{'fraction_non_alphanumeric': 0.017905102954341987, 'fraction_numerical': 0.006266786034019696, 'mean_word_length': 5.654761904761905, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Anti-myelin basic protein T cells protect hippocampal neurons against trimethyltin-induced damage

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.