Abstract
The Ca2+-independent phospholipase A2β (iPLA2β) is a member of the PLA2 family that has been proposed to have roles in multiple biological processes including membrane remodeling, cell proliferation, bone formation, male fertility, cell death, and signaling. Such involvement has led to the identification of iPLA2β activation in several diseases such as cancer, cardiovascular abnormalities, glaucoma, periodontitis, neurological disorders, diabetes, and other metabolic disorders. More recently, there has been heightened interest in the role that iPLA2β plays in promoting inflammation. Recognizing the potential contribution of iPLA2β in the development of autoimmune diseases, we review this issue in the context of an iPLA2β link with macrophages and T-cells.
Highlights
Phospholipases A2 (PLA2 s) hydrolyze the sn-2 substituent of glycerophospholipids to release a lysophospholipid and a free fatty acid [1]
Summary independent PLA2 s (iPLA2 s)β is a member of the family of PLA2 s that hydrolyzes the sn-2 substituent from membrane glycerophospholipids
Activation of iPLA2 β can lead to the production of a variety of bioactive lipid mediators
Summary
Phospholipases A2 (PLA2 s) hydrolyze the sn-2 substituent of glycerophospholipids to release a lysophospholipid and a free fatty acid [1]. Crystal structure studies suggest that iPLA2 β forms a dimer through the interaction of the catalytic domains and that CAM binds to the dimer to cause a closed state, denying the access of substrates to the active site [4]. Relief from this inhibitory state is achieved through activation of calmodulin kinase IIβ, which forms a signaling complex with iPLA2 β [5]. In this paper, the basic functionality of these cells is discussed first, followed by a review of the specific impact of iPLA2 β in these immune cells, in the context of different pathophysiologies
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