Table 1 The role of important immune cells that involve in kidney disease

Immune cells

Macrophage

Macrophages can induce kidney lymphangiogenesis through upregulated expression level of VEGF-C and can also directly promote lymphangiogenesis through transdifferentiating into LECs[43, 114, 116]

M1 macrophages enhance lymphangiogenesis and promote kidney inflammation response, aggravating kidney injury[51, 53]

M2 macrophages promote tissue fibrosis process in the context of chronic kidney disease and kidney fibrosis [53]

Macrophages aggravate kidney damage and elevating blood pressure level. Meanwhile, hypertensive condition activates TonEBP in VEGF-C-expressing macrophages, leading to expression of VEGF-C, which promotes lymphangiogenesis, subsequently enhancing removal of excessive interstitial fluid [102]

M1 macrophages are the predominant macrophages within DKD, which enhance the inflammation response through secreting pro-inflammatory cytokines and presenting antigens to initiate immune response, ultimately causing renal injury. M2 macrophages can suppress the immune response within DKD through expressing anti-inflammatory cytokines [155,156,157]

CD137L-secreted macrophages interact with CD137 on LECs, inducing lymphatics autophagy and lymphangiogenesis [140]

M2 macrophages promote tissue fibrosis process in the context of chronic kidney disease and kidney fibrosis [53]

M2 macrophages are predominant macrophage within PKD. They promote the growing of cysts [144]

Cytotoxic T cell

Activated CD8 + T cells directly promote immune response at injury site. In contrast, infiltrated CD8 + T cells can induce LECs to produce PD-L1, further suppressing local CD8 + T cell [67]

IFN-γ-producing CD8 + T cells inhibit the differentiation of CD4 + T cell into Th2 cells, subsequently control kidney inflammation and fibrosis [88, 89]

CD11c + CD8 + T cells induce fibroblast apoptosis in obstructed kidney disease [88, 89]

CD8⁺ T cells present a protective role in the context of PKD [146]

Th cell

Th17 cells recruits neutrophils and other inflammatory cells to significantly aggravates kidney tissue damage and accelerates the progression to CKD [65, 66]

Th17 cells and Th2 cells present a profibrotic effect on injured site [86, 87]

Th1 cells and T17 cells secrete pro-inflammatory and pro-hypertensive cytokines, ultimately causing kidney tissue damage and sodium retention [110]

Th17 and Th1 cells conduct a strong pro-inflammatory response within DKD. Th 2 cells mainly suppress Th1 activation and therefore the inflammatory response, ameliorating the progression of kidney fibrosis [87, 158]

The distinct polarization patterns of Th1, Th2, and Th17 cells within IgAN lead to abnormalities of lymphocyte function. However, the differentiation of Th17 might improve the abnormal humoral immunity[137,138,139]

Th1/Th2 balance predominantly regulates transplant rejection [131]

Treg cell

Treg cells inhibit immune response by secreting suppressive cytokines and direct communication between cells. During AKI, T reg cells inhibit inflammation and facilitate tissue repair to reduce renal injury [72]

Treg cells protect the kidney against fibrosis progress [85]

Treg cells alleviate kidney inflammation response and improve sodium retention [72, 111]

Treg cells improve insulin resistance and suppress the immune response in kidney to ameliorate DN pathogenesis within the hyperglycemia setting [112]

Treg cells elicit attenuated immunosuppressive function within IgAN [159]

Treg cells mediate between transplant tolerance and rejection [160]

B cell

Recruitment of B cells in renal tissue exacerbates kidney fibrosis via increasing macrophage infiltration [82], inhibiting T cell differentiation and activation [83, 84]

Abnormally-functioned B cells exert a pathophysiological role within IgAN [133], [161]

B cells are crucial both in T cell-mediated graft rejection and antibody-mediated graft rejection [162]

Dendritic cell

CCR7 + dendritic cells at injury site dispose antigens and then present these antigens to CD8 + T cells in kidney draining lymph node, activating the activation and homing of antigen-specific CD8 + T cells. During AKI, dendritic cells contribute to a positive feedback that aggregates inflammation response [48, 57, 71, 72]