| First Author | Arnold J | Year | 2016 |
| Journal | Cell Death Differ | Volume | 23 |
| Issue | 5 | Pages | 853-64 |
| PubMed ID | 26586568 | Mgi Jnum | J:258905 |
| Mgi Id | MGI:6140844 | Doi | 10.1038/cdd.2015.149 |
| Citation | Arnold J, et al. (2016) Autophagy is dispensable for B-cell development but essential for humoral autoimmune responses. Cell Death Differ 23(5):853-64 |
| abstractText | To gain new insight into the role of B-cell autophagy, we generated two novel mouse models deficient for the autophagy-related gene (Atg)5, one from the outset pro-B cell stage (Atg5(f/-) Mb1 cre) and the other in mature B cells only (Atg5(f/-) CD21 cre). We show that autophagy is dispensable for pro- to pre-B cell transition, but necessary at a basal level to maintain normal numbers of peripheral B cells. It appears non-essential for B-cell activation under B-cell receptor stimulation but required for their survival after lipopolysaccharide stimulation that drives plasmablast differentiation and for specific IgM production after immunization. Results obtained using Atg5(f/-) CD21 cre x C57BL/6(lpr/lpr) autoimmune-prone mice show that B-cell autophagy is involved in the maintenance of anti-nuclear antibody secretion, elevated number of long-lived plasma cells, and sustains IgG deposits in the kidneys. Thus, treatments specifically targeting autophagy might be beneficial in systemic autoimmune diseases. |
