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Deficiency of invariant Vα14 natural killer T cells decreases atherosclerosis in LDL receptor null mice
| Content Provider | Semantic Scholar |
|---|---|
| Author | Rogers, Leah D. Burchat, Sarah Gage, Jessica Hasu, Mirela Thabet, Mohamad Wilcox, Lindsay Ramsamy, Tanya A. Whitman, Stewart C. |
| Copyright Year | 2008 |
| Abstract | AIMS CD1d-restricted natural killer T (NKT) cells function by regulating numerous immune responses during innate and adaptive immunity. Depletion of all populations of CD1d-dependent NKT cells has been shown by several groups to reduce atherosclerosis in two different mouse models of the disease. In this study, we determined if removal of a single (V alpha 14) NKT cell population protects mice from the disease. METHODS AND RESULTS Targeted deletion of the J alpha 18 gene results in selective depletion of CD1d-dependent V alpha 14 NKT cells in C57BL/6 mice without affecting the population of other NKT, NK, and conventional T cells. Therefore, to study the effect of V alpha 14 NKT cell depletion on the progression of atherosclerosis, we examined the extent of lesion formation using paired littermate LDL receptor null mice that were either +/+ or -/- for the J alpha 18 gene following the feeding of these mice a cholesterol- and fat-enriched diet for 8 weeks. At the end of the study, we found no difference in either serum total- or lipoprotein-cholesterol distributions between groups. However, quantification of atherosclerosis revealed that V alpha 14 NKT cell deficiency significantly decreased lesion size in the aortic root (20-28%) and arch (28-38%) in both genders of mice. By coupling the techniques of laser capture microdissection with quantitative real-time RT-PCR, we found that expression of the proatherogenic cytokine interferon (IFN)-gamma was significantly reduced in lesions from J alpha 18-/- mice. CONCLUSION This study is the first to identify a specific subpopulation of NKT cells that promotes atherosclerosis via a mechanism appearing to involve IFN-gamma expression. |
| Starting Page | 167 |
| Ending Page | 174 |
| Page Count | 8 |
| File Format | PDF HTM / HTML |
| DOI | 10.1093/cvr/cvn005 |
| Alternate Webpage(s) | https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/96/c1/cvn005.PMC5439367.pdf |
| PubMed reference number | 18192239 |
| Alternate Webpage(s) | https://doi.org/10.1093/cvr%2Fcvn005 |
| Journal | Medline |
| Volume Number | 78 |
| Journal | Cardiovascular research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
