Lymphotoxin organizes contributions to host defense and metabolic illness from innate lymphoid cells |
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| Institution: | 1. Committee on Immunology, University of Chicago, United States;2. Department of Pathology, University of Chicago, United States;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. 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. 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. 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. Department of Oncology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada;2. Department of Obstetrics and Gynecology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada;3. Department of Laboratory Medicine and Pathology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada |
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| Abstract: | The lymphotoxin (LT)-pathway is a unique constituent branch of the Tumor Necrosis Superfamily (TNFSF). Use of LT is a critical mechanism by which fetal innate lymphoid cells regulate lymphoid organogenesis. Within recent years, adult innate lymphoid cells have been discovered to utilize this same pathway to regulate IL-22 and IL-23 production for host defense. Notably, genetic studies have linked polymorphisms in the genes encoding LTα to several phenotypes contributing to metabolic syndrome. The role of the LT-pathway may lay the foundation for a bridge between host immune response, microbiota, and metabolic syndrome. The contribution of the LT-pathway to innate lymphoid cell function and metabolic syndrome will be visited in this review. |
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| Keywords: | Lymphotoxin Innate lymphoid cells Host defense Metabolic syndrome Microbiota |
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