scholarly journals Chemokines and Chemokine Receptors in the Development of Lupus Nephritis

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Xiaofeng Liao ◽  
Tharshikha Pirapakaran ◽  
Xin M. Luo
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Nephritis ◽  
Chemokine Receptor ◽  
Lupus Erythematosus ◽  
Chemokine Receptors ◽  
Leukocyte Recruitment ◽  
Systemic Lupus ◽  
Receptor System ◽  
Multiple Organs

Lupus nephritis (LN) is a major cause of morbidity and mortality in the patients with systemic lupus erythematosus (SLE), an autoimmune disease with damage to multiple organs. Leukocyte recruitment into the inflamed kidney is a critical step to promote LN progression, and the chemokine/chemokine receptor system is necessary for leukocyte recruitment. In this review, we summarize recent studies on the roles of chemokines and chemokine receptors in the development of LN and discuss the potential and hurdles of developing novel, chemokine-based drugs to treat LN.

scholarly journals The Role ofγδT Cells in Systemic Lupus Erythematosus

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Meng Wu ◽  
Jinhua Yang ◽  
Xiaofeng Li ◽  
Junwei Chen
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Multiple Organs ◽  
Minor Population ◽  
Neuronal Tissues ◽  
A Minor

Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by the overproduction of autoantibodies against an array of nuclear and cytoplasmic antigens and affects multiple organs, such as the skin, joints, kidneys, and neuronal tissues. T cells have been recognized as important players in the development of SLE due to their functions in cytokine secretion, antigen presentation, and supporting B cells for antibody production.γδT cells are a minor population of T cells that play important roles in infection and tumor-associated disease. In recent years, the role ofγδT cells in autoimmune diseases has been investigated. In this review, we discussed the role ofγδT cells in the pathogenesis of SLE.

scholarly journals HLA-DRB1*04 as a Risk Allele to Systemic Lupus Erythematosus and Lupus Nephritis in the Malay Population of Malaysia

2021 ◽  
Vol 7 ◽  
Author(s):  
Malarvili Selvaraja ◽  
Voon Kin Chin ◽  
Maha Abdullah ◽  
Masita Arip ◽  
Syafinaz Amin-Nordin
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Activity Index ◽  
Disease Activity Index ◽  
Systemic Lupus ◽  
Mortality And Morbidity ◽  
Curative Therapy ◽  
Multiple Organs ◽  
Increased Risk

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease afflicting multiple organs. Lupus nephritis (LN) is a serious complication of SLE and remains a major cause of mortality and morbidity. Curative therapy remains unavailable as etiology from genetic and environmental factors is still unclear. The present study was conducted to elucidate the link between HLA-DRB1 gene polymorphisms with SLE and LN through clinical and laboratory/biological presentations in a population of Malaysian Malay females with SLE. A total of 100 Malay female SLE patients inclusive of 70 SLE patients without LN and 30 patients with LN were included in this study. HLA-DRB1 allele examination in SLE patients was performed using PCR-SSO, and the alleles' frequencies were compared with 951 publicly available datasets representing Malay healthy controls in Malaysia. Cytokines and free radical levels were detected by ELISA and bead-based multiplexed Luminex assays. The association between HLA-DRB1 alleles with clinical and serological manifestations and immune mediators was analyzed using different statistical approaches whenever applicable. Our study showed that HLA-DRB1*0405, HLA-DRB1*1502, and HLA-DRB1*1602 were associated with the increased risk of SLE while HLA-DRB1*1201 and HLADRB1*1202 alleles were associated with a lower risk of SLE development. Furthermore, HLA-DRB1*04 showed significant association to LN and arthritis while HLA-DRB1*15 was significantly associated with oral ulcer in Malay SLE patients. Association analysis of HLA-DRB1*04 with clinical and biological factors revealed that HLA-DRB1*04 was significantly associated with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scores, anti-nuclear antibody (ANA), C-reactive protein (CRP) in the blood, and total protein in the urine. SLE carriers with the HLA-DRB1*04 allele were significantly correlated to the increased levels of cytokines (IFN-y, GM-CSF, IL-17F, IL-18, IL-21, and VEGF) and were significantly showing negative correlation to IL-5 and free radicals (LPO and catalase enzyme) levels compared to SLE carriers without HLA-DRB1*04 allele. The results suggested that disease severity in SLE may be determined by HLA-DRB1 alleles. The risk of HLA-DRB1*04 allele with LN was supported by the demonstration of an intense inflammatory response in Malay SLE patients in Malaysia. More studies inclusive of a larger and multiple SLE cohorts in the future are warranted to validate these findings.

scholarly journals Potentiation of Lupus Activity by Granulocyte Colony-Stimulating Factor

2021 ◽  
pp. 1-5
Author(s):  
Tsz Ching Mok ◽  
Lok Ping Ng ◽  
Eva Tsz Fung Chui ◽  
Ho Yin Chung
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Neutrophil Apoptosis ◽  
Cytokine Storm ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Systemic Lupus ◽  
Stimulating Factor

Recombinant human granulocyte colony-stimulating factor (G-CSF) is commonly used to accelerate recovery of neutropenia in patients with marrow suppression. We hereby report a patient with systemic lupus erythematosus (SLE) who developed diffuse lupus nephritis and impending cytokine storm after G-CSF therapy. The exact mechanisms by which G-CSF leads to lupus flares remains enigmatic. Increased neutrophil apoptosis and release of cytokines have been postulated. The use of G-CSF in patients with autoimmune disease should be cautious.

Lack of Association of C-C Chemokine Receptor 5 Δ32 Deletion Status with Rheumatoid Arthritis, Systemic Lupus Erythematosus, Lupus Nephritis, and Disease Severity

2010 ◽  
Vol 37 (11) ◽  
pp. 2226-2231 ◽  
Author(s):  
HENK A. MARTENS ◽  
SACHA GROSS ◽  
GERRIT van der STEEGE ◽  
ELISABETH BROUWER ◽  
JO H.M. BERDEN ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Disease Severity ◽  
Chemokine Receptor ◽  
Lupus Erythematosus ◽  
Disease Susceptibility ◽  
Systemic Lupus ◽  
Genotype Frequencies ◽  
Chemokine Receptor 5

Objective.C-C chemokine receptor 5 (CCR5) plays an important role in inflammation. A 32 base-pair (Δ32) deletion in the CCR5 gene leads to a nonfunctional receptor. This deletion has been reported to have a protective effect on the development and progression of several autoimmune diseases. We investigated whether the Δ32 deletion is associated with disease susceptibility in a population of patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and lupus nephritis (LN); and whether it is associated with disease severity.MethodsDNA samples from 405 RA patients, 97 SLE patients, 113 LN patients, and 431 healthy controls were genotyped for the CCR5 Δ32 deletion. Differences in genotype frequencies were tested between patients and controls. Association of genotypes with disease severity was analyzed.ResultsGenotype frequencies of each group were in Hardy-Weinberg equilibrium. The genotype frequencies of patients did not differ significantly from controls (CCR5/Δ32, Δ32/Δ32: RA 18.3% and 1.2%, respectively; SLE 17.5% and 2.1%; LN 13.3% and 1.8%; controls 20.0% and 2.8%). However, there was a trend for lower Δ32 deletion allele frequency in LN patients compared to controls (p = 0.08). There was no significant association between the CCR5 status and disease severity in RA, SLE, or LN.Conclusion.Although an association with LN cannot be excluded, the CCR5 Δ32 deletion does not seem to be a disease susceptibility genotype for RA, SLE, or LN. No significant effect of the Δ32 deletion on disease severity was demonstrated.

scholarly journals Overexpression of Cathepsin S Exacerbates Lupus Pathogenesis Through TLR7 and IFN-α in Transgenic Mice

2021 ◽  
Author(s):  
Jinhee Lee ◽  
Minjee Choi ◽  
Soyoung Jang ◽  
Mincheol Kang ◽  
Su-Geun Lim ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Cathepsin S ◽  
Toll Like Receptor ◽  
Systemic Lupus ◽  
Autoimmune Reaction ◽  
Multiple Organs ◽  
Lupus Pathogenesis ◽  
Chronic Autoimmune Disease

Abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were generated, and induced lupus-like symptoms. Eight months later, the TG mice spontaneously developed typical SLE symptoms regardless of the inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) expression with increased monocyte and neutrophil populations in the TG mice. In conclusion, overexpression of CTSS in mice influences TLR7 expression, autoantibodies and IFN-α, which leads to an autoimmune reaction and exacerbates lupus-like symptoms.

Negative Double Stranded DNA and Anti-Smith Antibodies in Lupus Nephritis

2012 ◽  
Vol 4 (2) ◽  
pp. 55-57
Author(s):  
Gagangeet Sandhu ◽  
Anip Bansal ◽  
Aditi Ranade ◽  
Ritu Aggarwal ◽  
Gopal Narayanswami ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Drug Induced ◽  
Serological Screening ◽  
Double Stranded Dna ◽  
Dsdna Antibodies

Systemic lupus erythematosus (SLE) is an autoimmune disease in which auto-antibodies are generated against a variety of intracellular antigens. Anti-Smith (Sm) and anti-double stranded DNA (dsDNA) antibodies in particular are considered to be nephritogenic and their role and correlation with lupus nephritis (LN) has been well established. We present here a case in which the patient had diffuse proliferative full house severe LN, yet negative ds-DNA and anti-Sm antibodies. Although extremely rare, a few subsets of patients with drug-induced LN (hydralazine) have been described in the literature to have negative dsDNA and anti-Sm antibodies on serological screening. Our patient, however, had no evidence of drug induced LN. On further review, and similar to our case, we found only 6 additional well documented cases of non-drug induced severe LN with negative dsDNA antibodies.

scholarly journals Efficacy and Cytokine Modulating Effects of Tacrolimus in Systemic Lupus Erythematosus: A Review

2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
Kam Hon Yoon
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Nephritis ◽  
Cytotoxic T Lymphocytes ◽  
Lupus Erythematosus ◽  
Calcineurin Inhibitor ◽  
Systemic Autoimmune Disease ◽  
Systemic Lupus ◽  
Established Role ◽  
Multitarget Therapy

Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease with involvement of both B cells and cytotoxic T lymphocytes and several cytokines aberrations. Standard therapy for SLE has its limitations. Tacrolimus, a novel calcineurin inhibitor with potent immunosuppressive effects, has been shown in the recent years to be effective in SLE therapy. This paper serves to collate the experimental and clinical data on the efficacy of tacrolimus in the treatment of SLE and lupus nephritis. Tacrolimus as a key component of multitarget therapy in SLE is also discussed. The immunocytokine modulatory effects of tacrolimus are also reviewed with reference to SLE. It can be concluded that tacrolimus has an established role in the management of SLE.

scholarly journals Lupus nephritis: Update on aetiopathogenesis and controversies in classification

2014 ◽  
Vol 4 (8) ◽  
pp. 672-676 ◽  
Author(s):  
AD Pant
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Direct Binding ◽  
Circulating Immune Complex ◽  
Loss Of Tolerance ◽  
Renal Antigens ◽  
Chronic Autoimmune Disease

Systemic Lupus Erythematosus; a chronic autoimmune disease; is characterized by loss of tolerance against its own antigens and leads to production of autoantibodies and causes formation and deposition of immune complexes in different organs. Recent articles have been trying to unravel the mysteries of SLE. Different theories that have been proposed for the aetiopathogenesis of SLE are a)The circulating immune complex theory, b) The direct binding to endogenous renal antigens theory, and c) binding of antibody to antigens that were previously ‘planted’ into the kidney.DOI: http://dx.doi.org/10.3126/jpn.v4i8.11596 Journal of Pathology of Nepal; Vol.4,No. 8 (2014) 672-676

scholarly journals Extracellular Vesicles as Biomarkers of Systemic Lupus Erythematosus

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Javier Perez-Hernandez ◽  
Raquel Cortes
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Extracellular Vesicles ◽  
Inflammatory Disease ◽  
Lupus Erythematosus ◽  
Apoptotic Bodies ◽  
Systemic Lupus ◽  
Surface Receptors ◽  
Multiple Organs ◽  
Inflammatory State

Systemic lupus erythematosus is an autoimmune disease that predominantly affects women and typically manifests in multiple organs. The damage caused by this disorder is characterized by a chronic inflammatory state. Extracellular vesicles (EVs), including microvesicles (also known as microparticles), apoptotic bodies, and exosomes, are recognized vehicles of intercellular communication, carrying autoantigens, cytokines, and surface receptors. Therefore, the evidence of EVs and their cargo as biomarkers of autoimmune disease is rapidly expanding. This review will focus on biogenesis of extracellular vesicles, their pathophysiological roles, and their potential as biomarkers and therapeutics in inflammatory disease, especially in systemic lupus erythematosus.

scholarly journals Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jinhee Lee ◽  
Soyoung Jang ◽  
Minjee Choi ◽  
Mincheol Kang ◽  
Su-Geun Lim ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Cathepsin S ◽  
Toll Like Receptor ◽  
Systemic Lupus ◽  
Autoimmune Reaction ◽  
Multiple Organs ◽  
Lupus Pathogenesis ◽  
Chronic Autoimmune Disease

AbstractSystemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were generated, and induced lupus-like symptoms. Eight months later, the TG mice spontaneously developed typical SLE symptoms regardless of the inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) expression with increased monocyte and neutrophil populations in the TG mice. In conclusion, overexpression of CTSS in mice influences TLR7 expression, autoantibodies and IFN-α, which leads to an autoimmune reaction and exacerbates lupus-like symptoms.

Sign in / Sign up

Export Citation Format

Share Document