FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2123097188> ?p ?o ?g. }

• W2123097188 endingPage "3663" @default.
• W2123097188 startingPage "3656" @default.
• W2123097188 abstract "Although reports documented aberrant cytokine expression in autoimmune bullous dermatoses (AIBDs), cytokine-targeting therapies have not been established in these disorders. We showed previously that IL-6 treatment protected against tissue destruction in experimental epidermolysis bullosa acquisita (EBA), an AIBD caused by autoantibodies to type VII collagen (COL7). The anti-inflammatory effects of IL-6 were mediated by induction of IL-1ra, and prophylactic IL-1ra administration prevented blistering. In this article, we demonstrate elevated serum concentrations of IL-1β in both mice with experimental EBA induced by injection of anti-COL7 IgG and in EBA patients. Increased IL-1α and IL-1β expression also was observed in the skin of anti-COL7 IgG-injected wild-type mice compared with the significantly less diseased IL-1R-deficient or wild-type mice treated with the IL-1R antagonist anakinra or anti-IL-1β. These findings suggested that IL-1 contributed to recruitment of inflammatory cells into the skin. Accordingly, the expression of ICAM-1 was decreased in IL-1R-deficient and anakinra-treated mice injected with anti-COL7. This effect appeared to be specifically attributable to IL-1 because anakinra blocked the upregulation of different endothelial adhesion molecules on IL-1-stimulated, but not on TNF-α-stimulated, cultured endothelial cells. Interestingly, injection of caspase-1/11-deficient mice with anti-COL7 IgG led to the same extent of skin lesions as in wild-type mice. Collectively, our data suggest that IL-1, independently of caspase-1, contributes to the pathogenesis of EBA. Because anti-IL-1β in a prophylactic setting and anakinra in a quasi-therapeutic setting (i.e., when skin lesions had already developed) improved experimental EBA, IL-1 appears to be a potential therapeutic target for EBA and related AIBDs." @default.
• W2123097188 created "2016-06-24" @default.
• W2123097188 creator A5006462331 @default.
• W2123097188 creator A5008159107 @default.
• W2123097188 creator A5012474305 @default.
• W2123097188 creator A5021559096 @default.
• W2123097188 creator A5022929399 @default.
• W2123097188 creator A5023586872 @default.
• W2123097188 creator A5043316836 @default.
• W2123097188 creator A5043602264 @default.
• W2123097188 creator A5059140139 @default.
• W2123097188 creator A5059824274 @default.
• W2123097188 creator A5067198663 @default.
• W2123097188 creator A5070449313 @default.
• W2123097188 creator A5075201374 @default.
• W2123097188 creator A5083484570 @default.
• W2123097188 creator A5089977110 @default.
• W2123097188 creator A5090549024 @default.
• W2123097188 date "2015-04-15" @default.
• W2123097188 modified "2023-10-13" @default.
• W2123097188 title "Caspase-1–Independent IL-1 Release Mediates Blister Formation in Autoantibody-Induced Tissue Injury through Modulation of Endothelial Adhesion Molecules" @default.
• W2123097188 cites W1510204727 @default.
• W2123097188 cites W1533217355 @default.
• W2123097188 cites W1583757072 @default.
• W2123097188 cites W1912288378 @default.
• W2123097188 cites W1951152790 @default.
• W2123097188 cites W1953849107 @default.
• W2123097188 cites W1976843984 @default.
• W2123097188 cites W1984289484 @default.
• W2123097188 cites W1986843662 @default.
• W2123097188 cites W1991155077 @default.
• W2123097188 cites W1998012332 @default.
• W2123097188 cites W2000111560 @default.
• W2123097188 cites W2003892236 @default.
• W2123097188 cites W2007033792 @default.
• W2123097188 cites W2014371671 @default.
• W2123097188 cites W2019678455 @default.
• W2123097188 cites W2031680195 @default.
• W2123097188 cites W2032259307 @default.
• W2123097188 cites W2035557737 @default.
• W2123097188 cites W2072785143 @default.
• W2123097188 cites W2075953207 @default.
• W2123097188 cites W2084180208 @default.
• W2123097188 cites W2089216091 @default.
• W2123097188 cites W2097207838 @default.
• W2123097188 cites W2102143428 @default.
• W2123097188 cites W2108373994 @default.
• W2123097188 cites W2110463517 @default.
• W2123097188 cites W2111620283 @default.
• W2123097188 cites W2118151585 @default.
• W2123097188 cites W2139935948 @default.
• W2123097188 cites W2142275262 @default.
• W2123097188 cites W2142709180 @default.
• W2123097188 cites W2150107812 @default.
• W2123097188 cites W4211003831 @default.
• W2123097188 cites W4233561050 @default.
• W2123097188 cites W4243974294 @default.
• W2123097188 doi "https://doi.org/10.4049/jimmunol.1402688" @default.
• W2123097188 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25795756" @default.
• W2123097188 hasPublicationYear "2015" @default.
• W2123097188 type Work @default.
• W2123097188 sameAs 2123097188 @default.
• W2123097188 citedByCount "38" @default.
• W2123097188 countsByYear W21230971882015 @default.
• W2123097188 countsByYear W21230971882016 @default.
• W2123097188 countsByYear W21230971882017 @default.
• W2123097188 countsByYear W21230971882018 @default.
• W2123097188 countsByYear W21230971882019 @default.
• W2123097188 countsByYear W21230971882020 @default.
• W2123097188 countsByYear W21230971882021 @default.
• W2123097188 countsByYear W21230971882023 @default.
• W2123097188 crossrefType "journal-article" @default.
• W2123097188 hasAuthorship W2123097188A5006462331 @default.
• W2123097188 hasAuthorship W2123097188A5008159107 @default.
• W2123097188 hasAuthorship W2123097188A5012474305 @default.
• W2123097188 hasAuthorship W2123097188A5021559096 @default.
• W2123097188 hasAuthorship W2123097188A5022929399 @default.
• W2123097188 hasAuthorship W2123097188A5023586872 @default.
• W2123097188 hasAuthorship W2123097188A5043316836 @default.
• W2123097188 hasAuthorship W2123097188A5043602264 @default.
• W2123097188 hasAuthorship W2123097188A5059140139 @default.
• W2123097188 hasAuthorship W2123097188A5059824274 @default.
• W2123097188 hasAuthorship W2123097188A5067198663 @default.
• W2123097188 hasAuthorship W2123097188A5070449313 @default.
• W2123097188 hasAuthorship W2123097188A5075201374 @default.
• W2123097188 hasAuthorship W2123097188A5083484570 @default.
• W2123097188 hasAuthorship W2123097188A5089977110 @default.
• W2123097188 hasAuthorship W2123097188A5090549024 @default.
• W2123097188 hasBestOaLocation W21230971881 @default.
• W2123097188 hasConcept C104317684 @default.
• W2123097188 hasConcept C126322002 @default.
• W2123097188 hasConcept C127561419 @default.
• W2123097188 hasConcept C149892131 @default.
• W2123097188 hasConcept C159654299 @default.
• W2123097188 hasConcept C16224149 @default.
• W2123097188 hasConcept C163764329 @default.
• W2123097188 hasConcept C170493617 @default.
• W2123097188 hasConcept C17991360 @default.

• next