{'fraction_non_alphanumeric': 0.022157434402332362, 'fraction_numerical': 0.023323615160349854, 'mean_word_length': 5.085106382978723, '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}}
Immune Response to the Antigen Arthritis Without Impairing the Systemic IL-10 Ameliorate Experimentally Induced Antigen-Specific T Cells Transduced with

For the treatment of rheumatoid arthritis, efﬁcient drug delivery methods to the inﬂamed joints need to be developed. Because T cells expressing an appropriate autoantigen-speciﬁc receptor can migrate to inﬂamed lesions, it has been reasoned that they can be employed to deliver therapeutic agents. To examine the ability and efﬁciency of such T cells as a vehicle, we employed an experimentally induced model of arthritis. Splenic T cells from DO11.10 TCR transgenic mice speciﬁc for OVA were transduced with murine IL-10. Adoptive transfer of the IL-10-transduced DO11.10 splenocytes ameliorated OVA-induced arthritis despite the presence of around 95% nontransduced cells. Using green ﬂuorescent protein as a marker for selection, the number of transferred cells needed to ameliorate the disease was able to be reduced to 10 4 . Preferential accumulation of the transferred T cells was observed in the inﬂamed joint, and the improvement in the disease was not accompanied by impairment of the systemic immune response to the Ag, suggesting that the transferred T cells exert their anti-inﬂammatory task locally, mainly in the joints where the Ag exists. In addition, IL-10-transduced DO11.10 T cells ameliorated methylated BSA-induced arthritis when the arthritic joint was coinjected with OVA in addition to methylated BSA. These results suggest that T cells speciﬁc for a joint-speciﬁc Ag would be useful as a therapeutic vehicle in rheumatoid arthritis for which the arthritic autoantigen is still unknown. The Journal of Immunology, 2000, 165: 5980–5986.