2004
DOI: 10.1126/science.1093889
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Modulation of Th1 Activation and Inflammation by the NF-κB Repressor Foxj1

Abstract: Forkhead transcription factors play key roles in the regulation of immune responses. Here, we identify a role for one member of this family, Foxj1, in the regulation of T cell activation and autoreactivity. Foxj1 deficiency resulted in multiorgan systemic inflammation, exaggerated Th1 cytokine production, and T cell proliferation in autologous mixed lymphocyte reactions. Foxj1 suppressed NF-kappaB transcription activity in vitro, and Foxj1-deficient T cells possessed increased NF-kappaB activity in vivo, corre… Show more

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Cited by 139 publications
(136 citation statements)
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References 20 publications
(38 reference statements)
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“…As judged by microsatellite markers, mice mutant for Foxj1, which is located on chromosome 11 at 78.0 cM, were homozygotic for C57BL/6 loci, including marker D11Mit333 (66.0 cM; 11qter is ϳ80.0 cM), indicating a Ͻ15 cM residual 129 contribution on chromosome 11. Foxj1 ϩ/ϩ and Ϫ/Ϫ fetal liver chimeras (FLCs) 3 were generated in irradiated Rag-2-deficient hosts as previously described (2). For B cell-only chimeras (BOC), fetal livers from Foxj1 ϩ/ϩ vs Ϫ/Ϫ (CD45.2 ϩ IgH b ) embryos were adoptively transferred into irradiated C57BL/6-nu/nu hosts, and reconstitution of the peripheral B cell lineage was allowed for 8 -12 wk.…”
Section: Methodsmentioning
confidence: 99%
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“…As judged by microsatellite markers, mice mutant for Foxj1, which is located on chromosome 11 at 78.0 cM, were homozygotic for C57BL/6 loci, including marker D11Mit333 (66.0 cM; 11qter is ϳ80.0 cM), indicating a Ͻ15 cM residual 129 contribution on chromosome 11. Foxj1 ϩ/ϩ and Ϫ/Ϫ fetal liver chimeras (FLCs) 3 were generated in irradiated Rag-2-deficient hosts as previously described (2). For B cell-only chimeras (BOC), fetal livers from Foxj1 ϩ/ϩ vs Ϫ/Ϫ (CD45.2 ϩ IgH b ) embryos were adoptively transferred into irradiated C57BL/6-nu/nu hosts, and reconstitution of the peripheral B cell lineage was allowed for 8 -12 wk.…”
Section: Methodsmentioning
confidence: 99%
“…Recent studies suggest that deficient functions in forkhead transcription factors, such as Foxj1 and Foxo3a, predispose to such diseases, because their activities are significantly diminished in lupus lymphocytes and their deficiency results in spontaneous, multisystem autoimmune syndromes characterized by autoreactive, hyperactivated T cells (2,3). Presumably, such hyperactivated T cells can promote pathogenic autoantibody production by overexpressing costimulatory molecules and/or effector cytokines, resulting in excessive autoreactive B cell activation.…”
Section: Restraint Of B Cell Activation Bymentioning
confidence: 99%
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