The Lymphotoxin Network: Orchestrating a Type I interferon response to optimize adaptive immunity |
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| Institution: | 1. Department of Immunology, University of Toronto, Toronto, Ontario, Canada;2. Department of Microbiology and Section of Rheumatology, Boston University School of Medicine, Boston, MA 02118, USA;3. Infectious and Inflammatory Disease Center, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA;1. Department of Biological Chemistry, The Weizmann Institute of Science, 76100 Rehovot, Israel;2. Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chung-Ju 380-701, Republic of Korea;1. Department of Microbiology, The University of Iowa, USA;2. The Graduate Program in Immunology, The University of Iowa, USA;3. Department of Internal Medicine, The University of Iowa, USA;4. Veterans Affairs Medical Center, Iowa City, IA 52242, USA;1. Joint Center for Translational Research of Chronic Diseases, Changhai Hospital, The Second Military Medical University, Shanghai 2000433, China;2. Department of Molecular Pharmacology and Chemistry, Sloan-Kettering Institute, New York, NY 10021, USA;3. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA;4. Program in Cellular and Molecular Medicine, Boston Children''s Hospital, Boston, MA 02115, USA;5. Department of Biochemistry, Weill Cornell Medical College, New York, NY 10065, USA;1. AbbVie Bioresearch Center, 100 Research Drive, Worcester, MA 01605, United States;2. Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6082, United States;1. Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, United States;2. Department of Immunology, Biogen Idec, 12 Cambridge Center, Cambridge, MA 02142, United States;1. Applied and Developmental Research Directorate, Laboratory of Human Retrovirology, Science Application International Corporation (SAIC)-Frederick, Inc., Frederick National Laboratory for Cancer Research, 1050 Boyles Street, Frederick, MD 21702, USA;2. Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, Rm. 4-1479, MSC 1460, Bethesda, MD 20892-1360, USA |
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| Abstract: | The Lymphotoxin (LT) pathway is best known for its role in orchestrating the development and homeostasis of lymph nodes and Peyer's patches through the regulation of homeostatic chemokines. More recently an appreciation of the LTβR pathway in the production of Type I interferons (IFN-I) during homeostasis and infection has emerged. LTβR signaling is essential in differentiating stromal cells and macrophages in lymphoid organs to rapidly produce IFN-I in response to virus infections independently of the conventional TLR signaling systems. In addition, LTβR signaling is required to produce homeostatic levels of IFN-I from dendritic cells in order to effectively cross-prime a CD8+ T cell response to protein antigen. Importantly, pharmacological inhibition of LTβR signaling in mice has a profound positive impact on a number of autoimmune disease models, although it remains unclear if this efficacy is linked to IFN-I production during chronic inflammation. In this review, we will provide a brief overview of how the “Lymphotoxin Network” is linked to the IFN-I response and its impact on the immune system. |
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| Keywords: | Autoimmunity Dendritic cells Interferon (IFN) Lymphotoxin-αβ (LTαβ) Stromal cells |
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