Inflammatory cells in renal allografts

Nickeleit,; Andreoni, Kenneth A.

doi:10.2741/3148

Cited by 13 publications

(6 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…33 These subtle inflammatory changes in renal allografts are likely very important, as an association between T-lymphocyte-mediated inflammation in scarred areas and graft outcome was demonstrated previously, 9 which suggests continuing effects of these inflammatory infiltrates on the scarring process. Importantly, however, especially in the light of possible therapeutic interventions, the current study supports the growing theory that other immune cell types such as B cells, 13,34,35 NK cells, 36–38 dendritic cells, 39–41 mast cells, 17,42,43 and granulocytes 44,45 are involved in chronic renal allograft damage and may be driving the immunological processes after transplantation, potentially by their implication in antigen presentation, in the secretion of inflammatory cytokines, and in the regulation of T cells.…”

Section: Discussionsupporting

confidence: 74%

Progressive histological damage in renal allografts is associated with expression of innate and adaptive immunity genes

Naesens

Khatri

et al. 2011

Kidney International

View full text Add to dashboard Cite

The degree of progressive chronic histological damage is associated with long-term renal allograft survival. In order to identify promising molecular targets for timely intervention, we examined renal allograft protocol and indication biopsies from 120 low-risk pediatric and adolescent recipients by whole-genome microarray expression profiling. In data-driven analysis, we found a highly regulated pattern of adaptive and innate immune gene expression that correlated with established or ongoing histological chronic injury, and also with development of future chronic histological damage, even in histologically pristine kidneys. Hence, histologically unrecognized immunological injury at a molecular level sets the stage for the development of chronic tissue injury, while the same molecular response is accentuated during established and worsening chronic allograft damage. Irrespective of the hypothesized immune or nonimmune trigger for chronic allograft injury, a highly orchestrated regulation of innate and adaptive immune responses was found in the graft at the molecular level. This occurred months before histologic lesions appear, and quantitatively below the diagnostic threshold of classic T-cell or antibody-mediated rejection. Thus, measurement of specific immune gene expression in protocol biopsies may be warranted to predict the development of subsequent chronic injury in histologically quiescent grafts and as a means to titrate immunosuppressive therapy.

show abstract

Section: Discussionsupporting

confidence: 74%

Progressive histological damage in renal allografts is associated with expression of innate and adaptive immunity genes

Naesens

Khatri

et al. 2011

Kidney International

View full text Add to dashboard Cite

show abstract

“…Besides CTLs and other leukocyte subtypes, the complement system contributes to the inflammation as well. Once activated, CTLs expanse and differentiate into effector cells, extravasate, and subsequently infiltrate the transplant [7, 17]. Different chemokines, cytokines, and the upregulation of vascular adhesion molecules guide this process [18], finally leading to necrotic parenchymal destruction or initiation of apoptosis [19, 20].…”

Section: Introductionmentioning

confidence: 99%

Renal Allograft Rejection: Noninvasive Ultrasound- and MRI-Based Diagnostics

Jehn

Schuette-Nuetgen

Kentrup

et al. 2019

Contrast Media & Molecular Imaging

View full text Add to dashboard Cite

To date, allogeneic kidney transplantation remains the best available therapeutic option for patients with end-stage renal disease regarding overall survival and quality of life. Despite the advancements in immunosuppressive drugs and protocols, episodes of acute allograft rejection, a sterile inflammatory process, continue to endanger allograft survival. Since effective treatment for acute rejection episodes is available, instant diagnosis of this potentially reversible graft injury is imperative. Although histological examination by invasive core needle biopsy of the graft remains the gold standard for the diagnosis of ongoing rejection, it is always associated with the risk of causing substantial graft injury as a result of the biopsy procedure itself. At the same time, biopsies are not immediately feasible for a considerable number of patients taking anticoagulants due to the high risk of complications such as bleeding and uneven distribution of pathological changes within the graft. This can result in the wrong diagnosis due to the small size of the tissue sample taken. Therefore, there is a need for a tool that overcomes these problems by being noninvasive and capable of assessing the whole organ at the same time for specific and fast detection of acute allograft rejection. In this article, we review current state-of-the-art approaches for noninvasive diagnostics of acute renal transplant inflammation, i.e., rejection. We especially focus on nonradiation-based methods using magnetic resonance imaging (MRI) and ultrasound.

show abstract

“…Vitamin D-binding protein-macrophage-activating factor (DBP-maf) is derived from serum vitamin D binding protein by selective deglycosylation during inflammation [21][22][23] . Evidence shows macrophages may play a role in promoting allograft injury [24] . Macrophages can enhance the activity of inducible nitric oxide synthase which causes endothelial cell cytotoxicity by nitric oxide generation.…”

Section: Discussionmentioning

confidence: 99%

Characterization of acute renal allograft rejection by human serum proteomic analysis

Gao

et al. 2009

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

View full text Add to dashboard Cite

To identify acute renal allograft rejection biomarkers in human serum, two-dimensional differential in-gel electrophoresis (2-D DIGE) and reversed phase high-performance liquid chromatography (RP-HPLC) followed by electrospray ionization mass spectrometry (ESI-MS) were used. Serum samples from renal allograft patients and normal volunteers were divided into three groups: acute rejection (AR), stable renal function (SRF) and normal volunteer (N). Serum samples were firstly processed using Multiple Affinity Removal Column to selectively remove the highest abundance proteins. Differentially expressed proteins were analyzed using 2-D DIGE. These differential protein spots were excised, digested by trypsin, and identified by RP-HPLC-ESI/MS. Twenty-two differentially expressed proteins were identified in serum from AR group. These proteins included complement C9 precursor, apolipoprotein A-IV precursor, vitamin D-binding protein precursor, beta-2-glycoprotein 1 precursor, etc. Vitamin D-binding protein, one of these proteins, was confirmed by ELISA in the independent set of serum samples. In conclusion, the differentially expressed proteins as serum biomarker candidates may provide the basis of acute rejection noninvasive diagnosis. Confirmed vitamin D-binding protein may be one of serum biomarkers of acute rejection. Furthermore, it may provide great insights into understanding the mechanisms and potential treatment strategy of acute rejection.

show abstract

Inflammatory cells in renal allografts

Cited by 13 publications

References 43 publications

Progressive histological damage in renal allografts is associated with expression of innate and adaptive immunity genes

Progressive histological damage in renal allografts is associated with expression of innate and adaptive immunity genes

Renal Allograft Rejection: Noninvasive Ultrasound- and MRI-Based Diagnostics

Characterization of acute renal allograft rejection by human serum proteomic analysis

Contact Info

Product

Resources

About