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Immunological Memory and Protective Immunity: Understanding Their Relation
Rafi Ahmed,David Gray +1 more
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TLDR
The current understanding of the cellular basis of immune memory is reviewed and the relative contributions made to protective immunity by memory and effector T and B cells are examined.Abstract:
The immune system can remember, sometimes for a lifetime, the identity of a pathogen. Understanding how this is accomplished has fascinated immunologists and microbiologists for many years, but there is still considerable debate regarding the mechanisms by which long-term immunity is maintained. Some of the controversy stems from a failure to distinguish between effector and memory cells and to define their roles in conferring protection against disease. Here the current understanding of the cellular basis of immune memory is reviewed and the relative contributions made to protective immunity by memory and effector T and B cells are examined.read more
Citations
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Two subsets of memory T lymphocytes with distinct homing potentials and effector functions
TL;DR: It is shown that expression of CCR7, a chemokine receptor that controls homing to secondary lymphoid organs, divides human memory T cells into two functionally distinct subsets, which are named central memory (TCM) and effector memory (TEM).
Journal ArticleDOI
Lymphocyte homing and homeostasis.
TL;DR: A review of the molecular basis of lymphocyte homing is presented, and mechanisms by which homing physiology regulates the homeostasis of immunologic resources are proposed.
Journal ArticleDOI
Regulation of endothelium-derived nitric oxide production by the protein kinase Akt.
David Fulton,Jean-Philippe Gratton,Timothy J. McCabe,Jason Fontana,Yasushl Fujio,Kenneth Walsh,Thomas F. Franke,Andreas Papapetropoulos,William C. Sessa +8 more
TL;DR: It is shown that the serine/threonine protein kinase Akt (protein kinase B) can directly phosphorylate eNOS on serine 1179 and activate the enzyme, leading to NO production, whereas mutant eN OS (S1179A) is resistant to phosphorylation and activation by Akt.
Journal ArticleDOI
Counting Antigen-Specific CD8 T Cells: A Reevaluation of Bystander Activation during Viral Infection
Kaja Murali-Krishna,John D. Altman,M. Suresh,David J. D. Sourdive,Allan J. Zajac,Joseph D. Miller,Jill E. Slansky,Rafi Ahmed +7 more
TL;DR: Much of the CD8 T cell expansion seen during viral infection represents antigen-specific cells and warrants a revision of current thinking on the size of the antiviral response.
Journal ArticleDOI
About sleep's role in memory
Bjoern Rasch,Jan Born,Jan Born +2 more
TL;DR: This review aims to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings.
References
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Journal ArticleDOI
The Fas Death Factor
Shigekazu Nagata,Pierre Golstein +1 more
TL;DR: Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells.
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Social controls on cell survival and cell death
TL;DR: For some mammalian cells, programmed death seems to occur by default unless suppressed by signals from other cells, so dependence on specific survival signals provides a simple way to eliminate misplaced cells, for regulating cell numbers and, perhaps, for selecting the fittest cells.
Journal ArticleDOI
A B cell-deficient mouse by targeted disruption of the membrane exon of the immunoglobulin μ chain gene
TL;DR: The importance of the membrane form of the μ chain in B-cell development is assessed by generating mice lacking this chain by disrupting one of the membranes exons of the gene encoding the μ-chain constant region by gene targeting in mouse embryonic stem cells.
Journal ArticleDOI
Fas and Perforin Pathways as Major Mechanisms of T Cell-Mediated Cytotoxicity
David Kägi,Françoise Vignaux,Birgit Ledermann,Kurt Bürki,Valérie Depraetere,Shigekazu Nagata,Hans Hengartner,Pierre Golstein +7 more
TL;DR: The perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays, and no third mechanism was detected.
Journal ArticleDOI
Generalized lymphoproliferative disease in mice, caused by a point mutation in the fas ligand
Tomohiro Takahashi,Masato Tanaka,Camllynn I. Brannan,Nancy A. Jenkins,Neal G. Copeland,Takashi Suda,Shigekazu Nagata +6 more
TL;DR: The results indicate that lpr and gld are mutations in Fas and Fasl, respectively, and suggest important roles of the Fas system in development of T cells as well as cytotoxic T lymphocyte-mediated cytotoxicity.