Abstract
Atherosclerosis is a lipid-driven inflammatory disease of blood vessels, and both innate and adaptive immune responses are involved in its development. The impact of B cells on atherosclerosis has been demonstrated in numerous studies and B cells have been found in close proximity to atherosclerotic plaques in humans and mice. B cells exert both atheroprotective and pro-atherogenic functions, which have been associated with their B cell subset attribution. While B1 cells and marginal zone B cells are considered to protect against atherosclerosis, follicular B cells and innate response activator B cells have been shown to promote atherosclerosis. In this review, we shed light on the role of B cells from a different, functional perspective and focus on the three major B cell functions: antibody production, antigen presentation/T cell interaction, and the release of cytokines. All of these functions have the potential to affect atherosclerosis by multiple ways and are dependent on the cellular milieu and the activation status of the B cell. Moreover, we discuss B cell receptor signaling and the mechanism of B cell activation under atherosclerosis-prone conditions. By summarizing current knowledge of B cells in and beyond atherosclerosis, we are pointing out open questions and enabling new perspectives.
Highlights
Cardiovascular diseases (CVDs) are the main cause of death worldwide
The presence of immunoglobulins against oxidation-specific epitopes (OSEs), development of germinal center (GC), and an increase in anti-oxLDL Ab-secreting plasma cells strongly support the idea that B cell receptor (BCR) do recognize some OSE-related antigens in atherosclerosis [30,31]; they likely induce BCR-dependent signaling in the B cell
Recent studies that have been focused on the role of B cell subsets have generated new insights and opportunities to reveal the components of B cell responses in CVD
Summary
Cardiovascular diseases (CVDs) are the main cause of death worldwide. An estimated 17.9 million people died from CVDs in 2016 with the main cause for these deaths due to heart attack and stroke driven by developed atherosclerosis (World Health Organization report). With the progression of the atherosclerotic plaque, further accumulation of modified LDL (mLDL) induces the recruitment of inflammatory monocytes that differentiate to either MΦs or vDCs serving as antigen-presenting cells that drive the T cell activation in atherosclerosis and further aggravate inflammatory responses [11]. IL-17-producing CD4+ and IL17+ γδ+ T cells are detected in the plaques, where they likely support the development of atherosclerosis via the regulation of myeloid cell migration to the aorta and provide plaque stability via TGFβ-dependent mechanisms; other studies suggest a protective role of Th17 cells [13]. While it is likely that the main activation of adaptive immunity occurs in secondary lymphoid tissues, data suggest that local antigen presentation, activation of T cells, and induction of Tregs take place in the aorta and in tertiary lymphoid structures that are formed in the adventitia of aged atherosclerotic vessels [16]. Five types of MΦs, five types of T cells, two types of monocytes, three types of DCs, NK, ILC2 cells as well as B1 (CD79a and b, CCR7, and MZB1) and B2 (TPPP33, S100A6, and CD9) cells were found in the murine aorta [17]
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