|Title||A switch from canonical to noncanonical autophagy shapes B cell responses.|
|Publication Type||Journal Article|
|Year of Publication||2017|
|Authors||Martinez-Martin N, Maldonado P, Gasparrini F, Frederico B, Aggarwal S, Gaya M, Tsui C, Burbage M, Keppler SJessica, Montaner B, Jefferies HBJ, Nair U, Zhao YG, Domart M-C, Collinson L, Bruckbauer A, Tooze SA, Batista FD|
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.
|Grant List||UM1 AI100663 / AI / NIAID NIH HHS / United States|
A switch from canonical to noncanonical autophagy shapes B cell responses.