title: Autophagy in T-cell development, activation and differentiation.
abstract: Autophagy is a vital catabolic process for degrading bulky cytosolic contents, which cannot be resorbed via the proteasome. First described as a survival mechanism during nutrient starvation conditions, recent reports have demonstrated that autophagy supports metabolic functions of T cells at various stages of maturation and effector function. Autophagy is crucial for T-cell development at the precursor stage as self-renewability and quiescence of hematopoietic stem cells depend on autophagy of the mitochondria and the endoplasmic reticulum. Later, during development in the thymus, autophagy regulates peptide presentation in stromal cells and professional antigen-presenting cells, which mediate thymocyte selection. Furthermore, the metabolic changes when mature T cells enter the periphery and when they are activated are both dependent on autophagy. Lastly, autophagy prevents early aging and, thus, ensures maintenance of memory T cells.
authors.affiliation: 1] Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany [2] Institute for Molecular and Clinical Immunology, Otto-von-Guericke University, Magdeburg, Germany.
authors.forename: Alisha W
authors.initials: AW
authors.lastname: Bronietzki
authors.affiliation: 1] Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany [2] Institute for Molecular and Clinical Immunology, Otto-von-Guericke University, Magdeburg, Germany.
authors.forename: Marc
authors.initials: M
authors.lastname: Schuster
authors.affiliation: 1] Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany [2] Institute for Molecular and Clinical Immunology, Otto-von-Guericke University, Magdeburg, Germany.
authors.forename: Ingo
authors.initials: I
authors.lastname: Schmitz
mesh_terms: D000375:Aging / Q000235:genetics / Q000276:immunology*; D000818:Animals; D017951:Antigen Presentation; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000276:immunology; D001343:Autophagy / Q000235:genetics / Q000276:immunology*; D002454:Cell Differentiation; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology*; D018507:Gene Expression Regulation, Developmental; D006412:Hematopoietic Stem Cells / Q000166:cytology / Q000276:immunology*; D006801:Humans; D007156:Immunologic Memory; D008213:Lymphocyte Activation; D008928:Mitochondria / Q000235:genetics / Q000276:immunology; D010588:Phagosomes / Q000235:genetics / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*; D013950:Thymus Gland / Q000166:cytology / Q000254:growth & development / Q000276:immunology*; D044763:Ubiquitin-Conjugating Enzymes / Q000235:genetics / Q000276:immunology
chemical_list: D051017:Apoptosis Regulatory Proteins; D044763:Ubiquitin-Conjugating Enzymes