| First Author | Conway KL | Year | 2013 |
| Journal | Autophagy | Volume | 9 |
| Issue | 4 | Pages | 528-37 |
| PubMed ID | 23327930 | Mgi Jnum | J:282702 |
| Mgi Id | MGI:6382369 | Doi | 10.4161/auto.23484 |
| Citation | Conway KL, et al. (2013) ATG5 regulates plasma cell differentiation. Autophagy 9(4):528-37 |
| abstractText | Autophagy is a conserved homeostatic process in which cytoplasmic contents are degraded and recycled. Two ubiquitin-like conjugation pathways are required for the generation of autophagosomes, and ATG5 is necessary for both of these processes. Studies of mice deficient in ATG5 reveal a key role for autophagy in T lymphocyte function, as well as in B cell development and B-1a B cell maintenance. However, the role of autophagy genes in B cell function and antibody production has not been described. Using mice in which Atg5 is conditionally deleted in B lymphocytes, we showed here that this autophagy gene is essential for plasma cell homeostasis. In the absence of B cell ATG5 expression, antibody responses were significantly diminished during antigen-specific immunization, parasitic infection and mucosal inflammation. Atg5-deficient B cells maintained the ability to produce immunoglobulin and undergo class-switch recombination, yet had impaired SDC1 expression, significantly decreased antibody secretion in response to toll-like receptor ligands, and an inability to upregulate plasma cell transcription factors. These results build upon previous data demonstrating a role for ATG5 in early B cell development, illustrating its importance in late B cell activation and subsequent plasma cell differentiation. |
