Exaggerated complement activation is a key event in the pathogenesis of a range of autoimmune and inflammatory diseases. Complement Receptor 1 (CR1) has emerged as a molecule of immense interest in gaining insight to the susceptibility, pathophysiology, diagnosis, prognosis and therapy of such diseases. This review brings forth a composite view of the current understanding on the structure, functions, genetics, disease associations and therapeutic implications of CR1.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125513 | PMC |
| http://dx.doi.org/10.1016/j.molimm.2008.09.026 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Innate Immune Activation with Multifunctional Nanoparticles for Cancer Immunotherapy.
Angew Chem Int Ed Engl
January 2025
University of Chicago Division of the Physical Sciences, chemistry, UNITED STATES OF AMERICA.
Immune checkpoint blockade (ICB) has revolutionized the treatment of many cancers by leveraging the immune system to combat malignancies. However, its efficacy is limited by the immunosuppressive tumor microenvironment and other regulatory mechanisms of the immune system. Innate immune modulators (IIMs) provide potent immune activation to complement adaptive immune responses and help overcome resistance to ICB.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Background: New methods developed to estimate when AD biomarkers became abnormal in individuals have shown considerable heterogeneity in amyloid and tau pathology onset age. This work used polygenic scores (PGS) generated from CSF Aβ and ptau GWAS, individual-level genetic data, and estimated tau onset age (ETOA) to identify genetic influences on tau onset beyond APOE.
Method: Participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) with genetic data, CSF biomarkers (Aβ and ptau), and longitudinal [F]Flortaucipir (FTP) tau PET were analyzed (N = 462).
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
UK Dementia Research Institute at Cardiff University, Cardiff, South Glamorgan, United Kingdom.
Background: Genome-wide association studies (GWAS) in Alzheimer's disease (AD) implicate complement in pathogenesis. Complement receptor 1 (CR1; CD35) is a top AD-associated GWAS hit; the long variant, CR1*2, associates with risk. The roles of CR1 in brain and how variants influence AD risk are poorly understood.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Brigham and Women's Hospital; Harvard Medical School, Boston, MA, USA.
Background: Anti-amyloid antibodies have been associated with amyloid-related-imaging-abnormalities (ARIA) in AD patients, causing vasogenic edema and microhemorrhages, especially in ApoE4 carriers. Here, we compared recombinant 3D6-L, a murine version of bapineuzumab, and an isotype control IgG2a monoclonal antibody (mAb) to investigate potential mechanisms, including complement activation, involved in these side effects (ARIA-H or microhemorrhages) following passive immunization.
Method: Plaque-rich 16.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
The Ohio State University, Columbus, OH, USA.
Background: Microglia, the innate immune cells of the brain, are a principal player in Alzheimer's Disease (AD) pathogenesis. Their surveillance of the brain leads to interaction with the protein aggregates that drive AD pathogenesis, most notably Amyloid Beta (Aβ). Aβ can elicit attempts from microglia to clear and degrade it using phagocytic machinery, spurring damaging neuroinflammation in the process.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!