R
Rille Pullerits
Researcher at Sahlgrenska University Hospital
Publications - 77
Citations - 1507
Rille Pullerits is an academic researcher from Sahlgrenska University Hospital. The author has contributed to research in topics: Arthritis & Rheumatoid arthritis. The author has an hindex of 19, co-authored 56 publications receiving 1244 citations. Previous affiliations of Rille Pullerits include University of Gothenburg.
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High mobility group box chromosomal protein 1, a DNA binding cytokine, induces arthritis.
Rille Pullerits,Ing-Marie Jonsson,Margareta Verdrengh,Maria Bokarewa,Ulf Andersson,Helena Erlandsson-Harris,Andrej Tarkowski +6 more
TL;DR: The results indicate that HMGB-1 is not a mere expression of inflammatory responses, but on its own, it triggers joint inflammation by activating macrophages and inducing production of IL-1 via NF-kappaB activation.
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Decreased levels of soluble receptor for advanced glycation end products in patients with rheumatoid arthritis indicating deficient inflammatory control
TL;DR: It is concluded that a decreased level of sRAGE in patients with RA might increase the propensity towards inflammation, whereas treatment with methotrexate counteracts this feature.
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Soluble receptor for advanced glycation end products triggers a proinflammatory cytokine cascade via beta2 integrin Mac-1.
TL;DR: It is concluded that sRAGE interacts with Mac-1, thereby acting as an important proinflammatory and chemotactic molecule and was proven to act as a Chemotactic stimulus for neutrophils.
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The Combination of a Tumor Necrosis Factor Inhibitor and Antibiotic Alleviates Staphylococcal Arthritis and Sepsis in Mice
Ying Fei,Wanzhong Wang,Jakub Kwiecinski,Elisabet Josefsson,Rille Pullerits,Ing-Marie Jonsson,Mattias Magnusson,Tao Jin +7 more
TL;DR: Treatment with the combination of a TNF inhibitor and an antibiotic resulted in a quicker relief of clinical arthritis in mice with septic arthritis, and it was demonstrated that anti-TNF treatment downregulates high-mobility group protein B1 in staphylococcal enterotoxin shock syndrome.
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Extracellular cytochrome c, a mitochondrial apoptosis-related protein, induces arthritis
TL;DR: It is hypothesized that decreased levels of cytochrome c in RA patients reflect consumption of this molecule in the synovial tissue, decreasing apoptosis and shifting the balance towards inflammation.