Role and therapeutic potential of Glycodelin A in systemic lupus erythematosus

2010 ◽  
Vol 31 (5) ◽  
pp. 563-565 ◽  
Author(s):  
Hai-Feng Pan ◽  
Rui-Xue Leng ◽  
Ning Zhang ◽  
Jin-Hui Tao ◽  
Dong-Qing Ye
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Therapeutic Potential ◽  
Systemic Lupus ◽  
Glycodelin A

scholarly journals Decreased miR-4512 Levels in Monocytes and Macrophages of Individuals With Systemic Lupus Erythematosus Contribute to Innate Immune Activation and Neutrsophil NETosis by Targeting TLR4 and CXCL2

2021 ◽  
Vol 12 ◽  
Author(s):  
Binbin Yang ◽  
Xinwei Huang ◽  
Shuangyan Xu ◽  
Li Li ◽  
Wei Wu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Target Genes ◽  
Mononuclear Cells ◽  
Therapeutic Potential ◽  
Luciferase Reporter ◽  
Systemic Lupus ◽  
Peripheral Blood Mononuclear ◽  
Monocytes And Macrophages

ObjectiveSystemic lupus erythematosus (SLE) is an autoimmune disease with complex etiology that is not yet entirely understood. We aimed to elucidate the mechanisms and therapeutic potential of microRNAs (miRNAs) in SLE in a Tibetan population.MethodsPeripheral blood mononuclear cells from SLE patients (n = 5) and healthy controls (n = 5) were used for miRNA–mRNA co-sequencing to detect miRNAs related to immune abnormalities associated with SLE. Luciferase reporter assay was used to identify potential targets of candidate miRNA. The target genes were verified in miRNA-agomir/antagomir transfection assays with multiple cells lines and by expression analysis. The effects of candidate miRNA on monocyte and macrophage activation were evaluated by multiple cytokine profiling. Neutrophil extracellular traps (NETs) formation was analyzed in vitro by cell stimulation with supernatants of monocytes and macrophages transfected with candidate miRNA. The rodent MRL/lpr lupus model was used to evaluate the therapeutic effect of CXCL2Ab on SLE and the regulation effect of immune disorders.ResultsIntegrated miRNA and mRNA expression profiling identified miRNA-4512 as a candidate miRNA involved in the regulation of neutrophil activation and chemokine-related pathways. MiR-4512 expression was significantly reduced in monocytes and macrophages from SLE patients. MiR-4512 suppressed the TLR4 pathway by targeting TLR4 and CXCL2. Decreased monocyte and macrophage miR-4512 levels led to the expression of multiple proinflammatory cytokines in vitro. Supernatants of miR-4512 antagomir-transfected monocytes and macrophages significantly promoted NETs formation (P < 0.05). Blocking of CXCL2 alleviated various pathogenic manifestations in MRL/lpr mice, including kidney damage and expression of immunological markers of SLE.ConclusionsWe here demonstrated the role of miR-4512 in innate immunity regulation in SLE. The effect of miR-4512 involves the regulation of monocytes, macrophages, and NETs formation by direct targeting of TLR4 and CXCL2, indicating the miR-4512-TLR4-CXCL2 axis as a potential novel therapeutic target in SLE.

Therapeutic potential of SIGIRR in systemic lupus erythematosus

2013 ◽  
Vol 33 (8) ◽  
pp. 1917-1921 ◽  
Author(s):  
Chao Wang ◽  
Chen-Chen Feng ◽  
Hai-Feng Pan ◽  
De-Guang Wang ◽  
Dong-Qing Ye
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Therapeutic Potential ◽  
Systemic Lupus

scholarly journals COVID-19 Prevalence and Outcomes among Individuals with Rheumatoid Arthritis and Systemic Lupus Erythematosus Taking Hydroxychloroquine; A Retrospective Analysis

2021 ◽  
Vol 15 (1) ◽  
pp. 69-76
Author(s):  
Arash Mollaeian ◽  
Daniel S. Kim ◽  
Christopher J. Haas
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Statistical Analysis ◽  
Lupus Erythematosus ◽  
Therapeutic Potential ◽  
Systemic Lupus ◽  
Global Pandemic ◽  
Therapeutic Properties ◽  
Secondary Outcomes ◽  
D Dimer

Introduction: The SARS-CoV-2 global pandemic has resulted in a universal search for potential treatments of Coronavirus Disease 2019 (COVID-19). Initial reports of the therapeutic potential of chloroquine (CQ) and hydroxychloroquine (HCQ) and early non-randomized non-controlled studies were followed by subsequent trials refuting such properties. The use of CQ and HCQ in diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), prompted us to examine the prevalence of COVID-19 and proposed prophylactic and therapeutic properties of HCQ in this population. Methods: A total of 103 patients with RA and SLE aged 18 to 75 diagnosed with COVID-19 were identified. The patients were categorized as those taking HCQ (cases) and those not on HCQ (controls) for at least 6 months. Primary (mechanical ventilation, length of stay, death) and secondary outcomes were defined, data were collected, and results were compared and statistically analyzed between cases and controls. Results: No statistical difference was observed in demographic features, baseline comorbidities, and medications. Primary outcomes’ statistical analysis did not reveal any differences between cases and controls. Statistical analysis of secondary outcomes revealed that cases had a statistically higher chance of being tachypneic (p 0.034). D-Dimer (p 0.017) and LDH levels (p 0.044) were found to be significantly lower in cases versus controls. Conclusion: This study highlights the lack of clinical prophylactic and therapeutic efficacy of HCQ against COVID-19 when taken at regular doses for patients with RA and SLE. It also shows that the prevalence of COVID-19 was similar in RA and SLE patients regardless of baseline consumption of HCQ.

scholarly journals Inflammatory Cytokines in Systemic Lupus Erythematosus

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Kim Ohl ◽  
Klaus Tenbrock
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cell ◽  
Lupus Erythematosus ◽  
Therapeutic Potential ◽  
Unknown Origin ◽  
Organ Damage ◽  
Cell Phenotype ◽  
Systemic Lupus ◽  
Activation Induced Cell Death ◽  
Organ Systems

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown origin affecting virtually all organ systems. Beyond genetic and environmental factors, cytokine imbalances contribute to immune dysfunction, trigger inflammation, and induce organ damage. The key cytokine that is involved in SLE pathogenesis is interferon alpha. Interferon secretion is induced by immune complexes and leads to upregulation of several inflammatory proteins, which account for the so-called IFN signature that can be found in the majority of SLE PBMCs. Additionally IL-6 and IFN-y as well as T-cell-derived cytokines like IL-17, IL-21, and IL-2 are dysregulated in SLE. The latter induce a T-cell phenotype that is characterized by enhanced B-cell help and enhanced secretion of proinflammatory cytokines but reduced induction of suppressive T cells and activation-induced cell death. This paper will focus on these cytokines and highlights pathophysiological approaches and therapeutic potential.

Structural insights into a human anti-IFN antibody exerting therapeutic potential for systemic lupus erythematosus

2012 ◽  
Vol 90 (7) ◽  
pp. 837-846 ◽  
Author(s):  
Songying Ouyang ◽  
Bin Gong ◽  
Jin-Zhi Li ◽  
Li-Xia Zhao ◽  
Wei Wu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Therapeutic Potential ◽  
Systemic Lupus ◽  
Structural Insights

scholarly journals Distinct cell-specific control of autoimmunity and infection by FcγRIIb

2008 ◽  
Vol 205 (4) ◽  
pp. 883-895 ◽  
Author(s):  
Rebecca J. Brownlie ◽  
Kate E. Lawlor ◽  
Heather A. Niederer ◽  
Antony J. Cutler ◽  
Zou Xiang ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
B Cells ◽  
Immune Responses ◽  
Lupus Erythematosus ◽  
Therapeutic Potential ◽  
Systemic Lupus ◽  
Collagen Induced Arthritis ◽  
Distinct Cell ◽  
Specific Control

FcγRIIb is an inhibitory Fc receptor expressed on B cells and myeloid cells. It is important in controlling responses to infection, and reduced expression or function predisposes to autoimmunity. To determine if increased expression of FcγRIIb can modulate these processes, we created transgenic mice overexpressing FcγRIIb on B cells or macrophages. Overexpression of FcγRIIb on B cells reduced the immunoglobulin G component of T-dependent immune responses, led to early resolution of collagen-induced arthritis (CIA), and reduced spontaneous systemic lupus erythematosus (SLE). In contrast, overexpression on macrophages had no effect on immune responses, CIA, or SLE but increased mortality after Streptococcus pneumoniae infection. These results help define the role of FcγRIIb in immune responses, demonstrate the contrasting roles played by FcγRIIb on B cells and macrophages in the control of infection and autoimmunity, and emphasize the therapeutic potential for modulation of FcγRIIb expression on B cells in inflammatory and autoimmune disease.

scholarly journals Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies.

1983 ◽  
Vol 158 (4) ◽  
pp. 1350-1355 ◽  
Author(s):  
N E Adelman ◽  
D L Watling ◽  
H O McDevitt
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Monoclonal Antibodies ◽  
Survival Rate ◽  
Renal Disease ◽  
Gene Product ◽  
Lupus Erythematosus ◽  
Therapeutic Potential ◽  
Systemic Lupus ◽  
Region Gene ◽  
Autoimmune Syndrome

(NZB x NZW)F1 mice spontaneously develop an autoimmune syndrome characterized by a fatal immune complex glomerulonephritis. Administration of monoclonal antibodies specific for an I region gene product (I-Az) of the H-2 haplotype associated with susceptibility to glomerulonephritis in these animals produced a remission in female mice with established renal disease. The results demonstrated that anti-I-A therapy stabilized the level of proteinuria and increased the 1-yr survival rate from 10% to greater than 90% in treated animals relative to control mice. These findings may ultimately have therapeutic potential for the treatment of systemic lupus erythematosus.

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