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Targeting Mitochondria to Revive Dysfunctional Regulatory T Cells
Elsa Brunet-Ratnasingham1, Mathieu Dubé2, Daniel E Kaufmann3
1Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada; Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montréal, QC, Canada.
Immunometabolism is important to T cell dysfunction in chronic infections. A recent publication in The Journal of Clinical Investigation (2018;128:5083-5094) [1] shows reduced mitochondrial fitness in regulatory CD4+ T cells (Tregs) of patients with HIV and failed immune restoration on antiretroviral therapy (ART). This defect can be reversed by IL-15, revealing a new immunotherapy target for regulatory T cell restoration.
Immunometabolism is important to T cell dysfunction in chronic infections. A recent publication in The Journal of Clinical Investigation (2018;128:5083-5094) [1] shows reduced mitochondrial fitness in regulatory CD4+ T cells (Tregs) of patients with HIV and failed immune restoration on antiretroviral therapy (ART). This defect can be reversed by IL-15, revealing a new immunotherapy target for regulatory T cell restoration.
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