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      Regulation of Immune Responses by mTOR

      Author(s): 1 , 1 , 1 , 2
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      Publication date (Print):
      Journal: Annual Review of Immunology
      Publisher: Annual Reviews

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          Abstract

          mTOR is an evolutionarily conserved serine/threonine kinase that plays a central role in integrating environmental cues in the form of growth factors, amino acids, and energy. In the study of the immune system, mTOR is emerging as a critical regulator of immune function because of its role in sensing and integrating cues from the immune microenvironment. With the greater appreciation of cellular metabolism as an important regulator of immune cell function, mTOR is proving to be a vital link between immune function and metabolism. In this review, we discuss the ability of mTOR to direct the adaptive immune response. Specifically, we focus on the role of mTOR in promoting differentiation, activation, and function in T cells, B cells, and antigen-presenting cells.

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          Understanding the Warburg effect: the metabolic requirements of cell proliferation.

          Craig B Thompson, Matthew Vander Heiden, Lewis Cantley (2009)
          In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient way to generate adenosine 5'-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here we propose that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass (e.g., nucleotides, amino acids, and lipids) needed to produce a new cell. Supporting this idea are recent studies showing that (i) several signaling pathways implicated in cell proliferation also regulate metabolic pathways that incorporate nutrients into biomass; and that (ii) certain cancer-associated mutations enable cancer cells to acquire and metabolize nutrients in a manner conducive to proliferation rather than efficient ATP production. A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer.
          Article 0 comments Cited 2500 times – based on 0 reviews     Review now
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            Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1.

            Mehrdad Matloubian, Charles G. Lo, Guy Cinamon … (2004)
            Adaptive immunity depends on T-cell exit from the thymus and T and B cells travelling between secondary lymphoid organs to survey for antigens. After activation in lymphoid organs, T cells must again return to circulation to reach sites of infection; however, the mechanisms regulating lymphoid organ exit are unknown. An immunosuppressant drug, FTY720, inhibits lymphocyte emigration from lymphoid organs, and phosphorylated FTY720 binds and activates four of the five known sphingosine-1-phosphate (S1P) receptors. However, the role of S1P receptors in normal immune cell trafficking is unclear. Here we show that in mice whose haematopoietic cells lack a single S1P receptor (S1P1; also known as Edg1) there are no T cells in the periphery because mature T cells are unable to exit the thymus. Although B cells are present in peripheral lymphoid organs, they are severely deficient in blood and lymph. Adoptive cell transfer experiments establish an intrinsic requirement for S1P1 in T and B cells for lymphoid organ egress. Furthermore, S1P1-dependent chemotactic responsiveness is strongly upregulated in T-cell development before exit from the thymus, whereas S1P1 is downregulated during peripheral lymphocyte activation, and this is associated with retention in lymphoid organs. We find that FTY720 treatment downregulates S1P1, creating a temporary pharmacological S1P1-null state in lymphocytes, providing an explanation for the mechanism of FTY720-induced lymphocyte sequestration. These findings establish that S1P1 is essential for lymphocyte recirculation and that it regulates egress from both thymus and peripheral lymphoid organs.
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              Alternative activation of macrophages: mechanism and functions.

              Siamon Gordon, Fernando Martinez (2010)
              The concept of an alternative pathway of macrophage activation has stimulated interest in its definition, mechanism, and functional significance in homeostasis and disease. We assess recent research in this field, argue for a restricted definition, and explore pathways by which the T helper 2 (Th2) cell cytokines interleukin-4 (IL-4) and IL-13 mediate their effects on macrophage cell biology, their biosynthesis, and responses to a normal and pathological microenvironment. The stage is now set to gain deeper insights into the role of alternatively activated macrophages in immunobiology. Copyright 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Title: Annual Review of Immunology
                Abbreviated Title: Annu. Rev. Immunol.
                Publisher: Annual Reviews
                ISSN (Print): 0732-0582
                ISSN (Electronic): 1545-3278
                Publication date Created: April 23 2012
                Publication date (Print): April 23 2012
                Volume: 30
                Issue: 1
                Pages: 39-68
                Affiliations
                [1 ]Department of Oncology, Sidney Kimmel Comprehensive Cancer Center,
                [2 ]Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231;, , ,
                Article
                DOI: 10.1146/annurev-immunol-020711-075024
                PMC ID: 3616892
                PubMed ID: 22136167
                SO-VID: a962d000-e58d-4221-9298-d8f43b3aa5ab
                Copyright © © 2012
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