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The study in Ldlr −/− mice found that Atg16l1-deficient CD11b + DCs produced a TGF-β-dependent tolerance phenotype and promoted CD4 + Treg cell expansion, reducing the development of atherosclerosis

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Size EU:37

In addition, RPE cell atrophy, photoreceptor cell death, drusen deposition, and inflammatory reactions are all induced by oxidative stress and caught in a vicious cycle 13