scholarly journals Autoantigen TRIM21/Ro52 as a Possible Target for Treatment of Systemic Lupus Erythematosus

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Ryusuke Yoshimi ◽  
Yoshiaki Ishigatsubo ◽  
Keiko Ozato
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Immunosuppressive Drugs ◽  
Systemic Autoimmune Disease ◽  
Type I ◽  
Systemic Lupus ◽  
Molecular Features ◽  
Attractive Therapeutic Target ◽  
Autoimmune Processes

Systemic lupus erythematosus (SLE) is a chronic, systemic, and autoimmune disease, whose etiology is still unknown. Although there has been progress in the treatment of SLE through the use of glucocorticoid and immunosuppressive drugs, these drugs have limited efficacy and pose significant risks of toxicity. Moreover, prognosis of patients with SLE has remained difficult to assess. TRIM21/Ro52/SS-A1, a 52-kDa protein, is an autoantigen recognized by antibodies in sera of patients with SLE and Sjögren's syndrome (SS), another systemic autoimmune disease, and anti-TRIM21 antibodies have been used as a diagnostic marker for decades. TRIM21 belongs to the tripartite motif-containing (TRIM) super family, which has been found to play important roles in innate and acquired immunity. Recently, TRIM21 has been shown to be involved in both physiological immune responses and pathological autoimmune processes. For example, TRIM21 ubiquitylates proteins of the interferon-regulatory factor (IRF) family and regulates type I interferon and proinflammatory cytokines. In this paper, we summarize molecular features of TRIM21 revealed so far and discuss its potential as an attractive therapeutic target for SLE.

scholarly journals Drug-Induced Gingival Overgrowth in an 8-Year-Old Girl: A Case Report

2021 ◽  
Vol 13 (3) ◽  
pp. 109-112
Author(s):  
Parviz Torkzaban ◽  
Amir Talaie
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Case Report ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Immunological Tolerance ◽  
Systemic Autoimmune Disease ◽  
Channel Blockers ◽  
Systemic Lupus ◽  
Drug Induced ◽  
Gingival Overgrowth

Systemic lupus erythematosus is a systemic autoimmune disease that involves multi organs. Genetic, endocrine, immunological, and environmental factors influence the loss of immunological tolerance against self-antigens leading to the formation of pathogenic autoantibodies that cause tissue damage through multiple mechanisms. The gingival overgrowth can be caused by three factors: noninflammatory, hyperplastic reaction to the medication; chronic inflammatory hyperplasia; or a combined enlargement due to chronic inflammation and drug-induced hyperplasia. Drug-Induced Gingival Overgrowth is associated with the use of three major classes of drugs, namely anticonvulsants, calcium channel blockers, and immunosuppressants. Due to recent indications for these drugs, their use continues to grow.

scholarly journals Resolution of the Expert Council «The role of type I interferon inhibitor in the treatment of patients with systemic lupus erythematosus»

2021 ◽  
Vol 15 (4) ◽  
pp. 126-128
Author(s):  
A. M. Lila ◽  
S. K. Soloviev ◽  
T. V. Popkova
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Organ Damage ◽  
Immunosuppressive Drugs ◽  
Type I ◽  
Type I Ifn ◽  
Systemic Lupus ◽  
Key Points

On April 28, 2021, a meeting of the Council of Experts was held with the participation of the leading experts in the field of rheumatic diseases, approaches to the treatment of patients with systemic lupus erythematosus (SLE) were discussed. The issues of medical care for patients with SLE and their routing, key points of Russian and international clinical guidelines for the management of patients with SLE, as well as the role of interferon (IFN) type I in the pathogenesis of the disease were discussed. It is noted that the management of patients with SLE requires a multidisciplinary approach. The basis of therapy is the use of glucocorticoids (GC), immunosuppressive drugs and their combinations. But long-term use of GC in patients with SLE leads to severe complications. Early prescription of biological disease-modifying antirheumatic drugs (bDMARDs) allows to achieve the greatest effect and prevent the development of irreversible organ damage associated with SLE. Currently data from three clinical trials on the efficacy and safety of the type I IFN inhibitor anifrolumab are available. During the discussion, experts defined the clinical profile of a patient with SLE, for whom administration of bDMARD therapy is indicated. According to experts, the use of a type I IFN inhibitor in routine clinical practice can improve disease outcomes in both short and long term.

scholarly journals The Role of Genetic Variation Near Interferon-Kappa in Systemic Lupus Erythematosus

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Isaac T. W. Harley ◽  
Timothy B. Niewold ◽  
Rebecca M. Stormont ◽  
Kenneth M. Kaufman ◽  
Stuart B. Glenn ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Type I Interferons ◽  
Systemic Autoimmune Disease ◽  
Type I ◽  
Nucleotide Polymorphisms ◽  
Type I Ifn ◽  
Systemic Lupus ◽  
Genome Wide

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by increased type I interferons (IFNs) and multiorgan inflammation frequently targeting the skin. IFN-kappa is a type I IFN expressed in skin. A pooled genome-wide scan implicated theIFNKlocus in SLE susceptibility. We studiedIFNKsingle nucleotide polymorphisms (SNPs) in 3982 SLE cases and 4275 controls, composed of European (EA), African-American (AA), and Asian ancestry. rs12553951C was associated with SLE in EA males (odds ratio=1.93,P=2.5×10−4), but not females. Suggestive associations with skin phenotypes in EA and AA females were found, and these were also sex-specific.IFNKSNPs were associated with increased serum type I IFN in EA and AA SLE patients. Our data suggest a sex-dependent association betweenIFNKSNPs and SLE and skin phenotypes. The serum IFN association suggests thatIFNKvariants could influence type I IFN producing plasmacytoid dendritic cells in affected skin.

scholarly journals Siglec-H protects from virus-triggered severe systemic autoimmunity

2016 ◽  
Vol 213 (8) ◽  
pp. 1627-1644 ◽  
Author(s):  
Heike Schmitt ◽  
Sabrina Sell ◽  
Julia Koch ◽  
Martina Seefried ◽  
Sophia Sonnewald ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Murine Cytomegalovirus ◽  
Systemic Autoimmune Disease ◽  
Type I ◽  
Type I Ifn ◽  
Virus Infections ◽  
Systemic Lupus ◽  
Mcmv Infection ◽  
Systemic Autoimmunity

It is controversial whether virus infections can contribute to the development of autoimmune diseases. Type I interferons (IFNs) are critical antiviral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus. Type I IFN is mainly produced by plasmacytoid dendritic cells (pDCs). The secretion of type I IFN of pDCs is modulated by Siglec-H, a DAP12-associated receptor on pDCs. In this study, we show that Siglec-H–deficient pDCs produce more of the type I IFN, IFN-α, in vitro and that Siglec-H knockout (KO) mice produce more IFN-α after murine cytomegalovirus (mCMV) infection in vivo. This did not impact control of viral replication. Remarkably, several weeks after a single mCMV infection, Siglec-H KO mice developed a severe form of systemic lupus–like autoimmune disease with strong kidney nephritis. In contrast, uninfected aging Siglec-H KO mice developed a mild form of systemic autoimmunity. The induction of systemic autoimmune disease after virus infection in Siglec-H KO mice was accompanied by a type I IFN signature and fully dependent on type I IFN signaling. These results show that Siglec-H normally serves as a modulator of type I IFN responses after infection with a persistent virus and thereby prevents induction of autoimmune disease.

Systemic Lupus Erythematosus

2016 ◽  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Symptomatic Treatment ◽  
The Body ◽  
Systemic Autoimmune Disease ◽  
Systemic Lupus ◽  
Specific Section ◽  
Onset Systemic Lupus Erythematosus ◽  
Management Issues

Systemic lupus erythematosus (SLE) is a systemic, autoimmune disease that can affect any part of the body, causing the immune system to attack the body’s cells and tissue, and resulting in inflammation and tissue damage. It is characterized by the presence of autoreactive B and T cells and the production of a broad, heterogeneous group of autoantibodies (autoAb); the absence of a unique presentation makes its diagnosis difficult, even for qualified clinicians. Systemic Lupus Erythematosus focuses on providing a practical approach to the assessment and management of patients with this complex, multisystem, autoimmune disease, in order to improve the diagnosis and treatment of the disease and its complications. It provides detail on the history and epidemiology of SLE alongside comprehensive sections on clinical features, treatment, and special situations. As well as detailing the challenging management issues of SLE, this title provides an overview of the numerous investigations specific to the condition, assessment of disease activity, symptomatic treatment, patient education, and biologic therapies. A specific section on juvenile-onset systemic lupus erythematosus also provides the practising clinician with the knowledge needed to manage this distinct and aggressive stage of SLE.

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 Why Do Patients With Systemic Lupus Erythematosus Suffer Pain?

2021 ◽  
pp. jrheum.210057
Author(s):  
Anisur Rahman
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Ethnic Groups ◽  
Lupus Erythematosus ◽  
Systemic Autoimmune Disease ◽  
Systemic Lupus ◽  
African Caribbean

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a prevalence of approximately 1 in 1000.1 It occurs 9 times more commonly in women than men and is more common in some ethnic groups, notably in people of African/Caribbean ethnicity.

Molecular mimicry in systemic lupus erythematosus

Lupus ◽  
2009 ◽  
Vol 18 (13) ◽  
pp. 1181-1185 ◽  
Author(s):  
N. Agmon-Levin ◽  
M. Blank ◽  
Z. Paz ◽  
Y. Shoenfeld
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Molecular Mimicry ◽  
Current Evidence ◽  
Systemic Autoimmune Disease ◽  
Infectious Agents ◽  
Systemic Lupus ◽  
Pivotal Mechanism

Systemic lupus erythematosus is a multi-systemic autoimmune disease distinguished by the presence of various autoantibodies. Like most autoimmune diseases, systemic lupus erythematosus is believed to be induced by a combination of genetic, immunologic, and environmental factors, mainly infectious agents. Molecular mimicry between an infectious antigen and self-components is implicated as a pivotal mechanism by which autoimmune diseases such as systemic lupus erythematosus are triggered. Here we review the current evidence of molecular mimicry between different infectious agents and systemic lupus erythematosus.

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