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      Aspects of Tryptophan and Nicotinamide Adenine Dinucleotide in Immunity: A New Twist in an Old Tale

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          Abstract

          Increasing evidence underscores the interesting ability of tryptophan to regulate immune responses. However, the exact mechanisms of tryptophan’s immune regulation remain to be determined. Tryptophan catabolism via the kynurenine pathway is known to play an important role in tryptophan’s involvement in immune responses. Interestingly, quinolinic acid, which is a neurotoxic catabolite of the kynurenine pathway, is the major pathway for the de novo synthesis of nicotinamide adenine dinucleotide (NAD+). Recent studies have shown that NAD+, a natural coenzyme found in all living cells, regulates immune responses and creates homeostasis via a novel signaling pathway. More importantly, the immunoregulatory properties of NAD+ are strongly related to the overexpression of tryptophan hydroxylase 1 (Tph1). This review provides recent knowledge of tryptophan and NAD+ and their specific and intriguing roles in the immune system. Furthermore, it focuses on the mechanisms by which tryptophan regulates NAD+ synthesis as well as innate and adaptive immune responses.

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          Most cited references97

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          Behavioural phenotyping assays for mouse models of autism.

          Autism is a heterogeneous neurodevelopmental disorder of unknown aetiology that affects 1 in 100-150 individuals. Diagnosis is based on three categories of behavioural criteria: abnormal social interactions, communication deficits and repetitive behaviours. Strong evidence for a genetic basis has prompted the development of mouse models with targeted mutations in candidate genes for autism. As the diagnostic criteria for autism are behavioural, phenotyping these mouse models requires behavioural assays with high relevance to each category of the diagnostic symptoms. Behavioural neuroscientists are generating a comprehensive set of assays for social interaction, communication and repetitive behaviours to test hypotheses about the causes of autism. Robust phenotypes in mouse models hold great promise as translational tools for discovering effective treatments for components of autism spectrum disorders.
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            IDO expression by dendritic cells: tolerance and tryptophan catabolism.

            Indoleamine 2,3-dioxygenase (IDO) is an enzyme that degrades the essential amino acid tryptophan. The concept that cells expressing IDO can suppress T-cell responses and promote tolerance is a relatively new paradigm in immunology. Considerable evidence now supports this hypothesis, including studies of mammalian pregnancy, tumour resistance, chronic infections and autoimmune diseases. In this review, we summarize key recent developments and propose a unifying model for the role of IDO in tolerance induction.
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              Advances in autism genetics: on the threshold of a new neurobiology.

              Autism is a heterogeneous syndrome defined by impairments in three core domains: social interaction, language and range of interests. Recent work has led to the identification of several autism susceptibility genes and an increased appreciation of the contribution of de novo and inherited copy number variation. Promising strategies are also being applied to identify common genetic risk variants. Systems biology approaches, including array-based expression profiling, are poised to provide additional insights into this group of disorders, in which heterogeneity, both genetic and phenotypic, is emerging as a dominant theme.
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                Author and article information

                Journal
                Int J Tryptophan Res
                Int J Tryptophan Res
                International Journal of Tryptophan Research
                International Journal of Tryptophan Research : IJTR
                SAGE Publications (Sage UK: London, England )
                1178-6469
                2017
                14 June 2017
                : 10
                : 1178646917713491
                Affiliations
                [1 ]Department of Cardiovascular Surgery, University Hospital Zurich, Zurich, Switzerland.
                [2 ]Angiogenesis and Brain Development Laboratory, Division of Basic Neuroscience, McLean Hospital and Harvard Medical School, Belmont, MA, USA.
                [3 ]Division of Transplant Surgery and Transplantation Surgery Research Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA.
                Author notes
                CORRESPONDING AUTHOR: Abdallah Elkhal, Division of Transplant Surgery and Transplantation Surgery Research Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA. Email: aelkhal@ 123456partners.org
                Article
                10.1177_1178646917713491
                10.1177/1178646917713491
                5476425
                28659716
                484ad610-33c5-43c2-8c7f-5738a7746ae5
                © The Author(s) 2017

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 30 November 2016
                : 07 April 2017
                Categories
                Review

                Biochemistry
                nicotinamide adenine dinucleotide,nad+,immune responses,tryptophan,kynurenine pathway
                Biochemistry
                nicotinamide adenine dinucleotide, nad+, immune responses, tryptophan, kynurenine pathway

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