Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 48, Issue 5, Pages 2273-2281Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST20200602
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Funding
- NIH [P01 HL136275, R35 HL145241, R01 HL148094, R01 HL146134, R01 HL140976]
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Atherosclerosis, the pathology underlying heart attacks, strokes and peripheral artery disease, is a chronic inflammatory disease of the artery wall initiated by elevated low-density lipoprotein (LDL) cholesterol levels. LDL accumulates in the artery wall, where it can become oxidized to oxLDL. T cell responses to ApoB, a core protein found in LDL and other lipoproteins, are detectable in healthy mice and people. Most of the ApoB-specific CD4T cells are FoxP3+ regulatory T cells (Treg). In the course of atherosclerosis development, the number of ApoB-reactive T cells expands. At the same time, their phenotype changes, showing cell surface markers, transcription factors and transcriptomes resembling other T-helper lineages like Th17, Th1 and follicular helper (TFH) cells. TFH cells enter germinal centers and provide T cell help to B cells, enabling antibody isotype switch from lgM to IgG and supporting affinity maturation. In people and mice with atherosclerosis, IgG and IgM antibodies to oxLDL are detectable. Higher IgM antibody titers to oxLDL are associated with less, IgG antibodies with more atherosclerosis. Thus, both T and B cells play critical roles in atherosclerosis. Modifying the adaptive immune response to ApoB holds promise for preventing atherosclerosis and reducing disease burden.
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