Tissue distribution of products of the mouse decay‐accelerating factor (DAF) genes. Exploitation of a <i>Daf1</i> knock‐out mouse and site‐specific monoclonal antibodies

Lin, Feng; Fukuoka, Yoshihiro; Spicer, Andrew P.; Ohta, Rieko; Okada, Noriko; Harris, Claire L.; Emancipator, Steven N.; Medof, M. Edward

doi:10.1046/j.1365-2567.2001.01287.x

Cited by 97 publications

(115 citation statements)

References 59 publications

Supporting

Mentioning

110

Contrasting

Order By: Relevance

“…These findings are consistent with the known tissue distribution patterns of CD55 and CD59 in the mouse kidney. Both proteins are highly expressed on vascular endothelial cells and, although they were detected by immunohistochemistry in the mouse glomeruli, CD55 and CD59 were minimally expressed, if at all, on proximal tubules of the mouse (29,30). Endothelial expression of CD55 is also known to be induced by inflammatory stimuli (31).…”

Section: Discussionmentioning

confidence: 99%

Critical Protection from Renal Ischemia Reperfusion Injury by CD55 and CD59

Yamada

Miwa

Liu

et al. 2004

The Journal of Immunology

153

135

View full text Add to dashboard Cite

Renal ischemia-reperfusion injury (IRI) is a feature of ischemic acute renal failure and it impacts both short- and long-term graft survival after kidney transplantation. Complement activation has been implicated in renal IRI, but its mechanism of action is uncertain and the determinants of complement activation during IRI remain poorly understood. We engineered mice deficient in two membrane complement regulatory proteins, CD55 and CD59, and used them to investigate the role of these endogenous complement inhibitors in renal IRI. CD55-deficient (CD55−/−), but not CD59-deficient (CD59−/−), mice exhibited increased renal IRI as indicated by significantly elevated blood urea nitrogen levels, histological scores, and neutrophil infiltration. Remarkably, although CD59 deficiency alone was inconsequential, CD55/CD59 double deficiency greatly exacerbated IRI. Severe IRI in CD55−/−CD59−/− mice was accompanied by endothelial deposition of C3 and the membrane attack complex (MAC) and medullary capillary thrombosis. Complement depletion in CD55−/−CD59−/− mice with cobra venom factor prevented these effects. Thus, CD55 and CD59 act synergistically to inhibit complement-mediated renal IRI, and abrogation of their function leads to MAC-induced microvascular injury and dysfunction that may exacerbate the initial ischemic assault. Our findings suggest a rationale for anti-complement therapies aimed at preventing microvascular injury during ischemia reperfusion, and the CD55−/−CD59−/− mouse provides a useful animal model in this regard.

show abstract

Section: Discussionmentioning

confidence: 99%

Critical Protection from Renal Ischemia Reperfusion Injury by CD55 and CD59

Yamada

Miwa

Liu

et al. 2004

The Journal of Immunology

153

135

View full text Add to dashboard Cite

show abstract

“…Factor D (fD Ϫ/Ϫ , H-2 b ) mice were a gift from Y. Ma (Birmingham, AL). Mice deficient in the Daf1 gene (Daf1 Ϫ/Ϫ ) were produced by Lin and colleagues 17 as described and backcrossed for Ͼ13 generations to B6 mice. B6 mice do not reject B6 Daf1 Ϫ/Ϫ skin (data not shown), confirming congenicity.…”

Section: Micementioning

confidence: 99%

“…12,16,17 Briefly, MultiScreen ELISPOT plates (Millipore, Bedford, MA) were coated overnight with the capture antibodies for IFN-␥, IL-4, or IL-17 (BD Biosciences). After a blocking step, recipient spleen or T cells (0.2 to 1 ϫ 10 6 per well) were plated and incubated with spleen cell stimulators (400,000 per well) at 37°C, 5% CO 2 , for 24 hours.…”

Section: Elispot Assaysmentioning

confidence: 99%

“…To test this hypothesis, we performed in vitro studies and in vivo transplant experiments, including those with APCs devoid of decay accelerating factor (DAF; CD55), 17 in which endogenous C3a/C5a production is tonically potentiated. 14 -16,18 We found that in the absence of either CD4 ϩ T cells or APC CD40, heightened bone marrow (BM) cell-derived C3a/C5a production provokes CD8 ϩ T-cell activation and cardiac allograft rejection.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Complement Regulates CD4 T-Cell Help to CD8 T Cells Required for Murine Allograft Rejection

Vieyra

Leisman

Raedler

et al. 2011

The American Journal of Pathology

Self Cite

View full text Add to dashboard Cite

Although induction of CD8 T-cell responses to transplants requires CD4-cell help, how this help is transmitted remains incompletely characterized. In vitro, cognate interactions between CD4 T cells and dendritic cells (DCs) induceC3a and C5a production. CD8 ؉ T cells lacking C3a receptor (C3aR) and C5a receptor (C5aR) proliferate weakly to allogeneic DCs despite CD4 help, indicating that CD4-cell help is mediated, in part, through DC-derived C3a/C5a acting on CD8 ؉ T cellexpressed C3aR/C5aR. In support of this concept, aug-

show abstract

“…These regulators are DAF, complement receptor-related protein-Y (Crry), and the membrane inhibitor of reactive lysis (CD59). In the mouse, two genes, Daf1 and Daf2, code for DAF protein (Spicer et al, 1995 glyco-phosphatidylinositol anchored and widely expressed in a distribution similar to that in humans, whereas DAF protein deriving from the Daf2 gene is predominantly transmembrane anchored and restricted in its expression to testis (Lin et al, 2001;Song et al, 1996;Spicer et al, 1995) and splenic dendritic cells (Lin et al, 2001). Previous studies have shown that DAF present in the kidney derives entirely from the Daf1 gene (Lin et al, 2001;Spicer et al, 1995) and that it is expressed at high levels in glomerular capillary walls (Lin et al, 2001).…”

mentioning

confidence: 99%

Decay-Accelerating Factor Confers Protection Against Complement-Mediated Podocyte Injury in Acute Nephrotoxic Nephritis

Lin

Emancipator

Salant

et al. 2002

Laboratory Investigation

Self Cite

View full text Add to dashboard Cite

SUMMARY:Decay-accelerating factor (DAF or CD55) is one of a set of regulators that function to protect self cells from deposition of autologous C3b on their surfaces. Its relative importance in vivo, however, is incompletely understood. As one approach to address this issue, we induced nephrotoxic serum (NTS) nephritis in wild-type mice and Daf1 gene-floxed mice devoid of renal DAF expression. For these experiments NTS IgG was administered at a dose (0.5 mg iv) that requires complement for glomerular injury. After 18 hours, renal injury was assessed by proteinuria and by histologic, immunohistochemical, and electron microscopic analyses of kidneys. Fifteen normal and 15 DAF-deficient mice were studied. Baseline albuminuria in the Daf1 Ϫ/Ϫ mice was 115.9 Ϯ 41.4 g/mg creatinine as compared with 85.7 Ϯ 32.3 g/mg creatinine in their Daf1 ϩ/ϩ littermates (p ϭ 0.075). After administration of NTS IgG, albuminuria increased to 2001.7 Ϯ 688.7 g/mg creatinine as compared with 799.7 Ϯ 340.5 g/mg creatinine in the controls (p ϭ 0.0003). Glomerular histology was similar in Daf1 Ϫ/Ϫ and Daf1 ϩ/ϩ mice, with essentially no infiltrating leukocytes. In contrast, electron microscopy revealed severe podocyte fusion in the Daf1 Ϫ/Ϫ mice but only mild focal changes in the controls. Immunohistochemical staining showed equivalent deposition of the administered (sheep) NTS IgG in the Daf1 Ϫ/Ϫ and Daf1 ϩ/ϩ animals. This contrasted with marked deposition of autologous murine C3 in the former and minimal deposition in the latter. The results show that DAF is essential physiologically for protecting glomeruli against autologous complement attack initiated by the classical pathway. (Lab Invest 2002, 82:563-569).D ifferent forms of nephrotoxic serum (NTS)-induced nephritis in rats and mice have been widely utilized as animal models for human antibodyinduced renal diseases (reviewed in Salant and Cybulsky, 1988). The mechanism of glomerular damage differs, depending on the source and dose of the antibody and the time after antibody administration (Boyce and Holdsworth, 1985;Salant and Cybulsky, 1988). When a low dosage of sheep NTS is given to mice, complement plays a significant role in the early heterologous phase of nephritis (Hebert et al, 1998;Quigg et al, 1998aQuigg et al, , 1998bSchrijver et al, 1988). This has been verified either by depleting serum complement proteins with cobra venom factor (Quigg et al, 1998b) or using C3 or C4 knock-out mice (Hebert et al, 1998). When the dosage of NTS is increased, the disease is in large part antibody mediated, and dependence on complement is diminished (Hebert et al, 1998). During the later autologous phase, especially if accelerated by preimmunization with heterologous IgG, a more fulminant, leukocyte-rich inflammatory lesion is induced (Lloyd et al, 1997).The sheep NTS used in these studies is specific for several podocyte cell surface proteins, including some that are known to be nephritogenic (Chugh et al, 2001). In addition, the proteinuria that develops in the early heterologous phase of g...

show abstract

Tissue distribution of products of the mouse decay‐accelerating factor (DAF) genes. Exploitation of a Daf1 knock‐out mouse and site‐specific monoclonal antibodies

Cited by 97 publications

References 59 publications

Critical Protection from Renal Ischemia Reperfusion Injury by CD55 and CD59

Critical Protection from Renal Ischemia Reperfusion Injury by CD55 and CD59

Complement Regulates CD4 T-Cell Help to CD8 T Cells Required for Murine Allograft Rejection

Decay-Accelerating Factor Confers Protection Against Complement-Mediated Podocyte Injury in Acute Nephrotoxic Nephritis

Contact Info

Product

Resources

About