Altered immune responses in apolipoprotein E-deficient mice
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Discussion
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Implication
Animal study reveals altered antibody and delayed-type hypersensitivity responses in apolipoprotein E-deficient mice, indicating that lipid metabolism regulates immunity.
Key Points
- To determine the biological mechanisms through which apolipoprotein E modulates immune function using human in vitro assays and an in vivo mouse model.
- Assessed human T cell proliferation following stimulation with phytohemagglutinin, anti-CD3 antibodies, and tetanus toxoid in the presence of human apoE3 and apoE4 isoforms.
- Analyzed lymphoid organ cell counts, in vitro splenocyte proliferative responses, antigen-specific IgM titers, and delayed-type hypersensitivity in apoE-deficient and control C57BL/6 mice.
- Human apoE3 and apoE4 isoforms induced similar suppression of human T lymphocyte proliferation in response to mitogenic and antigen-specific activation.
- ApoE-deficient mice displayed intact lymphoid cell populations and normal in vitro splenocyte proliferation, but produced significantly higher antigen-specific IgM titers after tetanus toxoid immunization.
- ApoE-deficient mice demonstrated impaired delayed-type hypersensitivity responses compared to wild-type controls.
Cite This Study
Laskowitz et al. (2000) studied this question.