The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Mitochondrial Respiration Controls Lysosomal Function during Inflammatory T Cell Responses
Open accessAbstract
Summary The endolysosomal system is critical for the maintenance of cellular homeostasis. However, how endolysosomal compartment is regulated by mitochondrial function is largely unknown. We have generated a mouse model with defective mitochondrial function in CD4+ T lymphocytes by genetic deletion of the mitochondrial transcription factor A (Tfam). Mitochondrial respiration-deficiency impairs lysosome function, promotes p62 and sphingomyelin accumulation and disrupts endolysosomal trafficking pathways and autophagy, thus linking a primary mitochondrial dysfunction to a lysosomal storage disorder. The impaired lysosome function in Tfam-deficient cells subverts T cell differentiation toward pro-inflammatory subsets and exacerbates the in vivo inflammatory response. Restoration of NAD+ levels improves lysosome function and corrects the inflammatory defects in Tfam-deficient T cells. Our results uncover a mechanism by which mitochondria regulate lysosome function to preserve T cell differentiation and effector functions, and identify novel strategies for intervention in mitochondrial-related diseases.
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Mitochondrial form and function
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“Mitochondria integrate their diverse functions through multiple pathways that ultimately converge on proper function of the respiratory complexes of the electron transport chain (Friedman and Nunnari, 2014).”
Functions and dysfunctions of mitochondrial dynamics
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Fueling Immunity: Insights into Metabolism and Lymphocyte Function
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Cited by
Mitochondria are the powerhouses of immunity
Mills, E. L., Kelly, B., & O'Neill, L. A. J. (2017) · Nature Immunology · doi:10.1038/ni.3704 · Cited by 1,161
NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential
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Mitonuclear communication in homeostasis and stress
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Self-citation
Metadata
- Authors
- Baixauli, F., Acín-Pérez, R., Villarroya-Beltrí, C., Mazzeo, C., Nuñez-Andrade, N., Gabandé-Rodriguez, E., Ledesma, M. D., Blázquez, A., Martin, M. A., Falcón-Pérez, J. M., Redondo, J. M., Enríquez, J. A., & Mittelbrunn, M.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2015-09
- Volume
- 22
- Issue
- 3
- Pages
- 485-498
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W1499820592
- Cited by
- 326
- References
- 15
- FWCI
- 12.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Baixauli, F., Acín-Pérez, R., Villarroya-Beltrí, C., Mazzeo, C., Nuñez-Andrade, N., Gabandé-Rodriguez, E., Ledesma, M. D., Blázquez, A., Martin, M. A., Falcón-Pérez, J. M., Redondo, J. M., Enríquez, J. A., & Mittelbrunn, M. (2015). Mitochondrial Respiration Controls Lysosomal Function during Inflammatory T Cell Responses. Cell Metabolism. https://doi.org/10.1016/j.cmet.2015.07.020
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
