Review article: Kidney dendritic cells: Their role in homeostasis, inflammation and transplantation

Rogers, Natasha M.; Matthews, Tyson J; Kausman, Josh Y; Kitching, A. Richard; Coates, P. Toby

doi:10.1111/j.1440-1797.2009.01200.x

Cited by 27 publications

(29 citation statements)

References 94 publications

(145 reference statements)

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“…Transfusion of functionally immature donor KDCs prolonged graft survival. 20,21 We also showed a protective role in nephrotoxic nephritis (NTN), 22 a widely studied murine model of crescentic GN. 23 KDCs from nephritic mice induced in Th cells not only production of typical Th type 1 (Th1) cytokines, but also of IL-10, 22 which can attenuate NTN.…”

mentioning

confidence: 92%

Kidney Dendritic Cells Become Pathogenic during Crescentic Glomerulonephritis with Proteinuria

Hochheiser¹,

Engel²,

Hammerich³

et al. 2011

Journal of the American Society of Nephrology

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It is unclear why kidney dendritic cells attenuate some models of kidney disease but aggravate others. Kidney dendritic cells ameliorate the early phase of nonaccelerated nephrotoxic nephritis, a murine model of crescentic glomerulonephritis, but their effect on the later phase is unknown. Here, we report that kidney dendritic cells at later stages of nephrotoxic nephritis expressed higher levels of costimulatory molecules but lower levels of the cosuppressor molecule ICOS-L and started production of IL-12/23p40 and TNF-␣. Furthermore, we noted that kidney dendritic cells captured more filterable antigen in proteinuric mice at late time points of nephrotoxic nephritis and started to capture molecules that were too large for filtration by a healthy kidney. They presented filtered antigen to Th cells, which responded by producing the proinflammatory cytokines IL-2, IFN-␥, TNF-␣, IL-6, and IL-17. Notably, production of the suppressive cytokine IL-10 further increased in late nephrotoxic nephritis. Depletion of kidney dendritic cells at a late stage attenuated nephrotoxic nephritis, in contrast to the exacerbation observed with depletion at an early stage, indicating that their acquired proinflammatory phenotype adversely affected disease. These findings indicate that the intrarenal inflammatory microenvironment determines how kidney dendritic cells affect nephritis. In addition, proteinuria may harm the kidney by providing dendritic cells with more antigens to stimulate potentially pathogenic Th cells.

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mentioning

confidence: 92%

Kidney Dendritic Cells Become Pathogenic during Crescentic Glomerulonephritis with Proteinuria

Hochheiser¹,

Engel²,

Hammerich³

et al. 2011

Journal of the American Society of Nephrology

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“…Maintaining Immune Tolerance against Renal Antigens Kidney DCs constantly probe their environment using their dendrites, suggesting a sentinel role (26,36,46,49). Indeed, DCs in healthy kidneys continuously sample glomerular and tubular self-antigens and small molecular weight antigens that can constitutively pass the glomerular filter from the tubular lumen (50).…”

Section: Homeostatic and Anti-infectious Sentinel Functionsmentioning

confidence: 99%

Dendritic Cells and Macrophages

Weisheit¹,

Engel

Kurts

2015

Clinical Journal of the American Society of Nephrology

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The mononuclear phagocytes (dendritic cells and macrophages) are closely related immune cells with central roles in anti-infectious defense and maintenance of organ integrity. The canonical function of dendritic cells is the activation of T cells, whereas macrophages remove apoptotic cells and microbes by phagocytosis. In the kidney, these cell types form an intricate system of mononuclear phagocytes that surveys against injury and infection and contributes to organ homeostasis and tissue repair but may also promote progression of CKD. This review summarizes the general functions and classification of dendritic cells and macrophages in the immune system and recapitulates why overlapping definitions and historically separate research have created controversy about their tasks. Their roles in acute kidney disease, CKD, and renal transplantation are described, and therapeutic strategy to modify these cells for therapeutic purposes is discussed.

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“…18 Because the TSP1-CD47 axis has been documented to inhibit tissue blood flow, we hypothesized that CD47 2/2 mice would experience less tissue injury post-IRI. To further test the importance of CD47 in renal IRI, we compared serum creatinine levels in CD47 2/2 versus congenic WT (CD47 +/+ ) mice.…”

Section: Cd47mentioning

confidence: 99%

Activation of Parenchymal CD47 Promotes Renal Ischemia-Reperfusion Injury

Rogers

Thomson

Isenberg

2012

Journal of the American Society of Nephrology

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Ischemia-reperfusion injury (IRI) contributes to decreased allograft function and allograft rejection in transplanted kidneys. Thrombospondin-1 is a stress protein typically secreted in response to hypoxia and the ligand activator for the ubiquitously expressed receptor CD47. The function of activated CD47 in IRI remains completely unknown. Here, we found that both CD47 and its ligand thrombospondin-1 were upregulated after renal IRI in mice. CD47-knockout mice were protected against renal dysfunction and tubular damage, suggesting that the development of IRI requires intact CD47 signaling. Chimeric CD47-knockout mice engrafted with wild-type hematopoietic cells had significantly lower serum creatinine and less tubular damage than wild-type controls after IRI, suggesting that CD47 signaling in parenchymal cells predominantly mediates renal damage. Treatment with a CD47-blocking antibody protected mice from renal dysfunction and tubular damage compared with an isotype control. Taken together, these data imply that CD47 on parenchymal cells promotes injury after renal ischemia and reperfusion. Therefore, CD47 blockade may have therapeutic potential to prevent or suppress ischemia-reperfusion-mediated damage.

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Review article: Kidney dendritic cells: Their role in homeostasis, inflammation and transplantation

Cited by 27 publications

References 94 publications

Kidney Dendritic Cells Become Pathogenic during Crescentic Glomerulonephritis with Proteinuria

Kidney Dendritic Cells Become Pathogenic during Crescentic Glomerulonephritis with Proteinuria

Dendritic Cells and Macrophages

Activation of Parenchymal CD47 Promotes Renal Ischemia-Reperfusion Injury

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