NEUROIMMUNOLOGYAnti-myelin basic protein T cells protect hippocampal neurons against trimethyltin-induced damageKurkowska-Jastrzebska, Iwonaa; Joniec, Ilonac; Zaremba, Malgorzatab; Fiedorowicz, Annab; Czlonkowska, Annaa c; Oderfeld-Nowak, BarbarabAuthor Information a2nd Department of Neurology, Institute of Psychiatry and Neurology bLaboratory of Mechanisms of Neurodegeneration and Neuroprotection, Department of Molecular and Cellular Neurobiology Nencki Institute of Experimental Biology cDepartment of Clinical and Experimental Pharmacology, Medical University, Warsaw, Poland Correspondence to Dr Iwona Kurkowska-Jastrzebska, MD, PhD, 2nd Department of Neurology, Institute of Psychiatry and Neurology, ul. Sobieskiego 9, 02-957 Warsaw, Poland Tel: +48 22 8262116; fax: +48 22 8262116; e-mail: email@example.com, firstname.lastname@example.org Received 23 November 2006; accepted 13 December 2006 NeuroReport: March 26th, 2007 - Volume 18 - Issue 5 - p 425-429 doi: 10.1097/WNR.0b013e3280586777 Buy Metrics Abstract We investigated the influence of administration of autoimmune T cells on trimethyltin-induced degeneration of hippocampal neurons. Female Lewis rats received 8 mg/kg trimethyltin intraperitoneally alone, or followed 24 h later by a second intravenous injection of anti-myelin basic protein T cells (green fluorescent protein-tagged). Neurodegeneration was assessed by NeuN and Nissl cell counts 21 days after trimethyltin injection. We found that neurodegeneration in the CA4 region of the hippocampus was significantly reduced in the group receiving T cells. T cells also caused an augmentation of trimethyltin-induced hippocampal astrocytic activation and astrocytic TrkA expression, which was particularly intense in the CA4 region. Our study provides the first evidence of neuroprotection evoked by transferred T cells following a neurotoxic brain insult. The data suggest that mediation of the neuroprotective effects of T-cell-released nerve growth factor occurs mainly via hippocampal astroglial TrkA receptors. © 2007 Lippincott Williams & Wilkins, Inc.