In the past 10 years, autophagy has emerged as a crucial regulator of T-cell homeostasis, activation, and differentiation. Through the ability to adjust the cell's proteome in response to different stimuli, different forms of autophagy have been shown to control T-cell homeostasis and survival. Autophagic processes can also determine the magnitude of the T-cell response to TCR engagement, by regulating the cellular levels of specific signaling intermediates and modulating the metabolic output in activated T cells. In this review we will examine the mechanisms that control autophagy activity in T cells, such as ROS signaling and signaling through common gamma-chain cytokine receptors, and the different aspect of T-cell biology, including T-cell survival, effector cell function, and generation of memory, which can be regulated by autophagy.
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http://dx.doi.org/10.1002/eji.201545955 | DOI Listing |
Blood Adv
March 2025
National Institutes of Health, Bethesda, Maryland, United States.
Megakaryocytes (MKs) serve diverse roles beyond platelet production, including hematopoietic stem cell maintenance and immune response modulation. In our mouse model of immune bone marrow failure (BMF), we observed the unexpected persistence of MKs despite thrombocytopenia. These MKs exhibited heightened expression of immune activation markers, such as IA-IE and CD53, compared to MKs from healthy controls.
View Article and Find Full Text PDFSci Immunol
March 2025
Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Regulatory T cells (T) have diverse functional specification in homeostasis and disease. However, how liver T function and are transcriptionally regulated in obesity is not well understood. Here, we identified that effector T expressing activating transcription factor 4 (ATF4) were enriched in the livers of obese mice.
View Article and Find Full Text PDFJ Immunol
March 2025
Leiden University Center for Infectious Diseases, Leiden University Medical Center, Leiden, The Netherlands.
The virtually monomorphic antigen presentation molecule HLA-E can present self- and non-self peptides to the NKG2A/CD94 co-receptor inhibitory complex expressed on natural killer (NK) cells and to T cell receptors (TCRs) expressed on T cells. HLA-E presents self-peptides to NKG2A/CD94 to regulate tissue homeostasis, whereas HLA-E restricted T cells mediate regulatory and cytotoxic responses toward pathogen-infected cells. In this study, we directly compared HLA-E/peptide recognition and signaling between NKG2A/CD94 and 2 HLA-E restricted TCRs that can recognize self-peptides or identical peptide mimics from the viral UL40 protein of cytomegalovirus using position substituted peptide variants.
View Article and Find Full Text PDFFront Immunol
March 2025
Department of Gastroenterology, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China.
Ulcerative colitis (UC) is an autoimmune disease with an incompletely understood pathogenesis. The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway plays a key role in immune response and inflammation. More and more studies demonstrated that JAK/STAT signaling pathway is associated with the pathogenesis of UC.
View Article and Find Full Text PDFBrain Commun
February 2025
Neuroscience, Clinical and Biomedical Sciences, University of Exeter Medical School, Exeter EX2 4TH, UK.
Alzheimer's disease and other cognitive impairments are a growing problem in the healthcare world with the ageing population. There are currently no effective treatments available; however, it has been suggested that targeting neuroinflammation may be a successful approach in slowing the progression of neurodegeneration. Reducing the destructive hyperinflammatory pathology to maintain homeostasis in neural tissue is a promising option to consider.
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