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. 2020 Mar 20;8:185. doi: 10.3389/fcell.2020.00185

FIGURE 3.

FIGURE 3

Changes in the immune system in CKD lead to the development of CVD. The populations of classical (CD14++CD16-) monocytes in CKD decrease, while those of intermediate (CD14++CD16+) and non-classical (CD14+CD16+) monocytes increase. The intermediate (CD14++CD16+) and non-classical (CD14+CD16+) monocytes promote inflammation and proatherogenic milieu by upregulating the expression of adhesion molecules and production of microvesicles (MVs) in the endothelium; this contributes to the development of CVD in patients with CKD. Lymphopenia of both T and B lymphocytes is observed in CKD. The T lymphopenia is caused by the reduction of T regulatory cells (Treg), contrariwise the increase of pro-inflammatory T helper 17 lymphocytes (Th17). These changes in proportion of regulatory cells to proinflammatory cells can lead to inflammation. B lymphopenia is caused by decreased numbers of B1 and B2 cells. The numbers of B1 lymphocytes generally show a greater decline than those of B2, resulting in a B-lymphocyte imbalance. These two processes also participate in the development of CKD-associated CVD.