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T-bet deficiency reduces atherosclerosis and alters plaque antigen-specific immune responses
Open accessAbstract
The influence of the immune system on atherosclerosis involves both helper T (Th) cell and antibody responses to plaque antigens. These responses may have proatherogenic and protective effects. T-bet is a transcription factor required for Th1 differentiation and regulates the balance between Th1 and Th2 responses in inflammatory diseases. To clarify how helper T cell subset differentiation influences atherosclerosis, we compared lesion development and immune responses to plaque antigens in low-density lipoprotein receptor-deficient ( Ldlr -/- ) mice with or without functional T-bet genes. Atherosclerosis was significantly reduced in T-bet-deficient Ldlr -/- mice compared with Ldlr -/- controls, and the lesions that did develop in the absence of T-bet had less smooth muscle cell content. Furthermore, T-bet deficiency caused a Th2 switch in the response to the atherosclerosis-associated antigen heat shock protein-60, and a change in T-dependent isotypes of oxidized LDL-specific antibodies. Of particular significance, T-bet deficiency caused a >250% increase in the titer of E06 antibodies, which are known to be atheroprotective and whose production by B-1 B cells is enhanced by IL-5. These findings establish that T cell subset differentiation influences both T cell and antibody responses that modulate atherosclerosis, and validate the therapeutic goal of skewing T responses to atherosclerosis-associated antigens.
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Citations
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Metadata
- Authors
- Buono, C., Binder, C. J., Stavrakis, G., Witztum, J. L., Glimcher, L. H., & Lichtman, A. H.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2005-01-21
- Volume
- 102
- Issue
- 5
- Pages
- 1596-1601
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2142462591
- Cited by
- 358
- References
- 0
- FWCI
- 4.94
- Type
- journal article
- Language
- en
- Open access
- green
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