Publication: A switch from canonical to noncanonical autophagy shapes B cell responses.

Publié dans: Science 2017 Feb; 355(6325): 641-647

Auteurs: Martinez-Martin N, Maldonado P, Gasparrini F, Frederico B, Aggarwal S, Gaya M, Tsui C, Burbage M, Keppler SJ, Montaner B, Jefferies HB, Nair U, Zhao YG, Domart MC, Collinson L, Bruckbauer A, Tooze SA, Batista FD

Résumé

Autophagy is important in a variety of cellular and pathophysiological situations; however, its role in immune responses remains elusive. Here, we show that among B cells, germinal center (GC) cells exhibited the highest rate of autophagy during viral infection. In contrast to mechanistic target of rapamycin complex 1-dependent canonical autophagy, GC B cell autophagy occurred predominantly through a noncanonical pathway. B cell stimulation was sufficient to down-regulate canonical autophagy transiently while triggering noncanonical autophagy. Genetic ablation of WD repeat domain, phosphoinositide-interacting protein 2 in B cells alone enhanced this noncanonical autophagy, resulting in changes of mitochondrial homeostasis and alterations in GC and antibody-secreting cells. Thus, B cell activation prompts a temporal switch from canonical to noncanonical autophagy that is important in controlling B cell differentiation and fate.

Lien vers Pubmed [PMID] – 28183981

Lien vers le DOI – 10.1126/science.aal3908