Omega-3 fatty acids have been shown to disrupt inflammation cell signaling pathways by binding to the GPR120 receptor.  This benefit however can be inhibited or even reversed if the ratio of Omega-6 / Omega-3 is too high as Omega-6 serves as a precursor to inflammatory chemicals ( prostaglandin and leukotriene eicosanoids ) in the body.   A high proportion of omega-6 to omega-3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, proinflammatory and proconstrictive.  Omega-6 competes with Omega-3 for the same rate limiting factor which is required for the health-benefits of Omega-3, directly reducing the action of Omega-3 in addition to pharmacologically counteracting Omega-3 benefits through its own action as a pro-inflammatory agent.
Interleukin-10 (IL-10) is a key immunoregulatory cytokine that can be produced by almost all leukocytes, including innate immune cells such as monocytes, macrophages, DCs, mast cells, natural killer cells, eosinophils, and neutrophils, and adaptive immune cells such as Th1, Th2, Treg, Tr1, Th3, γδ T, CD8 + T, and B cells [ 21 , 22 ], and the recently discovered Th17 and Th22 cells [ 23 , 24 ], with macrophages, DCs, and Th cells are the major sources. It has now been established that the production of IL-10 can be induced by Toll-like receptor (TLR) or non-TLR signaling in macrophages and myeloid DCs [ 25 ].