Scientific reports · 2017
ATP-degrading ENPP1 is required for survival (or persistence) of long-lived plasma cells.
СтатьяResearch Support, N.I.H., IntramuralНазвание и аннотация: Перевод пока не подготовлен
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Wang Hongsheng, Gonzalez-Garcia Ines, Traba Javier, Jain Shweta, Conteh Solomon, Shin Dong-Mi, Qi Chenfeng, Gao Yuanyuan, Sun Jiafang, Kang Sungyun, Abbasi Sadia, Naghashfar Zohreh, Yoon Jeongheon, DuBois Wendy, Kovalchuk Alexander L, Sack Michael N, Duffy Patrick, Morse Herbert C
Аннотация
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.