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Cited by 64 publications
(71 citation statements)
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References 82 publications
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“…In CIA and EAE, both endogenous IL-10 and IFN-γ have a clearcut disease-protective role, and it is intriguing to speculate that at least part of the protective role of IFN-γ resides in the stimulation of CpG-induced IL-10 [82][83][84][85][86]. Furthermore, together with the knowledge that autoimmune symptoms are exacerbated in the absence of TLR9 [87][88][89] and the observation that CpG stimulation can inhibit disease in experimental autoimmune animal models [90,91], our data and others [87,92] identify TLR9-triggering as a potential key event in the regulation of autoimmunity.…”
Section: Discussionmentioning
confidence: 99%
“…In CIA and EAE, both endogenous IL-10 and IFN-γ have a clearcut disease-protective role, and it is intriguing to speculate that at least part of the protective role of IFN-γ resides in the stimulation of CpG-induced IL-10 [82][83][84][85][86]. Furthermore, together with the knowledge that autoimmune symptoms are exacerbated in the absence of TLR9 [87][88][89] and the observation that CpG stimulation can inhibit disease in experimental autoimmune animal models [90,91], our data and others [87,92] identify TLR9-triggering as a potential key event in the regulation of autoimmunity.…”
Section: Discussionmentioning
confidence: 99%
“…Leadbetter et al, showed that BCR-mediated delivery of TLR antigens is a potential mechanism for delivery of autoantigens (chromatin) that can activate autoreactive B cells [37]. Data from our lab provides further mechanistic insights into this phenomenon; when a B cell is stimulated via this route and survives, it expresses T-bet in the presence of IL-21 or IFNγ and promotes class-switching to antibodies of the IgG 2a/c isotype [38]. This points to the existence of a TLR-driven checkpoint to regulate survival of autoreactive clones and the implication of T-bet in promoting detrimental autoimmune responses.…”
Section: Signals Driving T-bet In B Cellsmentioning
confidence: 93%
“…73 Interestingly, treatment with the Th2-type cytokine IL-4 pre- T-bet + B cell development is peculiar in that it does not require BCR signaling in vitro. 74 Presumably, this phenomenon acts as a peripheral tolerance mechanism to prevent autoimmune responses against DNA antigens, but cells can be saved from apoptosis by survival signals or appropriate cytokines produced during infection responses. 74 Presumably, this phenomenon acts as a peripheral tolerance mechanism to prevent autoimmune responses against DNA antigens, but cells can be saved from apoptosis by survival signals or appropriate cytokines produced during infection responses.…”
Section: Innatesensorsignalsandth1cytokinespoise Bcellstoadoptt-betmentioning
confidence: 99%