A
Ann Marshak-Rothstein
Researcher at University of Massachusetts Medical School
Publications - 202
Citations - 19938
Ann Marshak-Rothstein is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Antigen & B cell. The author has an hindex of 58, co-authored 194 publications receiving 18851 citations. Previous affiliations of Ann Marshak-Rothstein include Fox Chase Cancer Center & Boston University.
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Journal ArticleDOI
Chromatin–IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors
Elizabeth A. Leadbetter,Ian R. Rifkin,Andreas Hohlbaum,Britte C. Beaudette,Mark J. Shlomchik,Ann Marshak-Rothstein +5 more
TL;DR: It is shown that effective activation of RF+ B cells is mediated by IgG2a–chromatin immune complexes and requires the synergistic engagement of the antigen receptor and a member of the MyD88-dependent Toll-like receptor (TLR) family.
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Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation
Shyr-Te Ju,David J. Panka,Haili Cui,Rachel Ettinger,Maan El-Khatib,David H. Sherr,Ben Z. Stanger,Ann Marshak-Rothstein +7 more
TL;DR: It is shown that receptor crosslinking induces Fas ligand and upregulates Fas, and that the ensuing engagement of Fas by Fasligand activates the cell-death programme.
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Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE.
Jane Tian,Ana M. Avalos,Su-Yau Mao,Bo Chen,Kannaki Senthil,Herren Wu,Peggy Parroche,Stacey Drabic,Douglas T. Golenbock,Cherilyn M. Sirois,Jing Hua,Ling-Ling An,Laurent P. Audoly,Greg La Rosa,Angelika Bierhaus,Peter Naworth,Ann Marshak-Rothstein,Mary K. Crow,Katherine A. Fitzgerald,Eicke Latz,Peter A. Kiener,Anthony J. Coyle +21 more
TL;DR: HMGB1, a nuclear DNA-binding protein released from necrotic cells, was an essential component of DNA-containing immune complexes that stimulated cytokine production through a TLR9–MyD88 pathway involving the multivalent receptor RAGE.
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Toll-like receptors in systemic autoimmune disease
TL;DR: Data are beginning to emerge showing that this is the case that in vivo activation of both autoreactive B cells and plasmacytoid dendritic cells by mammalian TLR ligands translates to an in vivo role in either the initiation or the progression of systemic autoimmune disease.
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RNA-associated autoantigens activate B cells by combined B cell antigen receptor/Toll-like receptor 7 engagement
Christina M. Lau,Courtney Broughton,Abigail S. Tabor,Shizuo Akira,Richard A. Flavell,Mark J. Mamula,Sean R. Christensen,Mark J. Shlomchik,Gregory A. Viglianti,Ian R. Rifkin,Ann Marshak-Rothstein +10 more
TL;DR: The response to RNA-associated autoantigens was markedly enhanced by IFN-α, a cytokine strongly linked to disease progression in patients with systemic lupus erythematosus (SLE), and this data implicate TLR recognition of endogenous ligands in the response to both DNA- and RNA- associated autoantIGens.