ArticleJournal of immunology (Baltimore, Md. : 1950)2010
The complement inhibitors Crry and factor H are critical for preventing autologous complement activation on renal tubular epithelial cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- The Reduction of Uromodulin, Complement Factor H, and Their Interaction Is Associated with Acute Kidney Injury to Chronic Kidney Disease Transition in a Four-Time Cisplatin-Injected Rat Model.International journal of molecular sciences · 2023Article
- Complement Components C3 and C4 Indicate Vasculitis Manifestations to Distinct Renal Compartments in ANCA-Associated Glomerulonephritis.International journal of molecular sciences · 2021Article
- Generation of a novel decay accelerating factor (DAF) knock-out rat model using clustered regularly-interspaced short palindromic repeats, (CRISPR)/associated protein 9 (Cas9), genome editing.Transgenic research · 2021Article
- Circadian Clock and Complement Immune System-Complementary Control of Physiology and Pathology?Frontiers in cellular and infection microbiology · 2020Review
- Complement Inhibitor CRIg/FH Ameliorates Renal Ischemia Reperfusion Injury via Activation of PI3K/AKT Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Complement factor H protects mice from ischemic acute kidney injury but is not critical for controlling complement activation by glomerular IgM.European journal of immunology · 2018Article
- Modulation of the Alternative Pathway of Complement by Murine Factor H-Related Proteins.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Factor H C-Terminal Domains Are Critical for Regulation of Platelet/Granulocyte Aggregate Formation.Frontiers in immunology · 2017Article
- Distinct roles for the complement regulators factor H and Crry in protection of the kidney from injury.Kidney international · 2016Article
- Complement Factor B Production in Renal Tubular Cells and Its Role in Sodium Transporter Expression During Polymicrobial Sepsis.Critical care medicine · 2016Article
- Annexin A2 Enhances Complement Activation by Inhibiting Factor H.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.Nature reviews. Nephrology · 2015Review
- Structural basis for sialic acid-mediated self-recognition by complement factor H.Nature chemical biology · 2015Article
- Tissue-specific deletion of Crry from mouse proximal tubular epithelial cells increases susceptibility to renal ischemia-reperfusion injury.Kidney international · 2014Article
- Complement as a multifaceted modulator of kidney transplant injury.The Journal of clinical investigation · 2014Review
- The role of the complement system in acute kidney injury.Seminars in nephrology · 2013Review
- Cyclosporine induces endothelial cell release of complement-activating microparticles.Journal of the American Society of Nephrology : JASN · 2013Article
- Blocking properdin, the alternative pathway, and anaphylatoxin receptors ameliorates renal ischemia-reperfusion injury in decay-accelerating factor and CD59 double-knockout mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Acute kidney injury: a conspiracy of Toll-like receptor 4 on endothelia, leukocytes, and tubules.Pediatric nephrology (Berlin, Germany) · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
Congenital and acquired deficiencies of complement regulatory proteins are associated with pathologic complement activation in several renal diseases. To elucidate the mechanisms by which renal tubular epithelial cells (TECs) control the complement system, we examined the expression of complement regulatory proteins by the cells. We found that Crry is the only membrane-bound complement regulator expressed by murine TECs, and its expression is concentrated on the basolateral surface. Consistent with the polarized localization of Crry, less complement activation was observed when the basolateral surface of TECs was exposed to serum than when the apical surface was exposed. Furthermore, greater complement activation occurred when the basolateral surface of TECs from Crry(-/-)fB(-/-) mice was exposed to normal serum compared with TECs from wild-type mice. Complement activation on the apical and basolateral surfaces was also greater when factor H, an alternative pathway regulatory protein found in serum, was blocked from interacting with the cells. Finally, we injected Crry(-/-)fB(-/-) and Crry(+/+)fB(-/-) mice with purified factor B (an essential protein of the alternative pathway). Spontaneous complement activation was seen on the tubules of Crry(-/-)fB(-/-) mice after injection with factor B, and the mice developed acute tubular injury. These studies indicate that factor H and Crry regulate complement activation on the basolateral surface of TECs and that factor H regulates complement activation on the apical surface. However, congenital deficiency of Crry or reduced expression of the protein on the basolateral surface of injured cells permits spontaneous complement activation and tubular injury.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.