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Mrp8 and Mrp14 are endogenous activators of Toll-like receptor 4, promoting lethal, endotoxin-induced shock
TLDR
It is demonstrated that mice lacking Mrp8-Mrp14 complexes are protected from endotoxin-induced lethal shock and Escherichia coli–induced abdominal sepsis, indicating new inflammatory components that amplify phagocyte activation during sepsi upstream of TNFα–dependent effects.
Inhibition of dendritic cell differentiation and accumulation of myeloid-derived suppressor cells in cancer is regulated by S100A9 protein
TLDR
It is reported here that STAT3-inducible up-regulation of the myeloid-related protein S100A9 enhances MDSC production in cancer and reveals a novel molecular mechanism of immunological abnormalities in cancer.
S100 proteins expressed in phagocytes: a novel group of damage‐associated molecular pattern molecules
TLDR
Analyzing the molecular basis of the specific effects exhibited by S100 proteins in greater detail bears the potential to elucidate important mechanisms of innate immunity, to establish valid biomarkers of phagocytic inflammation, and eventually to reveal novel targets for innovative anti‐inflammatory therapies.
The endogenous Toll–like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancer
TLDR
S 100A8/S100A9 is not only involved in promoting the inflammatory response in infections but was also identified as a potent amplifier of inflammation in autoimmunity as well as in cancer development and tumor spread.
Staphylococcus aureus Panton-Valentine Leukocidin Is a Very Potent Cytotoxic Factor for Human Neutrophils
TLDR
The results question the value of infection-models in mice and non-human primates to elucidate the impact of PVL and suggest that PVL has an important cytotoxic role in human neutrophils, which has major implications for the pathogenesis of CA-MRSA infections.
Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel
TLDR
It is shown that Ni2+ triggered an inflammatory response by directly activating human Toll-like receptor 4 (TLR4), which implicate site-specific human TLR4 inhibition as a potential strategy for therapeutic intervention in CHS that would not affect vital immune responses.
Identification of Human S100A9 as a Novel Target for Treatment of Autoimmune Disease via Binding to Quinoline-3-Carboxamides
TLDR
The specific binding of quinoline-3-carboxamides to S100A9 explains the immunomodulatory activity of this class of compounds and defines S 100A9 as a novel target for treatment of human autoimmune diseases.
Loss of S100A9 (MRP14) Results in Reduced Interleukin-8-Induced CD11b Surface Expression, a Polarized Microfilament System, and Diminished Responsiveness to Chemoattractants In Vitro
TLDR
The data suggest that loss of the calcium-binding S100A9 protein reduces the responsiveness of the neutrophils upon chemoattractant stimuli at least in vitro, which may be responsible for the lack of any effect in the two in vivo models the authors have investigated so far.
Myeloid-related Protein (MRP) 8 and MRP14, Calcium-binding Proteins of the S100 Family, Are Secreted by Activated Monocytes via a Novel, Tubulin-dependent Pathway*
TLDR
The data provide evidence that the S100 proteins MRP8 and MRP14 are secreted after activation of protein kinase C via a novel pathway requiring an intact microtubule network and is associated with down-regulation of their de novo synthesis.
The Toll-like receptor 4 ligands Mrp8 and Mrp14 are crucial in the development of autoreactive CD8+ T cells
TLDR
It is shown in a mouse autoimmune model that local Mrp8 and Mrp14 production is essential for the induction of autoreactive CD8+ T cells and the development of systemic autoimmunity.
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