First Author | Elhage R | Year | 2004 |
Journal | Am J Pathol | Volume | 165 |
Issue | 6 | Pages | 2013-8 |
PubMed ID | 15579444 | Mgi Jnum | J:94976 |
Mgi Id | MGI:3522392 | Doi | 10.1016/s0002-9440(10)63252-x |
Citation | Elhage R, et al. (2004) Deleting TCR alpha beta+ or CD4+ T lymphocytes leads to opposite effects on site-specific atherosclerosis in female apolipoprotein E-deficient mice. Am J Pathol 165(6):2013-8 |
abstractText | Recent studies have demonstrated the importance of lymphocytes, especially CD4(+) T cells, in early lesions of atherosclerosis in hypercholesterolemic mice. However, the role of other T cell subpopulations, like CD8(+) T cells or TCR gamma delta T lymphocytes, is not yet clear. We have therefore generated apolipoprotein E-deficient mice genetically deficient in specific T lymphocyte subpopulations and measured atherosclerotic lesions in the aortic sinus and en face whole aorta preparation at 18 weeks and at 1 year of age. Whereas TCR gamma delta(+) T lymphocytes appeared to play a modest role, TCR alpha beta(+) T lymphocytes played a major role as their deficiency significantly prevented early and late atherosclerosis at all arterial sites. However, neither CD4(+) nor CD8(+) T cells induced any significant decrease of the lesions at the aortic sinus, suggesting that compensatory proatherogenic mechanisms are operating at this site. Interestingly, the absence of CD4(+) T cells led to a dramatic increase in early lesion abundance at the level of the descending thoracic and abdominal aorta, which was still obvious at 1 year. In conclusion, whereas the TCR alpha beta(+) lymphocyte subset in its whole contribute to aggravate both early and late atherosclerosis, the CD4(+) T subpopulation appears to be critically protective at the level of the lower part of the aorta. |