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000119439 1001_ $$0P:(DE-He78)22a10e47ef85d2b98a12b21a7f332e56$$aLanz, Tobias$$b0$$eFirst author$$udkfz
000119439 245__ $$aTryptophan-2,3-Dioxygenase (TDO) deficiency is associated with subclinical neuroprotection in a mouse model of multiple sclerosis.
000119439 260__ $$aLondon$$bNature Publishing Group$$c2017
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000119439 520__ $$aThe catabolism of tryptophan to immunosuppressive and neuroactive kynurenines is a key metabolic pathway regulating immune responses and neurotoxicity. The rate-limiting step is controlled by indoleamine-2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO). IDO is expressed in antigen presenting cells during immune reactions, hepatic TDO regulates blood homeostasis of tryptophan and neuronal TDO influences neurogenesis. While the role of IDO has been described in multiple immunological settings, little is known about TDO's effects on the immune system. TDO-deficiency is neuroprotective in C. elegans and Drosophila by increasing tryptophan and specific kynurenines. Here we have determined the role of TDO in autoimmunity and neurodegeneration in experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. We created reporter-TDO mice for in vivo imaging to show that hepatic but not CNS TDO expression is activated during EAE. TDO deficiency did not influence myelin-specific T cells, leukocyte infiltration into the CNS, demyelination and disease activity. TDO-deficiency protected from neuronal loss in the spinal cord but not in the optic nerves. While this protection did not translate to an improved overt clinical outcome, our data suggest that spatially distinct neuroprotection is conserved in mammals and support TDO as a potential target for treatment of diseases associated with neurodegeneration.
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000119439 7001_ $$aWilliams, Sarah K$$b1
000119439 7001_ $$aStojic, Aleksandar$$b2
000119439 7001_ $$aIwantscheff, Simeon$$b3
000119439 7001_ $$0P:(DE-He78)1f1efec9a95d1778031cb6f0b19ba58b$$aSonner, Jana$$b4$$udkfz
000119439 7001_ $$aGrabitz, Carl$$b5
000119439 7001_ $$0P:(DE-He78)a7dd606f37ce122c7f1c4140e754d515$$aBecker, Simon$$b6$$udkfz
000119439 7001_ $$0P:(DE-He78)1afad4d0b5b6ef348b8fdcd72739b278$$aBöhler, Laura-Inés$$b7$$udkfz
000119439 7001_ $$0P:(DE-He78)0a6d2d4e161256f6ce1ca4b630bcf246$$aMohapatra, Soumya Ranjan$$b8$$udkfz
000119439 7001_ $$0P:(DE-He78)a1f4b408b9155beb2a8f7cba4d04fe88$$aSahm, Felix$$b9$$udkfz
000119439 7001_ $$0P:(DE-He78)b8759faaf3e907bcd8b6a34983994a3c$$aKüblbeck, Günter$$b10$$udkfz
000119439 7001_ $$aNakamura, Toshikazu$$b11
000119439 7001_ $$aFunakoshi, Hiroshi$$b12
000119439 7001_ $$0P:(DE-He78)14aa02d2ca0515d0c53f1d6678e3ca34$$aOpitz, Christiane$$b13$$udkfz
000119439 7001_ $$0P:(DE-He78)92e9783ca7025f36ce14e12cd348d2ee$$aWick, Wolfgang$$b14$$udkfz
000119439 7001_ $$0P:(DE-He78)0b1c40947becd495c5aa9778ef098ef4$$aDiem, Ricarda$$b15$$udkfz
000119439 7001_ $$0P:(DE-He78)5ef8651b0f857b9c640aa5b1498c43b5$$aPlatten, Michael$$b16$$eLast author$$udkfz
000119439 773__ $$0PERI:(DE-600)2615211-3$$a10.1038/srep41271$$gVol. 7, p. 41271 -$$p41271 -$$tScientific reports$$v7$$x2045-2322$$y2017
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