ArticleThe Journal of clinical investigation2010
Genetic and therapeutic targeting of properdin in mice prevents complement-mediated tissue injury.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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.
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Who cites it
51 citing papers in PubMed, 73 citations in OpenAlex.
- Properdin deficiency or anti-properdin treatment ameliorates disease in the C3 gain-of-function mouse model of atypical haemolytic uraemic syndrome.Frontiers in immunology · 2026Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Differential expression of complement Properdin and Factor H in the placentae and umbilical cords of mothers with Preeclampsia, Gestational Diabetes Mellitus and Recurrent Pregnancy Loss.Frontiers in immunology · 2025Article
- Local complement activation and modulation in mucosal immunity.Mucosal immunology · 2024Review
- Article
- Neutrophil-activating therapy for the treatment of cancer.Cancer cell · 2023Article
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- Properdin inhibition ameliorates hepatic ischemia/reperfusion injury without interfering with liver regeneration in mice.Frontiers in immunology · 2023Article
- Structural studies offer a framework for understanding the role of properdin in the alternative pathway and beyond.Immunological reviews · 2023Review
- Exploration of Serum Marker Proteins in Mice Induced by Babesia microti Infection Using a Quantitative Proteomic Approach.The protein journal · 2021Article
- Article
- Properdin Is a Key Player in Lysis of Red Blood Cells and Complement Activation on Endothelial Cells in Hemolytic Anemias Caused by Complement Dysregulation.Frontiers in immunology · 2020Article
- Prognostic Value of Complement Properdin in Cancer.Frontiers in immunology · 2020Article
- Complement activation on neutrophils initiates endothelial adhesion and extravasation.Molecular immunology · 2019Article
- The role of properdin in complement-mediated renal diseases: a new player in complement-inhibiting therapy?Pediatric nephrology (Berlin, Germany) · 2019Article
- Fat-Produced Adipsin Regulates Inflammatory Arthritis.Cell reports · 2019Article
- Properdin: A Novel Target for Neuroprotection in Neonatal Hypoxic-Ischemic Brain Injury.Frontiers in immunology · 2019Article
- Structural Basis for Properdin Oligomerization and Convertase Stimulation in the Human Complement System.Frontiers in immunology · 2019Article
- Properdin: A multifaceted molecule involved in inflammation and diseases.Molecular immunology · 2018Review
- Timing and mechanism of conceptus demise in a complement regulatory membrane protein deficient mouse.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The alternative pathway (AP) of complement activation is constitutively active and must be regulated by host proteins to prevent autologous tissue injury. Dysfunction of AP regulatory proteins has been linked to several human inflammatory disorders. Properdin is a positive regulator of AP complement activation that has been shown to extend the half-life of cell surface–bound C3 convertase C3bBb; it may also initiate AP complement activation. Here, we demonstrate a critical role for properdin in autologous tissue injury mediated by AP complement activation. We identified myeloid lineage cells as the principal source of plasma properdin by generating mice with global and tissue-specific knockout of Cfp (which encodes properdin) and by generating BM chimeric mice. Properdin deficiency rescued mice from AP complement–mediated embryonic lethality caused by deficiency of the membrane complement regulator Crry and markedly reduced disease severity in the K/BxN model of arthritis. Ab neutralization of properdin in WT mice similarly ameliorated arthritis development, whereas reconstitution of properdin-null mice with exogenous properdin restored arthritis sensitivity. These data implicate systemic properdin as a key contributor to AP complement–mediated injury and support its therapeutic targeting in complement-dependent human diseases.
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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.