Matches in SemOpenAlex for { <https://semopenalex.org/work/W2142623408> ?p ?o ?g. }
- W2142623408 endingPage "1255" @default.
- W2142623408 startingPage "1248" @default.
- W2142623408 abstract "Abstract Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the CNS, most frequently starting with a series of bouts, each followed by complete remission and then a secondary, progressive phase during which the neurological deficit increases steadily. The underlying molecular mechanisms responsible for disease progression are still unclear. Herein, we demonstrate that high mobility group box chromosomal protein 1 (HMGB1), a DNA-binding protein with proinflammatory properties, is evident in active lesions of MS and experimental autoimmune encephalomyelitis (EAE) and that HMGB1 levels correlate with active inflammation. Furthermore, the expression of the innate HMGB1 receptors—receptor for advanced glycation end products, TLR2, and TLR4—was also highly increased in MS and rodent EAE. Additionally, in vitro activation of rodent CNS-derived microglia and bone marrow-derived macrophages demonstrated that microglia were equally as capable as macrophages of translocating HMGB1 following LPS/IFN-γ stimulation. Significant expression of HMGB1 and its receptors on accumulating activated macrophages and resident microglia may thus provide a positive feedback loop that amplifies the inflammatory response during MS and EAE pathogenesis." @default.
- W2142623408 created "2016-06-24" @default.
- W2142623408 creator A5005108165 @default.
- W2142623408 creator A5012427776 @default.
- W2142623408 creator A5016015447 @default.
- W2142623408 creator A5032636253 @default.
- W2142623408 creator A5038376395 @default.
- W2142623408 creator A5038736969 @default.
- W2142623408 creator A5050861407 @default.
- W2142623408 creator A5056853471 @default.
- W2142623408 creator A5070191665 @default.
- W2142623408 creator A5078164607 @default.
- W2142623408 creator A5084870559 @default.
- W2142623408 date "2008-07-21" @default.
- W2142623408 modified "2023-10-01" @default.
- W2142623408 title "Pivotal Advance: HMGB1 expression in active lesions of human and experimental multiple sclerosis" @default.
- W2142623408 cites W1489842152 @default.
- W2142623408 cites W1492105728 @default.
- W2142623408 cites W1503511302 @default.
- W2142623408 cites W1590156932 @default.
- W2142623408 cites W1930867397 @default.
- W2142623408 cites W1966921625 @default.
- W2142623408 cites W1977724594 @default.
- W2142623408 cites W1998505004 @default.
- W2142623408 cites W2000281764 @default.
- W2142623408 cites W2004266769 @default.
- W2142623408 cites W2005640704 @default.
- W2142623408 cites W2016232550 @default.
- W2142623408 cites W2021736304 @default.
- W2142623408 cites W2026885016 @default.
- W2142623408 cites W2029068688 @default.
- W2142623408 cites W2034311142 @default.
- W2142623408 cites W2059217150 @default.
- W2142623408 cites W2061163173 @default.
- W2142623408 cites W2061449596 @default.
- W2142623408 cites W2065427271 @default.
- W2142623408 cites W2075316492 @default.
- W2142623408 cites W2079407096 @default.
- W2142623408 cites W2080126967 @default.
- W2142623408 cites W2092272732 @default.
- W2142623408 cites W2096678432 @default.
- W2142623408 cites W2097391811 @default.
- W2142623408 cites W2100706488 @default.
- W2142623408 cites W2101520046 @default.
- W2142623408 cites W2103272567 @default.
- W2142623408 cites W2105490558 @default.
- W2142623408 cites W2107865650 @default.
- W2142623408 cites W2109342780 @default.
- W2142623408 cites W2115293825 @default.
- W2142623408 cites W2117340207 @default.
- W2142623408 cites W2117783767 @default.
- W2142623408 cites W2118296597 @default.
- W2142623408 cites W2134106169 @default.
- W2142623408 cites W2164714222 @default.
- W2142623408 cites W2168643298 @default.
- W2142623408 cites W2339472091 @default.
- W2142623408 doi "https://doi.org/10.1189/jlb.1207844" @default.
- W2142623408 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18644848" @default.
- W2142623408 hasPublicationYear "2008" @default.
- W2142623408 type Work @default.
- W2142623408 sameAs 2142623408 @default.
- W2142623408 citedByCount "189" @default.
- W2142623408 countsByYear W21426234082012 @default.
- W2142623408 countsByYear W21426234082013 @default.
- W2142623408 countsByYear W21426234082014 @default.
- W2142623408 countsByYear W21426234082015 @default.
- W2142623408 countsByYear W21426234082016 @default.
- W2142623408 countsByYear W21426234082017 @default.
- W2142623408 countsByYear W21426234082018 @default.
- W2142623408 countsByYear W21426234082019 @default.
- W2142623408 countsByYear W21426234082020 @default.
- W2142623408 countsByYear W21426234082021 @default.
- W2142623408 countsByYear W21426234082022 @default.
- W2142623408 countsByYear W21426234082023 @default.
- W2142623408 crossrefType "journal-article" @default.
- W2142623408 hasAuthorship W2142623408A5005108165 @default.
- W2142623408 hasAuthorship W2142623408A5012427776 @default.
- W2142623408 hasAuthorship W2142623408A5016015447 @default.
- W2142623408 hasAuthorship W2142623408A5032636253 @default.
- W2142623408 hasAuthorship W2142623408A5038376395 @default.
- W2142623408 hasAuthorship W2142623408A5038736969 @default.
- W2142623408 hasAuthorship W2142623408A5050861407 @default.
- W2142623408 hasAuthorship W2142623408A5056853471 @default.
- W2142623408 hasAuthorship W2142623408A5070191665 @default.
- W2142623408 hasAuthorship W2142623408A5078164607 @default.
- W2142623408 hasAuthorship W2142623408A5084870559 @default.
- W2142623408 hasConcept C136449434 @default.
- W2142623408 hasConcept C164027704 @default.
- W2142623408 hasConcept C170493617 @default.
- W2142623408 hasConcept C203014093 @default.
- W2142623408 hasConcept C2776070231 @default.
- W2142623408 hasConcept C2776914184 @default.
- W2142623408 hasConcept C2778486448 @default.
- W2142623408 hasConcept C2779830541 @default.
- W2142623408 hasConcept C2780545709 @default.
- W2142623408 hasConcept C2780640218 @default.
- W2142623408 hasConcept C2780942790 @default.
- W2142623408 hasConcept C2781236682 @default.