scholarly journals The in Vivo Metabolism of the Third Component of Complement in Systemic Lupus Erythematosus

1977 ◽  
Vol 20 (7) ◽  
pp. 1304-1313 ◽  
Author(s):  
Lawrence D. Petz ◽  
Runas Powers ◽  
James R. Fries ◽  
Neil R. Cooper ◽  
Halsted R. Holman
1981 ◽  
Vol 24 (10) ◽  
pp. 1255-1260 ◽  
Author(s):  
Yuji Sano ◽  
Hiroaki Nishimukai ◽  
Hajime Kitamura ◽  
Kazuyoshi Nagaki ◽  
Shinya Inai ◽  
...  

2020 ◽  
Vol 19 (4) ◽  
pp. 102488 ◽  
Author(s):  
Irene Cecchi ◽  
Carlos Perez-Sanchez ◽  
Savino Sciascia ◽  
Massimo Radin ◽  
Ivan Arias de la Rosa ◽  
...  

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1291 ◽  
Author(s):  
Ritprajak ◽  
Kaewraemruaen ◽  
Hirankarn

Tolerogenic dendritic cells (tolDCs) are central players in the initiation and maintenance of immune tolerance and subsequent prevention of autoimmunity. Recent advances in treatment of autoimmune diseases including systemic lupus erythematosus (SLE) have focused on inducing specific tolerance to avoid long-term use of immunosuppressive drugs. Therefore, DC-targeted therapies to either suppress DC immunogenicity or to promote DC tolerogenicity are of high interest. This review describes details of the typical characteristics of in vivo and ex vivo tolDC, which will help to select a protocol that can generate tolDC with high functional quality for clinical treatment of autoimmune disease in individual patients. In addition, we discuss the recent studies uncovering metabolic pathways and their interrelation intertwined with DC tolerogenicity. This review also highlights the clinical implications of tolDC-based therapy for SLE treatment, examines the current clinical therapeutics in patients with SLE, which can generate tolDC in vivo, and further discusses on possibility and limitation on each strategy. This synthesis provides new perspectives on development of novel therapeutic approaches for SLE and other autoimmune diseases.


2014 ◽  
Vol 41 (9) ◽  
pp. 1834-1842 ◽  
Author(s):  
Mary A. Mahieu ◽  
Camelia P. Guild ◽  
Carolyn J. Albert ◽  
George T. Kondos ◽  
James J. Carr ◽  
...  

Objective.Alpha-chlorofatty acid (α-ClFA) is one product of myeloperoxidase activity in vivo during atherogenesis and may be a biomarker for cardiovascular disease (CVD). We investigated if serum α-ClFA is associated with subclinical CVD as measured by coronary artery and aorta calcium scores (CAC and AC, respectively) in women with and without systemic lupus erythematosus (SLE).Methods.This pilot project analyzed baseline data from 173 women with SLE and 186 women without SLE participating in a 5-year longitudinal investigation of the Study of Lupus Vascular and Bone Long-term Endpoints (SOLVABLE). Data collection included demographic information, CVD and SLE risk factors, and laboratory assessments. Alpha-ClFA was measured in stored serum by liquid chromatography-mass spectrometry. CAC and AC were measured by computed tomography. Outcome measures were CAC and AC present (CAC > 0 or AC > 0) versus absent (CAC = 0 or AC = 0). Associations between risk factors and CAC or AC were tested with descriptive statistics and multivariate analyses.Results.Women with SLE had higher α-ClFA levels than women without SLE (42.0 fmol/25 µl ± 37.3 vs 34.5 fmol/25 µl ± 21.9; p = 0.020). In analyses including individual CVD risk factors, having SLE was independently associated with the presence of CAC (OR 3.42, 95% CI 1.72 to 6.78) but not AC. Alpha-ClFA was not associated with the presence of CAC or AC in patients with SLE.Conclusion.SLE, but not serum α-ClFA, was associated with the presence of CAC in this pilot project.


1958 ◽  
Vol 17 (4) ◽  
pp. 426-428 ◽  
Author(s):  
G. Bencze ◽  
S. Cserhati ◽  
J. Kovacs ◽  
T. Tiboldi

1987 ◽  
Vol 166 (3) ◽  
pp. 798-803 ◽  
Author(s):  
C O Jacob ◽  
P H van der Meide ◽  
H O McDevitt

The (NZB X NZW)F1 mouse is recognized as an important animal model of the human disease systemic lupus erythematosus (SLE). Groups of NZB/W F1 mice were treated either with IFN-gamma or with PBS. The results demonstrate that IFN-treated animals have accelerated development of fatal immune complex glomerulonephritis relative to age-matched controls. On the other hand, administration of mAbs specific for IFN-gamma to such mice from 4 to 7 mo of age resulted in significant remission. Development of both proteinuria and anti-DNA antibodies were delayed and survival at 11 mo was increased from less than 20% to 95% in treated mice relative to controls (p less than or equal to 0.001). These findings may have therapeutic implications for the treatment of SLE.


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