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Quantitative and qualitative differences in proatherogenic NKT cells in apolipoprotein E-deficient mice
Amy S Major1, Michael T Wilson, Jennifer L McCaleb
1Department of Medicine, Division of Cardiovascular Medicine, 2220 Pierce Avenue, Room 383 PRB, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. amy.major@vanderbilt.edu
Arteriosclerosis, Thrombosis, and Vascular Biology
|October 9, 2004
Summary
Natural killer T (NKT) cells play a significant role in atherosclerosis development. These immune cells are proatherogenic, meaning they promote the progression of atherosclerosis.
Area of Science:
- Immunology
- Cardiovascular Research
- Autoimmune Diseases
Background:
- Atherosclerosis involves lipid accumulation and inflammation, increasingly viewed as an autoimmune-type syndrome.
- Natural killer T (NKT) cells bridge innate and adaptive immunity, recognizing lipid antigens via CD1d molecules.
- NKT cell's immune-modulating capacity suggests a role in the development of atherosclerosis.
Purpose of the Study:
- To investigate the role of NKT cells in atherogenesis.
- To determine how the atherosclerotic environment impacts NKT cell populations.
Main Methods:
- Examined NKT cell function in apolipoprotein E-deficient (apoE(0)) mice, a model for atherosclerosis.
- Utilized CD1d-deficient mice and alpha-galactosylceramide (a specific NKT cell activator) treatment.
- Assessed age-dependent differences in NKT cell responses and interferon-gamma production.
Main Results:
- CD1d deficiency in apoE(0) mice reduced atherosclerosis.
- Activation of NKT cells with alpha-galactosylceramide increased atherosclerosis by twofold in apoE(0) mice.
- NKT cell responses and numbers exhibited age-dependent variations in apoE(0) mice compared to wild-type controls.
Conclusions:
- Hyperlipidemia and atherosclerosis significantly impact NKT cell responses.
- NKT cells are identified as proatherogenic, contributing to the progression of atherosclerosis.