2022
DOI: 10.1016/j.redox.2022.102422
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NCF4 dependent intracellular reactive oxygen species regulate plasma cell formation

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Cited by 6 publications
(3 citation statements)
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“…The Ncf1 m1J mutation leads to expression of only small amounts of deficient NCF1 protein, abrogating both intracellular and extracellular ROS response by the NOX2 complex [ 11 , 30 ]. We also showed that mice with the NCF4 58A mutation developed severe CIA due to dysregulated B cells and lost the ability to regulate plasma cell differentiation [ 31 ]. These data suggested that NCF4 and NCF1 regulate autoimmunity and the development of arthritis differentially.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…The Ncf1 m1J mutation leads to expression of only small amounts of deficient NCF1 protein, abrogating both intracellular and extracellular ROS response by the NOX2 complex [ 11 , 30 ]. We also showed that mice with the NCF4 58A mutation developed severe CIA due to dysregulated B cells and lost the ability to regulate plasma cell differentiation [ 31 ]. These data suggested that NCF4 and NCF1 regulate autoimmunity and the development of arthritis differentially.…”
Section: Discussionmentioning
confidence: 99%
“…To induce GIA in mice, all the male mice over 3 months of age were given a single intradermal injection of 100 μL of emulsified hGPI 325-339 peptide (10 μg per mouse) 1:1 complete Freund's adjuvant (CFA) (10 mg/mL Mycobacterium tuberculosis H37Ra (BD 231141) in incomplete Freund's adjuvant (IFA) (BD 263910)) as described previously [ 54 ]. To induce CIA in mice, all the mice over 3 months were given a single intradermal injection of 100 μL of emulsified type II collagen (50 μg per mouse) 1:1 CFA (BD, 263810) as described previously [ 31 ]. Arthritis severity was scored daily after immunization, as earlier described in detail [ 55 ].…”
Section: Methodsmentioning
confidence: 99%
“…Only recently, in vivo study on animal model showed that the deletion of NCF4, through impaired intracellular ROS production in activated B cells, led to increased differentiation of B cells into plasma cells as well as decreased expression of C-X-C Motif Chemokine Receptor 4 (CXCR4, CD184) and increased C-X-C Motif Chemokine Receptor 3 (CXCR3, CD183) [32]. CXCR3 and CXCR4 are chemokine receptors, highly expressed in RA patients.…”
Section: Introductionmentioning
confidence: 99%