{"entity": "journal", "iuid": "5d842dc2022d4001b598feac0d7c8ec6", "timestamp": "2026-08-10T19:38:37.871Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Neuroinflammation.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Neuroinflammation"}}, "title": "J Neuroinflammation", "issn": "1742-2094", "issn-l": "1742-2094", "publications_count": 2, "publications": [{"entity": "publication", "iuid": "e4ec50a777b949658a766bb79bf10e0f", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/e4ec50a777b949658a766bb79bf10e0f.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/e4ec50a777b949658a766bb79bf10e0f"}}, "title": "Electroconvulsive therapy suppresses the neurotoxic branch of the kynurenine pathway in treatment-resistant depressed patients.", "authors": [{"family": "Schwieler", "given": "Lilly", "initials": "L"}, {"family": "Samuelsson", "given": "Martin", "initials": "M"}, {"family": "Frye", "given": "Mark A", "initials": "MA"}, {"family": "Bhat", "given": "Maria", "initials": "M"}, {"family": "Schuppe-Koistinen", "given": "Ina", "initials": "I"}, {"family": "Jungholm", "given": "Oscar", "initials": "O"}, {"family": "Johansson", "given": "Anette G", "initials": "AG"}, {"family": "Land\u00e9n", "given": "Mikael", "initials": "M"}, {"family": "Sellgren", "given": "Carl M", "initials": "CM"}, {"family": "Erhardt", "given": "Sophie", "initials": "S"}], "type": "journal article", "published": "2016-02-29", "journal": {"title": "J Neuroinflammation", "issn": "1742-2094", "volume": "13", "issue": "1", "pages": "51", "issn-l": "1742-2094"}, "abstract": "Neuroinflammation is increasingly recognized as contributing to the pathogenesis of depression. Key inflammatory markers as well as kynurenic acid (KYNA) and quinolinic acid (QUIN), both tryptophan metabolites, have been associated with depressive symptoms and suicidality. The aim of the present study is to investigate the peripheral concentration of cytokines and tryptophan and kynurenine metabolites in patients with unipolar treatment-resistant depression before and after electroconvulsive therapy (ECT), the most effective treatment for depression.\n\nCytokines in plasma from patients with major depressive disorder (MDD; n\u2009=\u200919) and healthy volunteers (n\u2009=\u200914) were analyzed with electrochemiluminescence detection. Tryptophan and kynurenine metabolites were detected with high-performance liquid chromatography (HPLC) and LC/MS. KYNA was analyzed in a second healthy control cohort (n\u2009=\u200922).\n\nPatients with MDD had increased plasma levels of interleukin (IL)-6 compared to healthy volunteers (P\u2009<\u20090.05). We also found an altered kynurenine metabolism in these patients displayed by decreased plasma levels of KYNA (P\u2009<\u20090.0001) as well as a significantly increased QUIN/KYNA ratio (P\u2009<\u20090.001). Plasma levels of tryptophan, kynurenine, and QUIN did not differ between patients and controls. Treatment with ECT was associated with a significant decrease in the plasma levels of tryptophan (P\u2009<\u20090.05), kynurenine (P\u2009<\u20090.01), and QUIN (P\u2009<\u20090.001), whereas plasma levels of KYNA did not change. The QUIN/KYNA ratio was found to significantly decrease in ECT-treated patients (P\u2009<\u20090.05). There was a significant inverse correlation between symptom severity and kynurenine levels at baseline (r\u2009=\u2009-0.67, P\u2009=\u20090.002).\n\nThis study confirms an imbalanced kynurenine pathway in MDD supporting the hypothesis of a netstimulation of N-methyl-D-aspartic acid (NMDA) receptors in the disorder. Treatment with ECT profoundly decreased QUIN, an NMDA-receptor agonist previously suggested to be implicated in the pathogenesis of depression, an effect that might have bearing for the good clinical outcome of ECT.", "doi": "10.1186/s12974-016-0517-7", "pmid": "26925576", "labels": {"Affiliated researcher": null}, "xrefs": [{"db": "pii", "key": "10.1186/s12974-016-0517-7"}, {"db": "pmc", "key": "PMC4772340"}], "notes": [], "created": "2018-12-05T09:40:43.984Z", "modified": "2018-12-05T09:40:44.004Z"}, {"entity": "publication", "iuid": "8089c98f3ad848b7b112a18ad794076c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/8089c98f3ad848b7b112a18ad794076c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/8089c98f3ad848b7b112a18ad794076c"}}, "title": "CAR/FoxP3-engineered T regulatory cells target the CNS and suppress EAE upon intranasal delivery.", "authors": [{"family": "Fransson", "given": "Moa", "initials": "M"}, {"family": "Piras", "given": "Elena", "initials": "E"}, {"family": "Burman", "given": "Joachim", "initials": "J"}, {"family": "Nilsson", "given": "Berith", "initials": "B"}, {"family": "Essand", "given": "Magnus", "initials": "M"}, {"family": "Lu", "given": "Binfeng", "initials": "B"}, {"family": "Harris", "given": "Robert A", "initials": "RA"}, {"family": "Magnusson", "given": "Peetra U", "initials": "PU"}, {"family": "Brittebo", "given": "Eva", "initials": "E"}, {"family": "Loskog", "given": "Angelica S I", "initials": "AS"}], "type": "journal article", "published": "2012-05-30", "journal": {"title": "J Neuroinflammation", "issn": "1742-2094", "volume": "9", "issue": null, "pages": "112", "issn-l": "1742-2094"}, "abstract": "Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). In the murine experimental autoimmune encephalomyelitis (EAE) model of MS, T regulatory (Treg) cell therapy has proved to be beneficial, but generation of stable CNS-targeting Tregs needs further development. Here, we propose gene engineering to achieve CNS-targeting Tregs from na\u00efve CD4 cells and demonstrate their efficacy in the EAE model.\n\nCD4+ T cells were modified utilizing a lentiviral vector system to express a chimeric antigen receptor (CAR) targeting myelin oligodendrocyte glycoprotein (MOG) in trans with the murine FoxP3 gene that drives Treg differentiation. The cells were evaluated in vitro for suppressive capacity and in C57BL/6 mice to treat EAE. Cells were administered by intranasal (i.n.) cell delivery.\n\nThe engineered Tregs demonstrated suppressive capacity in vitro and could efficiently access various regions in the brain via i.n cell delivery. Clinical score 3 EAE mice were treated and the engineered Tregs suppressed ongoing encephalomyelitis as demonstrated by reduced disease symptoms as well as decreased IL-12 and IFNgamma mRNAs in brain tissue. Immunohistochemical markers for myelination (MBP) and reactive astrogliosis (GFAP) confirmed recovery in mice treated with engineered Tregs compared to controls. Symptom-free mice were rechallenged with a second EAE-inducing inoculum but remained healthy, demonstrating the sustained effect of engineered Tregs.\n\nCNS-targeting Tregs delivered i.n. localized to the CNS and efficiently suppressed ongoing inflammation leading to diminished disease symptoms.", "doi": "10.1186/1742-2094-9-112", "pmid": "22647574", "labels": {"Affiliated researcher": null}, "xrefs": [{"db": "pii", "key": "1742-2094-9-112"}, {"db": "pmc", "key": "PMC3403996"}], "notes": [], "created": "2018-12-05T08:46:15.364Z", "modified": "2018-12-05T08:46:15.396Z"}], "created": "2018-12-05T08:46:15.378Z", "modified": "2020-11-27T13:12:56.655Z"}