Expression of the Decay-Accelerating Factor (CD55) in Renal Transplants—A Possible Prediction Marker of Allograft Survival

Brodsky, Sergey V.; Nadasdy, Gyongyi; Pelletier, Ronald P.; Satoskar, Anjali A.; Birmingham, Daniel J.; Hadley, Gregg A.; Obeidat, Khaled; Nádasdy, Tibor

doi:10.1097/tp.0b013e3181b0517d

Cited by 26 publications

(14 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent study identified Cd55 as a key indicator in renal allograft survival. Patients with increased peritubular capillary Cd55 expression had increased graft survival over those with low Cd55 expression (50). Our data are consistent with these findings in patients, thus reinforcing the importance of this regulatory mechanism of complement in controlling the vasculature in disease states.…”

Section: Discussionmentioning

confidence: 99%

The alternative complement pathway regulates pathological angiogenesis in the retina

et al. 2014

View full text Add to dashboard Cite

A defining feature in proliferative retinopathies is the formation of pathological neovessels. In these diseases, the balance between neovessel formation and regression determines blindness, making the modulation of neovessel growth highly desirable. The role of the immune system in these retinopathies is of increasing interest, but it is not completely understood. We investigated the role of the alternative complement pathway during the formation and resolution of aberrant neovascularization. We used alternative complement pathway-deficient (Fb(-/-)) mice and age- and strain-matched control mice to assess neovessel development and regression in an oxygen-induced retinopathy (OIR) mouse model. In the control mice, we found increased transcription of Fb after OIR treatment. In the Fb(-/-) mice, we prepared retinal flatmounts and identified an increased number of neovessels, peaking at postnatal day 17 (P17; P=0.001). Subjecting human umbilical vein endothelial cells (HUVECs) to low oxygen, mimicking a characteristic of neovessels, decreased the expression of the complement inhibitor Cd55. Finally, using laser capture microdissection (LCM) to isolate the neovessels after OIR, we found decreased expression of Cd55 (P=0.005). Together, our data implicate the alternative complement pathway in facilitating neovessel clearance by down-regulating the complement inhibitor Cd55 specifically on neovessels, allowing for their targeted removal while leaving the established vasculature intact.-Sweigard, J. H., Yanai, R., Gaissert, P., Saint-Geniez, M., Kataoka, K., Thanos, A., Stahl, G. L., Lambris, J. D., Connor, K. M. The alternative complement pathway regulates pathological angiogenesis in the retina.

show abstract

Section: Discussionmentioning

confidence: 99%

The alternative complement pathway regulates pathological angiogenesis in the retina

et al. 2014

View full text Add to dashboard Cite

show abstract

“…19 Accordingly to this, a lower expression of DAF by grafts has been related with accelerated T-cell-mediated rejection in renal or heart transplants. 28, 29 Therefore, a permanent immune suppression would be necessary in a hypothetical transplantation of human MABs in patients affected by this form of muscular dystrophy.…”

Section: Discussionmentioning

confidence: 99%

Partial dysferlin reconstitution by adult murine mesoangioblasts is sufficient for full functional recovery in a murine model of dysferlinopathy

Díaz‐Manera

Touvier²,

Dellavalle³

et al. 2010

Cell Death Dis

View full text Add to dashboard Cite

Dysferlin deficiency leads to a peculiar form of muscular dystrophy due to a defect in sarcolemma repair and currently lacks a therapy. We developed a cell therapy protocol with wild-type adult murine mesoangioblasts. These cells differentiate with high efficiency into skeletal muscle in vitro but differ from satellite cells because they do not express Pax7. After intramuscular or intra-arterial administration to SCID/BlAJ mice, a novel model of dysferlinopathy, wild-type mesoangioblasts efficiently colonized dystrophic muscles and partially restored dysferlin expression. Nevertheless, functional assays performed on isolated single fibers from transplanted muscles showed a normal repairing ability of the membrane after laser-induced lesions; this result, which reflects gene correction of an enzymatic rather than a structural deficit, suggests that this myopathy may be easier to treat with cell or gene therapy than other forms of muscular dystrophies.

show abstract

“…Interestingly, Schaub et al reported that not all sera containing strong complement fixing antibodies (IgG1/IgG3) fix complement in vitro (24). There are multiple explanations for this possibility, including the in vivo presence of complement-inhibiting molecules such as heparin sulfate (26) and/or increased levels of decay-accelerating factor (27). There are multiple explanations for this possibility, including the in vivo presence of complement-inhibiting molecules such as heparin sulfate (26) and/or increased levels of decay-accelerating factor (27).…”

Section: Merge: "Functional" Methods To Assess Antibody Pathogenicitymentioning

confidence: 99%

The Road to HLA Antibody Evaluation: Do Not Rely on MFI

Sullivan

Liwski

Bray

et al. 2017

American Journal of Transplantation

View full text Add to dashboard Cite

Technological advances in HLA laboratory testing undoubtedly improved the sensitivity and specificity of HLA antibody assessment but not without introducing a set of challenges regarding data interpretation. In particular, the introduction of solid-phase single-antigen bead (SAB) antibody assessment brought the belief that mean fluorescence intensity (MFI) was a quantifiable value. As such, MFI levels heavily influenced HLA antibody reporting, monitoring, and clinical practice. However, given that SAB testing was neither intended for nor approved to be quantifiable, is the use of MFI in current clinical and laboratory practice valid? What, if anything, does this numerical value actually reveal about the pathogenic potential of the antibody? What are the pitfalls and caveats associated with reporting MFI? Herein, we travel the road to HLA antibody assessment and explore the reliability of MFI values to make clinical decisions.

show abstract

Expression of the Decay-Accelerating Factor (CD55) in Renal Transplants—A Possible Prediction Marker of Allograft Survival

Abstract: These data suggest that CD55 expression has a protective effect on PTC C4d negative renal allografts, and the pattern of PTC CD55 expression may be used as a potential marker of renal allograft survival in patients with no evidence of AMR.

Cited by 26 publications

References 29 publications

The alternative complement pathway regulates pathological angiogenesis in the retina

The alternative complement pathway regulates pathological angiogenesis in the retina

Partial dysferlin reconstitution by adult murine mesoangioblasts is sufficient for full functional recovery in a murine model of dysferlinopathy

The Road to HLA Antibody Evaluation: Do Not Rely on MFI

Contact Info

Product

Resources

About