Significance
Lipid droplets (LDs) are ubiquitous organelles that play important roles in cellular energy homeostasis, tightly regulating the accumulation and release of lipids. In macrophages, lipids accumulate in LDs during inflammation. However, it is unclear how inflammatory activation promotes the accumulation of lipids in LDs, and how the dynamic between lipid accumulation and breakdown could drive or inhibit inflammation. Elucidating the role of lipid accumulation during inflammation may provide important knowledge to influence inflammatory processes during health and disease. We identify the importance of the hypoxia-inducible lipid droplet–associated protein and the intracellular adipose triglyceride lipase in the regulation of lipid accumulation and breakdown in inflammatory macrophages. Furthermore, we determine the regulatory effect of lipid breakdown from LDs in supporting inflammation.
As of late, evidence has been emerging that the Maillard reaction (MR, also referred to as glycation) affects the structure and function of food proteins. MR induces the conformational and chemical modification of food proteins, not only on the level of IgG/IgE recognition, but also by increasing the interaction and recognition of these modified proteins by antigen-presenting cells (APCs). This affects their biological properties, including digestibility, bioavailability, immunogenicity, and ultimately their allergenicity. APCs possess various receptors that recognize glycation structures, which include receptor for advanced glycation end products (RAGE), scavenger receptors (SRs), galectin-3 and CD36. Through these receptors, glycation structures may influence the recognition, uptake and antigen-processing of food allergens by dendritic cells (DCs) and monocytes. This may lead to enhanced cytokine production and maturation of DCs, and may also induce adaptive immune responses to the antigens/allergens as a result of antigen uptake, processing and presentation to T cells. Here, we aim to review the current literature on the immunogenicity of AGEs originating from food (exogenous or dietary AGEs) in relation to AGEs that are formed within the body (endogenous AGEs), their interactions with receptors present on immune cells, and their effects on the activation of the innate as well as the adaptive immune system. Finally, we review the clinical relevance of AGEs in food allergies.
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