期刊
ATHEROSCLEROSIS
卷 215, 期 2, 页码 471-474出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2010.12.034
关键词
IL-17A; Antibody; Bone marrow transplantation; Inflammation; Atherosclerosis
资金
- National Natural Science Foundation of China [30871067]
- Program for New Century Excellent Talents in University [NCET-09-0380]
- National Basic Research Program of China [2007CB512000, 2007CB512005]
- FP7 TOLERAGE network
- British Heart Foundation [RG/10/001/27643] Funding Source: researchfish
Objective: To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. Methods and results: ApoE(-/-) mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks (n = 8-10 per group). Ldlr(-/-) mice were transplanted with IL-17A-deficient or wild type bone marrow (n = 8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% (p < 0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production. Conclusions: Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE(-/-) and Ldlr(-/-) mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE(-/-) mice could not be attributed to blockade of IL-17A signaling. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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