Lanzavecchia, A. & Sallusto, F. Understanding the generation and function of memory T cell subsets. Curr. Opin. Immunol. 17, 326-332

Institute for Research in Biomedicine, Via Vincenzo Vela 6, CH-6500 Bellinzona, Switzerland.
Current Opinion in Immunology (Impact Factor: 7.48). 07/2005; 17(3):326-32. DOI: 10.1016/j.coi.2005.04.010
Source: PubMed


Memory T cells can be broadly divided into central memory and effector memory subsets, which are endowed with different capacities to home to lymphoid or non-lymphoid tissues, to proliferate in response to antigen or cytokines and to perform effector functions. In the past few years progress has been made in understanding the properties of these memory T cell subsets and, in particular, the signals required for their generation and maintenance. Collectively these data point to a critical role of central memory T cells in conferring long-term immunity.

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    • "Generally, the generation of memory T cells is characterized by different phases (41). The first encounter with an Ag, defined priming, determines a massive proliferation and clonal expansion of Ag-specific T cells followed by a phase of contraction, where the majority of these cells, named effector cells, are eliminated by apoptosis (42, 43). During this primary response, memory T cells develop and are maintained for extended periods due to several mechanisms such as the retention of Ag, stimulation/boosters, or homeostatic proliferation, that will insure the maintenance of a pool of cells that can rapidly respond to subsequent encounters with the pathogen. "
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    ABSTRACT: With 1.4 million deaths and 8.7 million new cases in 2011, tuberculosis (TB) remains a global health care problem and together with HIV and Malaria represents the one of the three infectious diseases world-wild. Control of the global TB epidemic has been impaired by the lack of an effective vaccine, by the emergence of drug-resistant forms of Mycobacterium tuberculosis (Mtb) and by the lack of sensitive and rapid diagnostics. It is estimated, by epidemiological reports, that one third of the world’s population is latently infected with Mtb, but the majority of infected individuals develops long-lived protective immunity, which controls and contains Mtb in a T cell-dependent manner. Development of TB disease results from interactions among the environment, the host, and the pathogen, and known risk factors include HIV coinfection, immunodeficiency, diabetes mellitus, overcrowding, malnutrition, and general poverty; therefore an effective T cell response determines whether the infection resolves or develops into clinically evident disease. Consequently, there is great interest in determining which T cells subsets mediate anti-mycobacterial immunity, delineating their effector functions. On the other hand, many aspects remain unsolved in understanding why some individuals are protected from Mtb infection while others go on to develop disease.Several studies have demonstrated that CD4+ T cells are involved in protection against Mtb, as supported by the evidence that CD4+ T cell depletion is responsible for Mtb reactivation in HIV-infected individuals. There are many subsets of CD4+ T cells, such as T-helper 1 (Th1), Th2, Th17, and regulatory T cells (Tregs), and all these subsets cooperate or interfere with each other to control infection; the dominant subset may differ between active and latent Mtb infection cases. Mtb-specific CD4+ Th1 cell response is considered to have a protective role for the ability to produce cytokines such as IFN- or TNF- that contribute to
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    • "During immune responses, T cells activated by recognizing their target antigens presented by antigen presenting cells (APCs) undergo clonal expansion to increase number of T cells reacting to invading microbial pathogens. At the same time, proliferating T cells differentiate into various subsets of effector and/or memory T cells to efficiently mount both acute and recurrent immune responses to infection [1]–[3]. Although the mechanisms that allow a single T cell to generate phenotypically distinct subsets of T cells remain incompletely understood [4]–[7], asymmetric division has been shown to be one of the mechanisms that generate this diversity by regulating effector/memory formation of CD8+ T cell and differentiation of CD4+ T cells [8]–[10]. "
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    ABSTRACT: Similar to stem cells, naïve T cells undergo asymmetric division following activation. While asymmetric division of T cells has been shown to be an important mechanism for the generation of lymphocyte fate diversity during immune responses, key factors that influence whether T cells will undergo symmetric or asymmetric divisions are not completely understood. Here, we utilized immunological synapse arrays (ISAs) to begin to dissect mechanisms of asymmetric T lymphocyte division. ISAs are protein micropatterned surfaces composed of two segregated regions, activation sites and adhesion fields. Activation sites are small spots presenting activation signals such as anti-CD3 and anti-CD28, and adhesion fields are the remaining regions surrounding activation sites immobilized with interintercel adhesion molecule 1 (ICAM-1). By varying the size and the distance between the activation sites and measuring the incidence of asymmetric cell divisions, we found that the distance between activation sites is an important regulator of asymmetric division. Further analysis revealed that more symmetric divisions occurred when two nascent daughter cells stably interacted with two distinct activation sites throughout and following cytokinesis. In contrast, more asymmetric divisions occurred when only one daughter cell remained anchored on an activation site while the other daughter became motile and moved away following cytokinesis. Together, these results indicate that TCR signaling events during cytokinesis may repolarize key molecules for asymmetric partitioning, suggesting the possibility that the density of antigen presenting cells that interact with T cells as they undergo cytokinesis may be a critical factor regulating asymmetric division in T cells.
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    • "In addition, according to the literature on memory T-cell generation, a low but sufficient activation of naïve T-cells is crucial to the differentiation of TCM cells.39 Associating this evidence with the fact that CLL B-cells are poor as antigen presenting cells,11 the interaction between CLL B-cells and naïve T-cells could result in a weak stimulation leading to the generation and/or accumulation of CD4 TCM cells. "
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    ABSTRACT: The role of T-cells in the pathogenesis of chronic lymphocytic leukemia has recently gained much attention due to the importance of the constant interaction between neoplastic B-cells with microenvironment substratum and T-cells. It is believed that these interactions modulate the clinical course of the disease, mainly through the regulation of the expansion, differentiation, and survival of chronic lymphocytic leukemia B-cells. Importantly, this crosstalk may also change the number, function, and memory phenotype of normal T-cells, thereby altering the amplitude and/or efficiency of adaptive immunity in chronic lymphocytic leukemia patients. The present study presents an overview on important aspects of this immunological crosstalk, particularly on the abnormalities of chronic lymphocytic leukemia B-cells and the alterations in normal T-cells, with focus on the CD4 memory T-cell compartment that could offer survival signals to chronic lymphocytic leukemia B-cell clone(s) and contribute to the establishment and progression of the disease. The authors believe that understanding the biological consequences of the interaction between normal T- and neoplastic B-cells in chronic lymphocytic leukemia may allow for improvements in the prognostic information and therapeutic approaches for this disease.
    Full-text · Article · Mar 2014 · Revista Brasileira de Hematologia e Hemoterapia
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