The diverging roles of dendritic cells in kidney allotransplantation

Podestà, Manuel Alfredo; Cucchiari, David; Ponticelli, Claudio

doi:10.1016/j.trre.2015.04.001

Cited by 19 publications

(16 citation statements)

References 86 publications

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“…After lymph node homing, mature DCs present antigens to T cells causing their differentiation toward Th1 and Th17 effector cells, which can contribute to graft failure. There are also reports indicating that resident DCs confer protective responses to limit I/R injury and damage induced by allotransplantation (420a, 639a). Although the non-stressed brain lacks DCs or functional counterparts that mediate antigen uptake and presentation, these cells do appear in brain parenchyma within 1 hr after induction of ischemia, where they act to exacerbate stroke-induced infarction (235a).…”

Section: Cell Types Involved In Postischemic Inflammationmentioning

confidence: 99%

“…Of course, T cells can also be activated by antigen-independent pathways by cytokines, ROS and other pro-inflammatory molecules such as TNFα and CGRP that are formed during I/R, as outlined above. In the setting of transplantation-induced I/R, danger signals released from dying cells are recognized by PRRs of the innate immune system with subsequent activation of inflammatory cells, including DCs, which are directed to a more mature phenotype (379a, 639a). After lymph node homing, mature DCs present antigens to T cells causing their differentiation toward Th1 and Th17 effector cells, which can contribute to graft failure.…”

Section: Cell Types Involved In Postischemic Inflammationmentioning

confidence: 99%

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Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

647

565

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Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms are also disrupted by the lack of ATP, which can induce lysis of organelle and plasma membranes. Reperfusion, although required to salvage oxygen-starved tissues, produces paradoxical tissue responses that fuel the production of reactive oxygen species (oxygen paradox), sequestration of proinflammatory immunocytes in ischemic tissues, endoplasmic reticulum stress, and development of postischemic capillary no-reflow, which amplify tissue injury. These pathologic events culminate in opening of mitochondrial permeability transition pores as a common end-effector of ischemia/reperfusion (I/R)-induced cell lysis and death. Emerging concepts include the influence of the intestinal microbiome, fetal programming, epigenetic changes, and microparticles in the pathogenesis of I/R. The overall goal of this review is to describe these and other mechanisms that contribute to I/R injury. Because so many different deleterious events participate in I/R, it is clear that therapeutic approaches will be effective only when multiple pathologic processes are targeted. In addition, the translational significance of I/R research will be enhanced by much wider use of animal models that incorporate the complicating effects of risk factors for cardiovascular disease.

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Section: Cell Types Involved In Postischemic Inflammationmentioning

confidence: 99%

Section: Cell Types Involved In Postischemic Inflammationmentioning

confidence: 99%

Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

647

565

View full text Add to dashboard Cite

show abstract

“…With respect to allorecognition upon solid organ transplantation, the danger hypothesis was first mentioned in the early 2000s (335-337, 340, 341, 351). A growing body of literature suggests that allograft injury results in DAMP release (2,116,124,148,159,247,343,345,384,460,499,513,652,692,729). This may be of particular importance for the "canonical" (oxidative) injury that has been demonstrated to be inevitably associated with donor brain death and during ischemia-reperfusion injury.…”

Section: Role Of Damps In Human Diseasesmentioning

confidence: 99%

Origin and Consequences of Necroinflammation

Sarhan

Land

Tonnus

et al. 2018

Physiological Reviews

166

152

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When cells undergo necrotic cell death in either physiological or pathophysiological settings in vivo, they release highly immunogenic intracellular molecules and organelles into the interstitium and thereby represent the strongest known trigger of the immune system. With our increasing understanding of necrosis as a regulated and genetically determined process (RN, regulated necrosis), necrosis and necroinflammation can be pharmacologically prevented. This review discusses our current knowledge about signaling pathways of necrotic cell death as the origin of necroinflammation. Multiple pathways of RN such as necroptosis, ferroptosis, and pyroptosis have been evolutionary conserved most likely because of their differences in immunogenicity. As the consequence of necrosis, however, all necrotic cells release damage associated molecular patterns (DAMPs) that have been extensively investigated over the last two decades. Analysis of necroinflammation allows characterizing specific signatures for each particular pathway of cell death. While all RN-pathways share the release of DAMPs in general, most of them actively regulate the immune system by the additional expression and/or maturation of either pro- or anti-inflammatory cytokines/chemokines. In addition, DAMPs have been demonstrated to modulate the process of regeneration. For the purpose of better understanding of necroinflammation, we introduce a novel classification of DAMPs in this review to help detect the relative contribution of each RN-pathway to certain physiological and pathophysiological conditions.

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“…In the field of organ transplantation, the danger/injury model was tackled for the first time in the early 2000s and, more recently, comprehensively addressed in a monograph . According to currently accepted models , any injury to an allograft, in particular, the “canonical” oxidative injury as occurring in the donor under brain death condition and in the recipient during postischemic reperfusion, leads to induction of various classes of DAMPs that activate intragraft PRR‐bearing cells of the donor's and recipient's innate immune system, a process that results in inflammation of the allograft. In parallel, donor‐derived and recipient‐derived dendritic cells (DCs), activated after uptake of alloantigens and recognition of various DAMPs by their corresponding PRRs, elicit—via the process of direct and indirect allorecognition—a robust adaptive anti‐donor alloimmune response ultimately resulting in allograft rejection .…”

Section: The Danger/injury Model In Immunologymentioning

confidence: 99%

Transplantation and Damage-Associated Molecular Patterns (DAMPs)

Land

Agostinis

Gasser

et al. 2016

American Journal of Transplantation

133

110

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Upon solid organ transplantation and during cancer immunotherapy, cellular stress responses result in the release of damage-associated molecular patterns (DAMPs). The various cellular stresses have been characterized in detail over the last decades, but a unifying classification based on clinically important aspects is lacking. Here, we provide an in-depth review of the most recent literature along with a unifying concept of the danger/injury model, suggest a classification of DAMPs, and review the recently elaborated mechanisms that result in the emission of such factors. We further point out the differences in DAMP responses including the release following a heat shock pattern, endoplasmic reticulum stress, DNA damage-mediated DAMP release, and discuss the diverse pathways of regulated necrosis in this respect. The understanding of various forms of DAMPs and the consequences of their different release patterns are prerequisite to associate serum markers of cellular stresses with clinical outcomes.

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The diverging roles of dendritic cells in kidney allotransplantation

Cited by 19 publications

References 86 publications

Ischemia/Reperfusion

Ischemia/Reperfusion

Origin and Consequences of Necroinflammation

Transplantation and Damage-Associated Molecular Patterns (DAMPs)

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