal regulation and quantitative
Hiroaki Kajiho   +3 more
wiley   +1 more source

Gut microbiome and aging—A dynamic interplay of microbes, metabolites, and the immune system

open access: yesFEBS Letters, EarlyView.
Age‐dependent shifts in microbial communities engender shifts in microbial metabolite profiles. These in turn drive shifts in barrier surface permeability of the gut and brain and induce immune activation. When paired with preexisting age‐related chronic inflammation this increases the risk of neuroinflammation and neurodegenerative diseases.
Aaron Mehl, Eran Blacher
wiley   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Immunology of Macrophage Activation Syndrome

open access: yes, 2021
Objectives Define Hemophagocytic LymphoHistiocytosis (HLH) and Macrophage Activation Syndrome (MAS) Describe genetic and immunological pathways involved in pathogenesis of MAS Explore immunological pathways as targets of ...
Ocon, Anthony
core  

PANoptosis in the pathogenesis of myelodysplastic syndromes

open access: yesMolecular Oncology, EarlyView.
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla   +4 more
wiley   +1 more source

Membrane changes in murine macrophages after in-vivo stimulation and activation [PDF]

open access: yes, 1983
The expression of various receptors and other surface determinants on resident, glycogen-and Corynebacterium parvum- elicited mouse peritoneal macrophages has been described.
GLASS, EJ, WEIR, DM, STEWART, J
core  

Systematic review: macrophage activation syndrome in inflammatory bowel disease [PDF]

open access: yes, 2013
BACKGROUND: Recently, there have been increasingly frequent reports on the occurrence of macrophage activation syndrome (MAS) in patients with inflammatory bowel disease (IBD).
Fries W, CASCIO, ANTONIO, COTTONE, Mario
core   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

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