期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 114, 期 9, 页码 1290-1298出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200422557
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资金
- NIAID NIH HHS [R01 AI009484, AI09484, U19 AI051973, AI44451, AI51973, R01 AI044451] Funding Source: Medline
- NIDDK NIH HHS [DK58541, R29 DK051091, R01 DK051091, R01 DK058541, DK51091] Funding Source: Medline
- NINDS NIH HHS [T32 NS041219, NS041219] Funding Source: Medline
We document here that infection of prediabetic mice with a virus expressing an H-2K(b)-restricted mimic ligand to a self epitope present on beta cells accelerates the development of autoimmune diabetes. Immunization with the mimic ligand expanded autoreactive T cell populations, which was followed by their trafficking to the islets, as visualized in situ by tetramer staining. In contrast, the mimic ligand did not generate sufficient autoreactive T cells in naive mice to initiate disease. Diabetes acceleration did not occur in H-2K(b)-deficient mice or in mice tolerized to the mimic ligand. Thus, arenavirus-expressed mimics of self antigens accelerate a previously established autoimmune process. Sequential heterologous viral infections might therefore act in concert to precipitate clinical autoimmune disease, even if single exposure to a viral mimic does not always cause sufficient tissue destruction.
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