المؤلفون: Arnaud Delpoux, Stephen M. Hedrick, Dominik Wieland, Maike Hofmann, Xin Huang, Daniel T. Utzschneider, Robert Thimme, Chen-Yen Lai

المصدر: Cell Reports, Vol 22, Iss 13, Pp 3454-3467 (2018)
Cell reports, vol 22, iss 13

مصطلحات موضوعية: 0301 basic medicine, T-Lymphocytes, Medical Physiology, FOXO1, Inbred C57BL, self-renewal, immune memory, Mice, 0302 clinical medicine, Leukocytes, 2.1 Biological and endogenous factors, homeostatic proliferation, Aetiology, lcsh:QH301-705.5, education.field_of_study, Forkhead Box Protein O1, TCF1/TCF7, 3. Good health, Infectious Diseases, medicine.anatomical_structure, Acute Disease, Infection, endocrine system, T cell, Population, Mononuclear, T cells, Biology, cell survival, General Biochemistry, Genetics and Molecular Biology, Article, Vaccine Related, 03 medical and health sciences, Immunity, Biodefense, Genetics, medicine, Animals, Humans, quiescence, education, LCMV, Transcription factor, Innate immune system, Prevention, chronic infection, Mice, Inbred C57BL, Chronic infection, Emerging Infectious Diseases, 030104 developmental biology, lcsh:Biology (General), Immunology, Chronic Disease, Leukocytes, Mononuclear, FOXO, Biochemistry and Cell Biology, Immunologic Memory, CD8, 030215 immunology

الوصف: Summary: Immunity following an acutely resolved infection or the long-term equipoise of chronic viral infections often depends on the maintenance of antigen-specific CD8+ T cells, yet the ongoing transcriptional requirements of these cells remain unclear. We show that active and continuous programming by FOXO1 is required for the functional maintenance of a memory population. Upon Foxo1 deletion following resolution of an infection, memory cells rapidly lost their characteristic gene expression, gradually declined in number, and were impaired in self-renewal. This was extended to chronic infections, as a loss of FOXO1 during a persistent viral infection led to a rapid decline of the TCF7 (a.k.a. TCF1)-expressing memory-like subset of CD8+ T cells. We further establish FOXO1 regulation as a characteristic of human memory CD8+ T cells. Overall, we show that the molecular and functional longevity of a memory T cell population is actively maintained by the transcription factor FOXO1. : Utzschneider et al. find that hallmarks of CD8+ T cell memory such as longevity, self-renewal, and the ability to cycle between quiescence and cell division depend on continued expression of FOXO1. Loss of FOXO1 during any of these stages leads to the interruption of T cell memory. Keywords: immune memory, homeostatic proliferation, self-renewal, quiescence, cell survival, T cells, FOXO, TCF1/TCF7, chronic infection, LCMV

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6d33eeb9aa9cd37b0a0b64e7e1532570Test
http://www.sciencedirect.com/science/article/pii/S2211124718303498Test

المؤلفون: Alexander Hoffmann, Stephen M. Hedrick, Irene L. Ch’en

مصطلحات موضوعية: Programmed cell death, Cell growth, Necroptosis, Cell, NF-κB, Phosphatidylserine, Biology, Cell fate determination, Cell biology, chemistry.chemical_compound, medicine.anatomical_structure, chemistry, Apoptosis, medicine

الوصف: The NF‐κB signaling system has important and distinct roles in determining cell fate decisions, such as cell proliferation and cell death. Specifically, recent evidence indicates that NF‐B regulates several types of programmed cell death, such as apoptosis, necroptosis, necrosis, as well as cellular senescence, but its precise role in these is not fully understood. Distinguishing these cell fates experimentally is therefore important, and several techniques are available to researchers. We summarize experimental strategies and protocols that reveal changes in nuclear morphology and cell shrinkage, exposure of phosphatidylserine, compromised membrane integrity, DNA fragmentation, and altered mitochondrial membrane potential. Together, these may discriminate distinct cell death pathways and lead to a better understanding of the underlying regulatory mechanisms.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::62438972c292a8de2f5e94adefae41d4Test
https://doi.org/10.1016/s0076-6879Test(08)01610-8

المؤلفون: Stephen M. Hedrick

المصدر: Advances in Immunology ISBN: 9780120224432

مصطلحات موضوعية: Genetics, Protein structure, Immune system, Antigen, T-cell receptor, chemical and pharmacologic phenomena, Human leukocyte antigen, Biology, Receptor, Gene, humanities, Epitope

الوصف: Publisher Summary This chapter discusses the evolutionary and organismal influences of the specificity of the T cell receptor that may have contributed to a particular strategy of immune recognition. Understanding the specificity of recognition in the immune system is uniquely complicated because of the vast diversity of the specific receptors. The chapter focuses on the structure of the determinant recognized by the T-cell receptor (TCR) and the structure of the receptor itself. A recently proposed model of the TCR–antigen–MHC interaction has been discussed in the chapter. The chapter discuses the specificity of the TCR and the mechanisms by which T cells carry out the process of self- and nonself-discrimination. The TCR α and β chains that determine clonal specificity are encoded by variable (V), diversity (D), and joining (J) region gene elements that rearrange to form a mature, transcribable gene, and the number and diversity of these gene elements determine the repertoire potential for TCR specificity. A description of the organization of these gene elements and of the structure of TCR heterodimer is reviewed in the chapter.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::756ba21a982617d5e1c4b666570baa4aTest
https://doi.org/10.1016/s0065-2776Test(08)60366-1

المؤلفون: Stephen M. Hedrick

مصطلحات موضوعية: Macrophage-1 antigen, Interleukin-4 receptor, Cytotoxic T cell, CD28, H antigen, Biology, Natural killer T cell, Antigen-presenting cell, Molecular biology, Interleukin 3

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::0ce0daa13ffc85c7a2650bed8fef92d1Test
https://doi.org/10.1016/b978-0-12-123062-3.50018-9Test