| First Author | Wang H | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 17867 |
| PubMed ID | 29259245 | Mgi Jnum | J:287506 |
| Mgi Id | MGI:6407632 | Doi | 10.1038/s41598-017-18028-z |
| Citation | Wang H, et al. (2017) ATP-degrading ENPP1 is required for survival (or persistence) of long-lived plasma cells. Sci Rep 7(1):17867 |
| abstractText | Survival of antibody-secreting plasma cells (PCs) is vital for sustained antibody production. However, it remains poorly understood how long-lived PCs (LLPCs) are generated and maintained. Here we report that ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) is preferentially upregulated in bone marrow LLPCs compared with their splenic short-lived counterparts (SLPCs). We studied ENPP1-deficient mice (Enpp1 (-/-) ) to determine how the enzyme affects PC biology. Although Enpp1 (-/-) mice generated normal levels of germinal center B cells and plasmablasts in periphery, they produced significantly reduced numbers of LLPCs following immunization with T-dependent antigens or infection with plasmodium C. chabaudi. Bone marrow chimeric mice showed B cell intrinsic effect of ENPP1 selectively on generation of bone marrow as well as splenic LLPCs. Moreover, Enpp1 (-/-) PCs took up less glucose and had lower levels of glycolysis than those of wild-type controls. Thus, ENPP1 deficiency confers an energetic disadvantage to PCs for long-term survival and antibody production. |
