| First Author | Erikson E | Year | 2022 |
| Journal | Cell Immunol | Volume | 375 |
| Pages | 104516 | PubMed ID | 35413621 |
| Mgi Jnum | J:330351 | Mgi Id | MGI:7283788 |
| Doi | 10.1016/j.cellimm.2022.104516 | Citation | Erikson E, et al. (2022) Impaired plasma cell differentiation associates with increased oxidative metabolism in IkappaBNS-deficient B cells. Cell Immunol 375:104516 |
| abstractText | Mutations causing loss of the NF-kappaB regulator IkappaBNS, result in impaired development of innate-like B cells and defective plasma cell (PC) differentiation. Since productive PC differentiation requires B cell metabolic reprogramming, we sought to investigate processes important for this transition using the bumble mouse strain, deficient for IkappaBNS. We report that LPS-activated bumble B cells exhibited elevated mTOR activation levels, mitochondrial accumulation, increased OXPHOS and mROS production, along with a reduced capacity for autophagy, compared to wildtype B cells. Overall, our results demonstrate that PC differentiation in the absence of IkappaBNS is characterized by excessive activation during early rounds of B cell division, increased mitochondrial metabolism and decreased autophagic capacity, thus improving our understanding of the role of IkappaBNS in PC differentiation. |
