Dendritic Cells and Macrophages

Weisheit, Christina; Engel, Daniel R.; Kurts, Christian

doi:10.2215/cjn.07100714

Cited by 83 publications

(58 citation statements)

References 121 publications

(118 reference statements)

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“…74 After acquiring antigens, dendritic cells process these to peptides, migrate to the secondary lymphoid organ, and present these antigenic peptides in the context of MHCs to T cells. Antigen-activated T cells proliferate and produce clones specific for the antigen.…”

Section: Antigens and Dendritic Cellsmentioning

confidence: 99%

Immune Mechanisms in Arterial Hypertension

Wenzel¹,

Turner²,

Krebs³

et al. 2016

Journal of the American Society of Nephrology

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171

148

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Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive endorgan damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.

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Section: Antigens and Dendritic Cellsmentioning

confidence: 99%

Immune Mechanisms in Arterial Hypertension

Wenzel¹,

Turner²,

Krebs³

et al. 2016

Journal of the American Society of Nephrology

Self Cite

171

148

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“…The renal tubular cell itself may have immunologic properties when appropriately activated, including phagocytosis and subsequent antigen presentation, 61 as well as co-stimulation of dendritic cells 62,63 or lymphocytes. 64 The proximal tubular cell is activated to migrate and proliferate in order to replenish the tubular structure, but it also produces chemoattractants and fibrogenic factors (reviewed in 65,66 ).…”

Section: The Pathophysiology Of Progressive Ckdmentioning

confidence: 99%

The Tubulointerstitial Pathophysiology of Progressive Kidney Disease

Schnaper

2017

Advances in Chronic Kidney Disease

115

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Accumulating evidence suggests that the central locus for the progression of chronic kidney disease (CKD) is the renal proximal tubule. As injured tubular epithelial cells dedifferentiate in attempted repair they stimulate inflammation and recruit myofibroblasts. At the same time, tissue loss stimulates remnant nephron hypertrophy. Increased tubular transport workload eventually exceeds the energy-generating capacity of the hypertrophied nephrons, leading to anerobic metabolism, acidosis, hypoxia, endoplasmic reticulum stress and the induction of additional inflammatory and fibrogenic responses. The result is a vicious cycle of injury, misdirected repair, maladaptive responses and more nephron loss. Therapy that might be advantageous at one phase of this progression pathway could be deleterious during other phases. Thus, interrupting this downward spiral requires narrowly targeted approaches that promote healing and adequate function without generating further entry into the progression cycle.

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“…How to distinguish between renal macrophages or dendritic cells is an area of controversy. Although the presence of CD11c + cells negative for expression of the macrophage markers F4/80 suggests the presence of myeloid DCs [37, 38], F4/80 is now recognized to also be expressed on renal resident CD11c + DCs [39, 40]. However, a substantial number of studies have demonstrated that the CD11c + /F4/80 - and CD11c + /F4/80 + subsets have distinct effects on recovery and regeneration following IRI.…”

Section: Discussionmentioning

confidence: 99%

Delayed Ischemic Preconditioning Attenuated Renal Ischemia-Reperfusion Injury by Inhibiting Dendritic Cell Maturation

Zhang

Song

Fang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Even though delayed ischemic preconditioning (DIPC) has been reported to produce renal protection, the underlying mechanism remains poorly understood. We reported that a 15-minute renal ischemic preconditioning (IPC) 4 days before subsequent ischemia-reperfusion attenuated renal injury Kidney dendritic cells (DCs) are abundant in the renal tubulointerstitium and, depending on their status, can induce immune activation or tolerance. The aim of the present study was to investigate the role of DCs in IPC of the kidney. Methods: Mouse kidneys were challenged by transient brief episodes of sublethal ischemia followed by subsequent prolonged ischemia. DC abundance and maturation in the spleen and kidney were measured by flow cytometry and immunohistochemical staining. To confirm the function of mature DCs in the renoprotective effect of IPC on renal ischemia-reperfusion injury the A2 adenosine receptor (A2AR) antagonist SCH58261 was administered to stimulate DC maturation prior to assessment of renal functional and histological injury and the inflammatory reaction. Results: Compared with sham-operated animals, preconditioned mice had a reduced injury with less CD11c⁺ cells, lower levels of the pro-inflammatory cytokine IL-17 and reduced expression of the mature DC marker CCR7. Preconditioned mice also produced more of the anti-inflammatory cytokine IL-10. Both renal cells and splenocytes from these mice had more DCs (CD45⁺/CD11c⁺/F4/80^-), but fewer of these DCs were mature (CD45⁺/CD11c⁺/ F4/80^-/MHC-II⁺/CD80⁺) compared with those from sham-treated animals, suggesting that the immunomodulatory effect of renal ischemic preconditioning is both local and systemic. Additionally, injection of the A2AR antagonist SCH58261 reversed IPC-induced inhibition of DC maturation and mitigated the protective effect of preconditioning, suggesting that DC maturation contributes to immune cell-mediated ischemic preconditioning. Conclusion: Our results show that DIPC of the kidney provides local and systemic immunosuppression by inhibiting DC maturation and hence mediates a renal protective effect.

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Dendritic Cells and Macrophages

Cited by 83 publications

References 121 publications

Immune Mechanisms in Arterial Hypertension

Immune Mechanisms in Arterial Hypertension

The Tubulointerstitial Pathophysiology of Progressive Kidney Disease

Delayed Ischemic Preconditioning Attenuated Renal Ischemia-Reperfusion Injury by Inhibiting Dendritic Cell Maturation

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