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Development of autoantibodies before the clinical onset of systemic lupus erythematosus.
- M. Arbuckle, M. McClain, J. Harley
- Medicine, BiologyThe New England journal of medicine
- 16 October 2003
The onset and progression of autoantibody development before the clinical diagnosis of systemic lupus erythematosus is investigated, with a progressive accumulation of specificAutoantibodies before the onset of SLE, while patients are still asymptomatic.
Genome-wide association scan in women with systemic lupus erythematosus identifies susceptibility variants in ITGAM, PXK, KIAA1542 and other loci
The results show that numerous genes, some with known immune-related functions, predispose to SLE, and evidence of association with replication is found at FCGR2A, PTPN22 and STAT4, regions previously associated with SLE and other autoimmune diseases.
A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans
It is shown that one intronic SNP in PDCD1 is associated with development of SLE in Europeans, and this SNP alters a binding site for the runt-related transcription factor 1 (RUNX1) located in an intronic enhancer, suggesting a mechanism through which it can contribute to the development ofSLE in humans.
A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities
A SNP in the promoter region of FCRL3, a member of the Fc receptor-like family, that is associated with susceptibility to rheumatoid arthritis is identified and this polymorphism alters the binding affinity of nuclear factor-κB and regulatesFCRL3 expression.
The microRNA miR-23b suppresses IL-17-associated autoimmune inflammation by targeting TAB2, TAB3 and IKK-α
It is shown that miR-23b is downregulated in inflammatory lesions of humans with lupus or rheumatoid arthritis, as well as in the mouse models of l upus, rheumatic arthritis or multiple sclerosis.
NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations.
- A. Fauci, J. Harley, W. Roberts, V. Ferrans, H. Gralnick, B. Bjornson
- MedicineAnnals of internal medicine
- 1 July 1982
Chemotherapy to lower the eosinophil counts has resulted in marked improvement of HES prognosis, as have agressive medical and surgical approaches to cardiovascular complications.
An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus.
- J. James, K. Kaufman, A. Farris, E. Taylor-Albert, T. Lehman, J. Harley
- Medicine, BiologyThe Journal of clinical investigation
- 15 December 1997
When considered with other evidence supporting a relationship between Epstein-Barr virus and lupus, these data are consistent with, but do not in themselves establish, Epstein- Barr virus infection as an etiologic factor in l upus.
Changes in the pattern of DNA methylation associate with twin discordance in systemic lupus erythematosus.
The findings not only identify potentially relevant DNA methylation markers for the clinical characterization of SLE patients but also support the notion that epigenetic changes may be critical in the clinical manifestations of autoimmune disease.
High serum IFN-alpha activity is a heritable risk factor for systemic lupus erythematosus.
High serum IFN-alpha activity is a complex heritable trait, which plays a primary role in SLE pathogenesis, and was clustered in specific families in both SLE patients and their healthy first-degree relatives, suggesting a heritable traits.
Early events in lupus humoral autoimmunity suggest initiation through molecular mimicry
- M. McClain, L. Heinlen, G. Dennis, J. Roebuck, J. Harley, J. James
- Biology, MedicineNature Medicine
The hypothesis that some humoral autoimmunity in human lupus arises through molecular mimicry between EBNA-1 and l upus autoantigens is supported and further evidence to suspect an etiologic role for Epstein-Barr virus in SLE is provided.