FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2149476900> ?p ?o ?g. }

• W2149476900 endingPage "4330" @default.
• W2149476900 startingPage "4319" @default.
• W2149476900 abstract "Abstract The K/BxN serum transfer model of arthritis is critically dependent on FcγR signaling events mediated by spleen tyrosine kinase (Syk). However, the specific cell types in which this signaling is required are not known. We report that deletion of Syk in neutrophils, achieved using sykf/f MRP8-cre+ mice, blocks disease development in serum transfer arthritis. The sykf/f MRP8-cre+ mice display absent joint disease and reduced deposition of pathogenic anti–glucose-6-phosphate isomerase Abs in the joint (with a reciprocal accumulation of these Abs in the peripheral circulation). Additionally, sykf/f MRP8-cre+ mice manifest poor edema formation within 3 h after formation of cutaneous immune complexes (Arthus reaction). Together, this suggests that neutrophil-dependent recognition of immune complexes contributes significantly to changes in vascular permeability during the early phases of immune complex disease. Using mixed chimeric mice, containing both wild-type and sykf/f MRP8-cre+ neutrophils, we find no impairment in recruitment of Syk-deficient neutrophils to the inflamed joint, but they fail to become primed, demonstrating lower cytokine production after removal from the joint. They also display an increased apoptotic rate compared with wild-type cells in the same joint. Mast cell-deficient c-kitsh/sh mice developed robust arthritis after serum transfer whereas c-kitW/Wv mice did not, suggesting that previous conclusions concerning the central role of mast cells in this model may need to be revised. Basophil-deficient mice also responded normally to K/BxN serum transfer. These results demonstrate that Syk-dependent signaling in neutrophils alone is critically required for arthritis development in the serum transfer model." @default.
• W2149476900 created "2016-06-24" @default.
• W2149476900 creator A5012670880 @default.
• W2149476900 creator A5022168593 @default.
• W2149476900 creator A5028062932 @default.
• W2149476900 creator A5051185090 @default.
• W2149476900 creator A5066993086 @default.
• W2149476900 creator A5082818365 @default.
• W2149476900 date "2011-10-15" @default.
• W2149476900 modified "2023-09-29" @default.
• W2149476900 title "Deletion of Syk in Neutrophils Prevents Immune Complex Arthritis" @default.
• W2149476900 cites W1494419854 @default.
• W2149476900 cites W1550658501 @default.
• W2149476900 cites W1578893636 @default.
• W2149476900 cites W1595293335 @default.
• W2149476900 cites W1638726768 @default.
• W2149476900 cites W1950593974 @default.
• W2149476900 cites W1980042341 @default.
• W2149476900 cites W1982709334 @default.
• W2149476900 cites W1993316162 @default.
• W2149476900 cites W1995455646 @default.
• W2149476900 cites W1996058409 @default.
• W2149476900 cites W1998533172 @default.
• W2149476900 cites W1999398455 @default.
• W2149476900 cites W2001328992 @default.
• W2149476900 cites W2011473183 @default.
• W2149476900 cites W2011515061 @default.
• W2149476900 cites W2012326387 @default.
• W2149476900 cites W2013216643 @default.
• W2149476900 cites W2014566875 @default.
• W2149476900 cites W2017014846 @default.
• W2149476900 cites W2017341404 @default.
• W2149476900 cites W2024939178 @default.
• W2149476900 cites W2028561950 @default.
• W2149476900 cites W2029993165 @default.
• W2149476900 cites W2032837321 @default.
• W2149476900 cites W2045980139 @default.
• W2149476900 cites W2050069950 @default.
• W2149476900 cites W2057148259 @default.
• W2149476900 cites W2069375519 @default.
• W2149476900 cites W2074171762 @default.
• W2149476900 cites W2075372304 @default.
• W2149476900 cites W2075675512 @default.
• W2149476900 cites W2081324045 @default.
• W2149476900 cites W2085035241 @default.
• W2149476900 cites W2086734015 @default.
• W2149476900 cites W2089782191 @default.
• W2149476900 cites W2091836237 @default.
• W2149476900 cites W2100690094 @default.
• W2149476900 cites W2110578003 @default.
• W2149476900 cites W2111167373 @default.
• W2149476900 cites W2111935270 @default.
• W2149476900 cites W2115079945 @default.
• W2149476900 cites W2117276705 @default.
• W2149476900 cites W2123473370 @default.
• W2149476900 cites W2124678205 @default.
• W2149476900 cites W2124927041 @default.
• W2149476900 cites W2133326206 @default.
• W2149476900 cites W2135276664 @default.
• W2149476900 cites W2135577920 @default.
• W2149476900 cites W2136389594 @default.
• W2149476900 cites W2136861118 @default.
• W2149476900 cites W2142739945 @default.
• W2149476900 cites W2143036393 @default.
• W2149476900 cites W2149622090 @default.
• W2149476900 cites W2151751911 @default.
• W2149476900 cites W2160211752 @default.
• W2149476900 cites W2165117650 @default.
• W2149476900 cites W2170532254 @default.
• W2149476900 doi "https://doi.org/10.4049/jimmunol.1100341" @default.
• W2149476900 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3186826" @default.
• W2149476900 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21918195" @default.
• W2149476900 hasPublicationYear "2011" @default.
• W2149476900 type Work @default.
• W2149476900 sameAs 2149476900 @default.
• W2149476900 citedByCount "86" @default.
• W2149476900 countsByYear W21494769002012 @default.
• W2149476900 countsByYear W21494769002013 @default.
• W2149476900 countsByYear W21494769002014 @default.
• W2149476900 countsByYear W21494769002015 @default.
• W2149476900 countsByYear W21494769002016 @default.
• W2149476900 countsByYear W21494769002017 @default.
• W2149476900 countsByYear W21494769002018 @default.
• W2149476900 countsByYear W21494769002019 @default.
• W2149476900 countsByYear W21494769002020 @default.
• W2149476900 countsByYear W21494769002021 @default.
• W2149476900 countsByYear W21494769002022 @default.
• W2149476900 countsByYear W21494769002023 @default.
• W2149476900 crossrefType "journal-article" @default.
• W2149476900 hasAuthorship W2149476900A5012670880 @default.
• W2149476900 hasAuthorship W2149476900A5022168593 @default.
• W2149476900 hasAuthorship W2149476900A5028062932 @default.
• W2149476900 hasAuthorship W2149476900A5051185090 @default.
• W2149476900 hasAuthorship W2149476900A5066993086 @default.
• W2149476900 hasAuthorship W2149476900A5082818365 @default.
• W2149476900 hasBestOaLocation W21494769001 @default.
• W2149476900 hasConcept C185592680 @default.
• W2149476900 hasConcept C203014093 @default.

• next