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B-lymphocyte deficiency increases atherosclerosis in LDL receptor-null mice
Amy S Major1, Sergio Fazio, MacRae F Linton
1Department of Medicine, Division of Cardiovascular Medicine, Vanderbilt University, Nashville, Tenn 37232-6300, USA.
Arteriosclerosis, Thrombosis, and Vascular Biology
|November 12, 2002
Summary
B cells and antibodies protect against atherosclerosis development. Their absence in mice significantly increased lesion size, indicating a crucial role for B cell-mediated immune regulation in preventing this inflammatory disease.
Area of Science:
- Immunology
- Cardiovascular Science
- Inflammation Biology
Background:
- Atherosclerosis is an inflammatory condition involving immune responses.
- The specific roles of B cells and antibodies in atherosclerosis progression are not fully understood.
Purpose of the Study:
- To investigate the impact of B cell deficiency on atherosclerosis development in low-density lipoprotein receptor-deficient (LDLR(-/-)) mice.
Main Methods:
- Generated LDLR(-/-) mice with severely reduced B cell populations using bone marrow transplantation.
- Administered a Western diet to assess atherosclerosis progression.
- Analyzed serum antibody levels, aortic lesion area, and cytokine expression (mRNA and protein).
- Evaluated splenocyte proliferation in response to oxidized low-density lipoprotein (oxLDL).
Main Results:
- B cell-deficient LDLR(-/-) mice exhibited significantly reduced serum antibodies, including anti-oxLDL antibodies.
- A 30-40% increase in aortic lesion area was observed in B cell-deficient mice.
- Decreased levels of proatherogenic (interferon-gamma) and antiatherogenic (interleukin-10, transforming growth factor-beta) cytokines were detected.
- Reduced splenocyte proliferation to oxLDL suggests a role for B cells in lipid antigen presentation.
Conclusions:
- B cells and antibodies demonstrate a protective effect against atherosclerosis.
- B cell-mediated immune regulation appears to be the mechanism conferring this protection.