Incidence of Donor and Recipient Toll-Like Receptor-4 Polymorphisms in Kidney Transplantation

Nogueira, Eliana; Ozaki, Kikumi S.; Macusso, Georgia Daniela; Quarim, R.F.; Câmara, Niels Olsen Saraiva; Pacheco-Silva, Álvaro

doi:10.1016/j.transproceed.2007.01.026

Cited by 21 publications

(21 citation statements)

References 10 publications

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“…In a rat allograft model, Pratt et al demonstrated less vascular injury and leukocyte infiltration in allografts of recipient rats pretreated with recombinant humanized sCR1 (TP10) (67). Also, a modified form of complement receptor 1 (CR1) which was targeted to renal endothelium and epithelium reduced the amount of complement deposition, histological signs of renal injury and improved renal function after transplantation (68). Further, administration or targeting of other complement regulator proteins such as CD59, CD55 or CD46 might be a potential way to reduce renal injury during renal transplantation.…”

Section: Targeting Complementmentioning

confidence: 99%

Crosstalk between Complement and Toll-like Receptor Activation in Relation to Donor Brain Death and Renal Ischemia-Reperfusion Injury

Damman¹,

Daha

Son

et al. 2011

American Journal of Transplantation

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Section: Targeting Complementmentioning

confidence: 99%

Crosstalk between Complement and Toll-like Receptor Activation in Relation to Donor Brain Death and Renal Ischemia-Reperfusion Injury

Damman¹,

Daha

Son

et al. 2011

American Journal of Transplantation

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“…TLR2-deficient mice were protected from tubular injury and renal function deterioration in a model of kidney ischemiareperfusion (115). The clinical significance of a role for TLR signaling in the pathogenesis of genitourinary inflammation is found in clinical studies in which the incidence of acute rejection after kidney transplantation is reduced in patients who received a graft heterozygous for either the TLR4 Asp299Gly or Thr399Ile polymorphism compared with grafts without these mutations (189), although conflicting results have been reported (190). Taken together, these studies suggest an important role for TLR signaling in the development of urinary tract inflammation in a variety of models.…”

Section: Tlr-dependent Signaling In the Uroepithelial Tract: A Role Imentioning

confidence: 99%

No Longer an Innocent Bystander: Epithelial Toll-Like Receptor Signaling in the Development of Mucosal Inflammation

Gribar

Richardson

Sodhi

et al. 2008

Mol Med

142

109

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Diseases of mucosal inflammation represent important causes of morbidity and mortality, and have led to intense research efforts to understand the factors that lead to their development. It is well accepted that a breakdown of the normally impermeant epithelial barrier of the intestine, the lung, and the kidney is associated with the development of inflammatory disease in these organs, yet significant controversy exists as to how this breakdown actually occurs, and how such a breakdown may lead to inflammation. In this regard, much work has focused upon the role of the epithelium as an "innocent bystander," a target of a leukocyte-mediated inflammatory cascade that leads to its destruction in the mucosal inflammatory process. However, recent evidence from a variety of laboratories indicates that the epithelium is not merely a passive component in the steps that lead to mucosal inflammation, but is a central participant in the process. In addressing this controversy, we and others have determined that epithelial cells express Toll-like receptors (TLRs) of the innate immune system, and that activation of TLRs by endogenous and exogenous ligands may play a central role in determining the balance between a state of "mucosal homeostasis," as is required for optimal organ function, and "mucosal injury," leading to mucosal inflammation and barrier breakdown. In particular, activation of TLRs within intestinal epithelial cells leads to the development of cellular injury and impairment in mucosal repair in the pathogenesis of intestinal inflammation, while activation of TLRs in the lung and kidney may participate in the development of pneumonitis and nephritis respectively. Recent work in support of these concepts is extensively reviewed, while essential areas of further study that are required to determine the significance of epithelial TLR signaling during states of health and disease are outlined.

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“…Furthermore, ischaemia-reperfusion injury leads to cellular death and release of immunologically active molecules called damage-activates molecular patterns (DAMPs) such as heatshock proteins, adenosine triphosphate (ATP), uric acid, ribonucleic acid (RNA), deoxyribonucleic acid (DNA), as well as proteins derived from extracellular matrix including hyaluronan fragments and heparin sulphate proteoglycans [29,30]. Epithelial, mesenchymal and endothelial cells within the donor kidney express receptors for which include toll-like receptors (TLRs) and nucleotide-binding oligomerization domain-like receptors (NLRs), Interaction of the products of cellular injury with TLR and NLR sets of production of cytokines and chemokines, which are strong attractants for recipient innate immune cells [31][32][33][34].…”

Section: Allorecognition and T Cell Activationmentioning

confidence: 99%

Immunology for Renal Transplantation: A Review

Shrestha¹

2013

J Transplant Technol Res

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The current success of renal transplantation (RT) is the result of advancement in the understanding of the transplant immunology from gross allograft rejection to cellular and antibody response to the current molecular level. Laboratory assay technologies have been developed to characterise patient sensitisation and to detect pre-existing donor-specific antibodies (DSA) in pre-transplant crossmatch, which has helped prevent premature transplant losses from early and late antibody-mediated rejection. After a RT, pre-existing or de novo DSA are routinely monitored for modulation of immunosuppressive regimens. Therefore, it is mandatory for the personnel involved in the management of RT recipients to have clear understanding of the components of transplantation immunology and be familiar with the modern immunological techniques used in RT.

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Incidence of Donor and Recipient Toll-Like Receptor-4 Polymorphisms in Kidney Transplantation

Cited by 21 publications

References 10 publications

Crosstalk between Complement and Toll-like Receptor Activation in Relation to Donor Brain Death and Renal Ischemia-Reperfusion Injury

Crosstalk between Complement and Toll-like Receptor Activation in Relation to Donor Brain Death and Renal Ischemia-Reperfusion Injury

No Longer an Innocent Bystander: Epithelial Toll-Like Receptor Signaling in the Development of Mucosal Inflammation

Immunology for Renal Transplantation: A Review

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