C
Caroline A. Jefferies
Researcher at Cedars-Sinai Medical Center
Publications - 91
Citations - 5876
Caroline A. Jefferies is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Innate immune system & Inflammation. The author has an hindex of 36, co-authored 84 publications receiving 5054 citations. Previous affiliations of Caroline A. Jefferies include Trinity College, Dublin & Royal College of Surgeons in Ireland.
Papers
More filters
Journal ArticleDOI
Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction
Katherine A. Fitzgerald,Eva M. Palsson-McDermott,Andrew G. Bowie,Andrew G. Bowie,Caroline A. Jefferies,Ashley Mansell,Gerard Brady,Elizabeth Brint,Aisling Dunne,Pearl Gray,Mary T. Harte,Diane McMurray,Dirk E. Smith,John E. Sims,T. A. Bird,Luke A. J. O'Neill +15 more
TL;DR: A protein is described, Mal (MyD88-adapter-like), which joins MyD88 as a cytoplasmic TIR-domain-containing protein in the human genome, which is therefore an adapter in TLR-4 signal transduction.
Journal ArticleDOI
Targeted Liposomal Drug Delivery to Monocytes and Macrophages
TL;DR: The goal for targeting monocytes/macrophages using liposomes includes not only drug delivery but also potentially a role in cell ablation and cell activation for the treatment of conditions including cancer, atherosclerosis, HIV, and chronic inflammation.
Journal ArticleDOI
Bruton's Tyrosine Kinase Is a Toll/Interleukin-1 Receptor Domain-binding Protein That Participates in Nuclear Factor κB Activation by Toll-like Receptor 4
Caroline A. Jefferies,Sarah L. Doyle,Cornelia Brunner,Aisling Dunne,Elizabeth Brint,Claudia Wietek,Eva Walch,Thomas Wirth,Luke A. J. O'Neill +8 more
TL;DR: Investigation revealed that the Btk-specific inhibitor, LFM-A13, inhibited the activation of NFκB by LPS in THP-1 cells, implicate Btk as a Toll/interleukin-1 receptor domain-binding protein that is important for NFκBs activation by TLR4.
Journal ArticleDOI
Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23–Th17 pathway
Alexander Espinosa,Valerie Dardalhon,Susanna Brauner,Aurélie Ambrosi,Rowan Higgs,Fransisco J. Quintana,Maria Sjöstrand,Maija-Leena Eloranta,Joan Ní Gabhann,Ola Winqvist,Birgitta Sundelin,Caroline A. Jefferies,Björn Rozell,Vijay K. Kuchroo,Marie Wahren-Herlenius +14 more
TL;DR: Data reveal that the lupus-associated Ro52 protein is an important negative regulator of proinflammatory cytokine production, and they provide a mechanism by which a defective Ro52 function can lead to tissue inflammation and systemic autoimmunity through the IL-23–Th17 pathway.
Journal ArticleDOI
The E3 Ubiquitin Ligase Ro52 Negatively Regulates IFN-β Production Post-Pathogen Recognition by Polyubiquitin-Mediated Degradation of IRF3
Rowan Higgs,Joan Ní Gabhann,Nadia Ben Larbi,Eamon P. Breen,Katherine A. Fitzgerald,Caroline A. Jefferies +5 more
TL;DR: A novel role for Ro52 is demonstrated in turning off and thus limiting IRF3-dependent type I IFN production by targeting the transcription factor for polyubiquitination and subsequent proteasomal degradation.