Delineating the genetic basis of systemic lupus erythematosus.
By E. Wakeland, Kui Liu, R. Graham, T. Behrens. Immunity, 2001
619 citations recorded by the source corpus.
Subfields: Oncology, Radiology, Nuclear Medicine and Imaging, Rheumatology
View Paper: https://www.semanticscholar.org/paper/fbac1ff01c2b1bd0bed59404cd049f2254bd4245
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In Oncology
- A. Strasser
- Jacques Banchereau
- Richard Hargreaves
- R. Coffman
- A. Palucka
- K. Ohtsubo
- Richard Frank
- F. Barrat
In Radiology, Nuclear Medicine and Imaging
In Rheumatology
Citations in the corpus
- Genetic association of the R620W polymorphism of protein tyrosine phosphatase PTPN22 with human SLE. (2004, background): “factors (Wakeland et al. 2001).”
- The role of BH3-only proteins in the immune system (2005, result): “These observations are consistent with many studies showing that defects in multiple genes must cooperate to precipitate autoimmune diseas”
- Immunology of multiple sclerosis. (2005, neutral): “, the fraction of animals that developed lupus was determined by the number of disease-linked genes under identical environmental influences (48).”
- Interferon and Granulopoiesis Signatures in Systemic Lupus Erythematosus Blood (2003, background): “Human SLE appears linked to at least 6 gene loci and numerous mouse genetic mutants show SLE-like syndromes (3).”
- A Common Dominant TLR5 Stop Codon Polymorphism Abolishes Flagellin Signaling and Is Associated with Susceptibility to Legionnaires' Disease (2003, background): “Linkage papers have mapped a major susceptibility locus for systemic lupus erythematosus in humans and mice to chromosome 1q41 where TLR5 resides (49, 50).”
- Glycosylation in cellular mechanisms of health and disease. (2006, background): “Therefore , in this model of autoimmune disease, pathogenesis may reflect endogenous epitope (N-glycan) modification (Wakeland et al., 2001).”
- Netting Neutrophils Are Major Inducers of Type I IFN Production in Pediatric Systemic Lupus Erythematosus (2011, background): “Common hypotheses about SLE pathogenesis suggest that environmental triggers, such as infectious agents, operate in the context of both susceptibility genes and epigenetic modifications, resulting in alterations in antigen presentation, lymphoid signaling, apoptosis, and antigen/IC clearance (2, 3).”
- Clinical biomarkers in drug discovery and development (2003, background): “The underlying aetiology can include both overactive immune responses and deficiencies in complement, impairing clearance of infectious agent”