Chromatin–IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors
By E. Leadbetter, I. Rifkin, A. Hohlbaum, Britte C. Beaudette, M. Shlomchik, A. Marshak‐Rothstein. Nature, 2002
2,079 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/71618a8982b9e3d63171df58c1399148e56e0ca4
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In Immunology
- Shizuo Akira
- R. Medzhitov
- Taro Kawai
- T. Mogensen
- Daniel B. Stetson
- O. Takeuchi
- B. Beutler
- Jonathan C. Kagan
Citations in the corpus
- Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “Binding of the immune complex by the BCR, or by the Fc R in the case of pDCs, is followed by BCR-mediated endocytosis and delivery of the immune complex to an endosomal compartment, which allows ssRNA and CpG DNA motifs within the autoantigen to activate the cell through TLR7 and TLR9, respectively ”
- Collaborative Induction of Inflammatory Responses by Dectin-1 and Toll-like Receptor 2 (2003, background): “One recent report has suggested that activation of autoreactive B cells by chromatin–IgG complexes occurs synergistically through the B cell receptor and a TLR (35).”
- Toll-like receptors in innate immunity. (2004, positive): “Sequential engagement of IgG2a–chromatin complex by the B cell receptor and TLR9 mediates effective production of rheumatoid factor by auto-reactive B cells (41).”
- Intracellular localization of Toll-like receptor 9 prevents recognition of self DNA but facilitates access to viral DNA (2006, background): “Mammalian DNA, for example, can stimulate TLR9 in some pathological situation”
- Endocytosis of HIV-1 activates plasmacytoid dendritic cells via Toll-like receptor-viral RNA interactions. (2005, neutral): “They are often utilized to demonstrate a TLR9 dependence in murine systems (27, 28, 65, 66).”
- Negative regulation of Toll-like receptor-mediated immune responses (2005, background): “fcgi?db=gene&cmd=Retrieve&dopt=Graphics&&list_uids=54106">TLR9 might also be involved in systemic lupus erythematosus by directly activating autoreactive B cell”