Oxidative stress and immune complexes: Pathogenic mechanisms in pristane induced murine model of lupus

Pannu, Naveet

doi:10.1016/j.imbio.2019.11.006

Cited by 16 publications

(8 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Oxidative damage has been observed to give rise to increased levels of IL-6. Concordantly, serum IL-6 level was doubled in lupus patients and pristane-induced lupus mouse models, 1,30 reflecting that oxidative stress might have an appreciable effect on Treg cell differentiation by regulating IL-6. Adipokines were found to have been overproduced and strongly correlated to oxidative stress in SLE patients.…”

Section: Oxidative Stress Dysregulates Immune Cells In Lupus Erythema...mentioning

confidence: 90%

“…There is a broad spectrum of its clinical manifestations involving multiple organ systems including the genitourinary, cardiopulmonary, neuromuscular-psychiatric, endocrine, integumentary, and hematologic systems. 1 , 2 The molecular mechanisms underlying this systemic autoimmune response remain largely unknown, and any further advancement in therapeutic approaches requires assessments in preclinical studies.…”

Section: Introductionmentioning

confidence: 99%

“… 12 Any disruption to the oxidant/antioxidant equilibrium in autoimmune diseases by either endogenous or exogenous toxic substances incites an aberrant innate and adaptative immune response with a continuing supply of autoantigens. 13 Some translational investigations 1 , 14 , 15 have associated oxidative stress with the pathogenesis of SLE. High levels of oxidative and nitrosative stress have been detected in individuals with active SLE.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Oxidative Stress Contributes to Inflammatory and Cellular Damage in Systemic Lupus Erythematosus: Cellular Markers and Molecular Mechanism

Zhu¹,

Chen²,

Xia³

2023

JIR

View full text Add to dashboard Cite

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease with complex pathogenesis, the treatment of which relies exclusively on the use of immunosuppressants. Increased oxidative stress is involved in causing inflammatory and cellular defects in the pathogenesis of SLE. Various inflammatory and cellular markers including oxidative modifications of proteins, lipids, and DNA contribute to immune system dysregulation and trigger an aggressive autoimmune attack through molecular mechanisms like enhanced NETosis, mTOR pathway activation, and imbalanced T-cell differentiation. Accordingly, the detection of inflammatory and cellular markers is important for providing an accurate assessment of the extent of oxidative stress. Oxidative stress also reduces DNA methylation, thus allowing the increased expression of affected genes. As a result, pharmacological approaches targeting oxidative stress yield promising results in treating patients with SLE. The purpose of this review is to examine the involvement of oxidative stress in the pathogenesis and management of SLE.

show abstract

Section: Oxidative Stress Dysregulates Immune Cells In Lupus Erythema...mentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative Stress Contributes to Inflammatory and Cellular Damage in Systemic Lupus Erythematosus: Cellular Markers and Molecular Mechanism

Zhu¹,

Chen²,

Xia³

2023

JIR

View full text Add to dashboard Cite

show abstract

“…This increase indicates the involvement of inflammation in the pathomechanism of SLE. The rise in TNF-α in this SLE model indicated the involvement of kidney manifestations, autoantibodies, and inflammation [21] . Macrophages directly induce TNF-α production in response to immune complexes [22] .…”

Section: Resultsmentioning

confidence: 70%

Green Tea Suppresses Serum TNF-? and TGF-?1 Levels In Mice Model of Systemic Lupus Erythematosus

Herin Mawarti,

Jusak Nugraha,

Djoko Agus Purwanto

et al. 2021

Indian Journal of Forensic Medicine & Toxicology

View full text Add to dashboard Cite

Objective: This study aims to investigate the effects of green tea administration on TNF-a, Hsp70, and TGF-b1 levels in the systemic lupus erythematosus (SLE). Material and methods: A total of 32 mice will be divided into four groups (each 8 mice), namely the control group, the SLE group, the SLE group who were given green tea extract at a dose of 500 mg/kg body weight, and the SLE group who were given green tea extract at a dose of 1000 mg/kg body weight. Analysis of TNF-a, Hsp70, and TGF-b1 levels was carried out using the enzyme-linked immunosorbent assay technique. Results: TNF-a and TGF-b1 levels were significantly increased in the SLE group compared to the control group (p < 0.05). This increase can be significantly reduced through the provision of green tea, even reaching levels comparable to the control group (p > 0.05). Conclusions: It was concluded that green tea containing EGCG can suppress TNF-a and TGF-b1 in the SLE model. Thus, green tea can be an alternative in immunology modulation in SLE.

show abstract

“…As we previously reported that ADAMTS7 was upregulated after H 2 O 2 and proinflammatory cytokine stimuli, 32 ADAMTS7 upregulation in both models was possibly due to oxidative stress and inflammatory response, which mediated the pathogenesis of SLE and renal I/R injury. 33–37 Moreover, we demonstrated that ADAMTS7 deficiency rescued CFH degradation and alleviated complement-mediated renal pathologies, but without affecting complement-dependent serum bactericidal activity. Therefore, ADAMTS7, which degrades CFH, would be a promising anticomplement therapeutic target for related renal injuries, potentially reducing the risk of infection.…”

Section: Discussionmentioning

confidence: 84%

ADAMTS7-Mediated Complement Factor H Degradation Potentiates Complement Activation to Contributing to Renal Injuries

Mao

Jia

et al. 2023

JASN

View full text Add to dashboard Cite

Background The dysfunction of complement factor H (CFH), the main soluble complement negative regulator, potentiates various complement-induced renal injuries. However, insights into the underlying mechanism of CFH dysfunction remain limited. In this study, we investigated whether extracellular protease-mediated degradation accounts for CFH dysfunction in complement-mediated renal injuries.Methods An unbiased interactome of lupus mice kidneys identified CFH-binding protease. In vitro cleavage assay clarified CFH degradation. Pristane-induced SLE or renal ischemia-reperfusion (I/R) injury models were used in wild-type and ADAMTS7 2/2 mice. ResultsWe identified the metalloprotease ADAMTS7 as a CFH-binding protein in lupus kidneys. Moreover, the upregulation of ADAMTS7 correlated with CFH reduction in both lupus mice and patients. Mechanistically, ADAMTS7 is directly bound to CFH complement control protein (CCP) 1-4 domain and degraded CCP 1-7 domain through multiple cleavages. In mice with lupus nephritis or renal I/R injury, ADAMTS7 deficiency alleviated complement activation and related renal pathologies, but without affecting complement-mediated bactericidal activity. Adeno-associated virus-mediated CFH silencing compromised these protective effects of ADAMTS7 knockout against complement-mediated renal injuries in vivo.Conclusion ADAMTS7-mediated CFH degradation potentiates complement activation and related renal injuries. ADAMTS7 would be a promising anticomplement therapeutic target that does not increase bacterial infection risk.

show abstract

Oxidative stress and immune complexes: Pathogenic mechanisms in pristane induced murine model of lupus

Cited by 16 publications

References 44 publications

Oxidative Stress Contributes to Inflammatory and Cellular Damage in Systemic Lupus Erythematosus: Cellular Markers and Molecular Mechanism

Oxidative Stress Contributes to Inflammatory and Cellular Damage in Systemic Lupus Erythematosus: Cellular Markers and Molecular Mechanism

Green Tea Suppresses Serum TNF-? and TGF-?1 Levels In Mice Model of Systemic Lupus Erythematosus

ADAMTS7-Mediated Complement Factor H Degradation Potentiates Complement Activation to Contributing to Renal Injuries

Contact Info

Product

Resources

About