Autoimmune effector memory T cells: the bad and the good
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IMMUNOLOGY & MICROBIOLOGY IN MIAMI
Autoimmune effector memory T cells: the bad and the good Priyadharshini Devarajan • Zhibin Chen
Zhibin Chen Published online: 8 November 2013 Ó Springer Science+Business Media New York 2013
Abstract Immunological memory is a hallmark of adaptive immunity, a defense mechanism endowed to vertebrates during evolution. However, an autoimmune pathogenic role of memory lymphocytes is also emerging with accumulating evidence, despite reasonable skepticism on their existence in a chronic setting of autoimmune damage. It is conceivable that autoimmune memory would be particularly harmful since memory cells would constantly ‘‘remember’’ and attack the body’s healthy tissues. It is even more detrimental given the resistance of memory T cells to immunomodulatory therapies. In this review, we focus on self-antigen-reactive CD4? effector memory T (TEM) cells, surveying the evidence for the role of the TEM compartment in autoimmune pathogenesis. We will also discuss the role of TEM cells in chronic and acute infectious disease settings and how they compare to their counterparts in autoimmune diseases. With their long-lasting potency, the autoimmune TEM cells could also play a critical role in anti-tumor immunity, which may be largely based on their reactivity to self-antigens. Therefore, although autoimmune TEM cells are ‘‘bad’’ due to their role in relentless perpetration of tissue damage in autoimmune disease settings, they are unlikely a by-product of industrial development along the modern surge of autoimmune disease prevalence. Rather, they may be a product of evolution for their ‘‘good’’ in clearing damaged host cells in chronic infections and malignant cells in cancer settings. Keywords
Autoimmunity Tumor T cells Memory CTLA4 Genomic
Introduction Autoimmune diseases, wherein the body’s immune system attacks self-tissues, collectively afflict 5–10 % of the world’s developed population. The incidence of many autoimmune diseases, including type 1 diabetes (T1D) [1], system lupus erythematosus (SLE) [2] and multiple sclerosis (MS) [3] have been increasing over the past decade and is estimated to increase further in the coming years [4]. The exact cause of this surge remains unclear, but environmental changes associated with industrialization have long been suspected. Those changes include sanitization
P. Devarajan Z. Chen (&) Department of Microbiology and Immunology, University of Miami Miller School of Medicine, RMSB 3035, 1600 NW 10th Ave, Miami, FL 33136, USA e-mail: [email protected]
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from parasitic and microbial agents, as formulated in the hygiene hypothesis [5], and industrial pollutants that may alter the differentiation of immune cells [6–8]. Despite advances in treating autoimmune diseases, many of them involve general immunosuppression, leading to adverse side effects. A better understanding of the immunological causes of autoimmune diseases is needed for developing therapies that specifically target the pathogenic immunological subsets responsible for the a
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