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JournalISSN: 0891-6934

Autoimmunity 

Informa
About: Autoimmunity is an academic journal published by Informa. The journal publishes majorly in the area(s): Autoantibody & Autoimmune disease. It has an ISSN identifier of 0891-6934. Over the lifetime, 2633 publications have been published receiving 62402 citations. The journal is also known as: Auto-immunity & Autoimmune.


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Journal ArticleDOI
TL;DR: In CIA, activation of AP-1 and NF-kappaB precede both clinical arthritis and metalloproteinase gene expression, and expression was increased in both RA and OA synovial intimal lining.
Abstract: Objective To determine the expression and regulation of nuclear transcription factors AP-1 and NF-KB in rheumatoid arthritis and in collagen-induced arthritis in mice.Methods AP-1 and NF-KB expression and function were determined in RA, OA and normal synovial tissue by electrophoretic mobility shift assay (EMSA) and immunohis-tochemistry. The kinetics of transcription factor expression were then examined in collagen-induced arthritis (CIA) in mice. EMSAs were performed with the nuclear extracts obtained from paws of CIA mice from 10 to 45 d after immunization to determine AP-1 and NF-KB binding activity. The expression of collagenase-3 (MMP13) and stromelysin (MMP3) mRNA was examined by northern blot analysis.Results Immunohistochemistry showed that NF-KB expression was increased in both RA and OA synovial intimal lining. AP-1 components Jun and Fos were also present in the intimal lining and was significantly greater in RA than OA. The DNA binding activities of both AP-1 and NF-KB were significantly high...

364 citations

Journal ArticleDOI
TL;DR: In this review various aspects of the relation between complement and SLE are discussed.
Abstract: The complement system involves both the innate and the adaptive immune systems and has important roles in the pathogenesis of SLE. Complement deficiencies within the classical pathway (C1q, C4 and C2) of activation predispose for development of the autoimmune disease SLE. The association between complement deficiencies and SLE could be explained by several mechanisms, including impaired clearance of immune complexes and impaired handling of apoptotic cells, aberrant tolerance induction or changes in cytokine regulation. Also during SLE disease flares, the complement system is activated giving rise to partial deficiency or dysfunction due to consumption. On the other hand, complement also takes part in the inflammatory reaction in the disease that gives rise to the tissue and organ damage. In this review various aspects of the relation between complement and SLE are discussed.

284 citations

Journal ArticleDOI
TL;DR: SLE patients are considered a high-risk population, where identification and treatment of chronic infections such as tuberculosis, hepatitis B or human immunodeficiency virus are important prior to the institution of immunosuppression so as to prevent reactivation or exacerbation of the infection.
Abstract: Viral and bacterial infections may serve as an environmental trigger for the development or exacerbation of systemic lupus erythematosus (SLE) in the genetically predetermined individual. In addition, SLE patients are more prone to develop common (pneumonia, urinary tract infection, cellulitis, sepsis), chronic (tuberculosis), and opportunistic infections possibly due to inherit genetic and immunologic defects (complement deficiencies, mannose-binding lectin [MBL] polymorphisms, elevated Fcgamma III and GM-CSF levels, osteopontion polymorphism), but also due to the broad spectrum immunosuppressive agents that are part of therapy for severe manifestations of the disease. Hence, SLE patients are considered a high-risk population, where identification and treatment of chronic infections such as tuberculosis, hepatitis B or human immunodeficiency virus, are important prior to the institution of immunosuppression so as to prevent reactivation or exacerbation of the infection. Infections in SLE patients remain a source of morbidity and mortality. A caveat often encountered is to distinguish between a lupus flare and an acute infection; in such cases parameters including elevated CRP (and adhesion molecules) may aid in the diagnosis of infection. Recent research has provided convincing evidence that EBV infection may play a major role not only in molecular mimicry but also in aberrations of B cells and apoptosis leading to a state of perpetual heightened immune response in SLE.

268 citations

Journal ArticleDOI
TL;DR: The role of TRAP in bone and immune cells is discussed and it is suggested that TRAP may be implicated in autoimmune disorders regulated by Th1 inflammatory responses as well as certain cancers.
Abstract: Tartrate-resistant acid phosphatase (TRAP), once considered to be just a histochemical marker of osteoclasts is now recognised to be a molecule of widespread occurrence with functions in both the skeleton and the immune system. TRAP is expressed by osteoclasts, macrophages, dendritic cells and a number of other cell types. It has a critical role in many biological processes including skeletal development, collagen synthesis and degradation, the mineralisation of bone, cytokine production by macrophages and dendritic cells, macrophage recruitment, dendritic cell maturation and a role in the development of Th1 responses. TRAP is able to degrade skeletal phosphoproteins including osteopontin (OPN), identical to the T-cell cytokine, Eta-1. In this review, we discuss the role of TRAP in bone and immune cells and suggest that TRAP may be implicated in autoimmune disorders regulated by Th1 inflammatory responses as well as certain cancers.

268 citations

Journal ArticleDOI
TL;DR: Estimation of the nature of the major IFNs, or other factors, that drive the IFN-regulated gene expression signature noted in SLE is an important area for investigation that may lead to new approaches to targeted therapy of SLE.
Abstract: Altered regulation of interferon-alpha (IFNalpha) in systemic lupus erythematosus (SLE) was first demonstrated nearly 25 years ago. However, only recently has due attention been directed towards the central role of this cytokine family in SLE. Several laboratories have used large-scale microarray technology to study global gene expression patterns in heterogeneous populations of peripheral blood cells from lupus patients and control subjects. The results of these studies demonstrate that IFN-regulated genes are among the most significantly overexpressed in SLE mononuclear cells. In view of the protean effects of IFNs on immune system function, increased activity of IFNs may account for many of the immune system alterations that characterize SLE and contribute to autoimmunity. Definition of the nature of the major IFNs, or other factors, that drive the IFN-regulated gene expression signature noted in SLE is an important area for investigation that may lead to new approaches to targeted therapy of SLE.

263 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202319
202257
202164
202054
201933
201848