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. Author manuscript; available in PMC: 2015 Apr 22.
Published in final edited form as: Circulation. 2014 Jan 31;129(16):1677–1687. doi: 10.1161/CIRCULATIONAHA.113.006381

Figure 6.

Figure 6

Model of IRA B cell-dependent TH1 skewing during atherosclerosis. During atherosclerosis IRA B cells arise in secondary lymphoid organs via Myd88-dependent signaling and promote the generation of classical IL-12 producing classical dendritic cells (cDC). CD4+ T-helper cells that recognize disease related antigens (i.e. oxidation specific epiptopes) presented by these cDC differentiate into IFNγ-producing TH1 cells. TH1 cells infiltrate atherosclerotic lesions and stimulate macrophages. Antigen-specific interaction between TH1 cells and B cells leads to IFNγ-dependent isotype switching from IgG1 to IgG2a/c which carry the highest Fcγ-receptor mediated activation capacity. By instructing TH1-priming cDC IRA B cells aid in bridging innate and adaptive immunity. Solid arrows depict functional relationship and dashed arrows depict spatial relationship.