A switch from canonical to noncanonical autophagy shapes B cell responses.
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| Title: | A switch from canonical to noncanonical autophagy shapes B cell responses. |
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| Authors: | Martinez-Martin, Nuria (AUTHOR), Maldonado, Paula (AUTHOR), Gasparrini, Francesca (AUTHOR), Frederico, Bruno (AUTHOR), Aggarwal, Shweta (AUTHOR), Gaya, Mauro (AUTHOR), Tsui, Carlson (AUTHOR), Burbage, Marianne (AUTHOR), Jessica Keppler, Selina (AUTHOR), Montaner, Beatriz (AUTHOR), Jefferies, Harold B. J. (AUTHOR), Nair, Usha (AUTHOR), Zhao, Yan G. (AUTHOR), Domart, Marie-Charlotte (AUTHOR), Collinson, Lucy (AUTHOR), Bruckbauer, Andreas (AUTHOR), Tooze, Sharon A. (AUTHOR), Batista, Facundo D. (AUTHOR) |
| Source: | Science (pre-March 2025). 2/10/2017, Vol. 355 Issue 6325, p641-647. 7p. 4 Graphs. |
| Subjects: | Autophagy, B cells, Immune response, Virus diseases, Rapamycin, Homeostasis |
| Abstract: | 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. [ABSTRACT FROM AUTHOR] |
| Copyright of Science (pre-March 2025) is the property of American Association for the Advancement of Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | 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. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 00368075 |
| DOI: | 10.1126/science.aal3908 |
