Similar Datasets
Project description:Isolevuglandins modify immune function in hypertension in systemic lupus erythematosus
| PRJNA825480 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-06-03 | E-GEOD-46923 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2014-06-03 | GSE46923 | GEO
Project description: Not available
| S-EPMC1440614 | biostudies-literature
Project description:The treatment of rheumatoid arthritis was revolutionized with the use of molecular-targeted drugs that target immunoregulatory molecules. The success of treatment with these drugs prompted the development of molecular-targeted drugs for systemic lupus erythematosus. However, systemic lupus erythematosus is a disease with high heterogeneous immune abnormalities, and diverse cells or molecules can be treatment targets. Thus, the identification of subpopulations based on immune abnormalities is essential for the development of effective treatment. One analytical method used to identify subpopulations is the immunophenotyping of peripheral blood samples of patients. This analysis evaluates the validity of target molecules for peripheral blood immune cell subsets, which are expected to be developed as biomarkers for precision medicine in which appropriate treatment targets are set for each subpopulation.
| S-EPMC10295858 | biostudies-literature
Project description:Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disorder. The study of diverse mouse models of lupus has provided clues to the etiology of SLE. Spontaneous mouse models of lupus have led to identification of numerous susceptibility loci from which several candidate genes have emerged. Meanwhile, induced models of lupus have provided insight into the role of environmental factors in lupus pathogenesis as well as provided a better understanding of cellular mechanisms involved in the onset and progression of disease. The SLE-like phenotypes present in these models have also served to screen numerous potential SLE therapies. Due to the complex nature of SLE, it is necessary to understand the effect specific targeted therapies have on immune homeostasis. Furthermore, knowledge gained from mouse models will provide novel therapy targets for the treatment of SLE.
| S-EPMC3042628 | biostudies-other
Project description:Systemic lupus erythematosus (SLE) is a prototypic inflammatory autoimmune disorder characterized by multisystem involvement and fluctuating disease activity. Symptoms range from rather mild manifestations such as rash or arthritis to life-threatening end-organ manifestations. Despite new and improved therapy having positively impacted the prognosis of SLE, a subgroup of patients do not respond to conventional therapy. Moreover, the risk of fatal outcomes and the damaging side effects of immunosuppressive therapies in SLE call for an improvement in the current therapeutic management. New therapeutic approaches are focused on B-cell targets, T-cell downregulation and costimulatory blockade, cytokine inhibition, and the modulation of complement. Several biological agents have been developed, but this encouraging news is associated with several disappointments in trials and provide a timely moment to reflect on biologic therapy in SLE.
| S-EPMC3303577 | biostudies-other
Project description:INTRODUCTION: Bullous systemic lupus erythematosus (BSLE) is an autoantibody-mediated disease with subepidermal blisters. It is a rare form of presentation of SLE that occurs in less than 5% of cases of lupus. CASE REPORT: A 27-year-old, female, FRS patient reported the appearance of painful bullous lesions in the left nasal wing and left buccal mucosa that displayed sudden and rapid growth. She sought advice from emergency dermatology staff 15 days after onset and was hospitalized with suspected bullous disease. Intravenous antibiotics and steroids were administered initially, but the patient showed no improvement during hospitalization. She displayed further extensive injuries to the trunk, axillae, and vulva as well as disruption of the bullous lesions, which remained as hyperemic scars. Incisional biopsy of a lesion in the left buccal mucosa was performed, and pathological results indicated mucositis with extensive erosion and the presence of a predominantly neutrophilic infiltrate with degeneration of basal cells and apoptotic keratinocytes. Under direct immunofluorescence, the skin showed anti-IgA, anti-IgM, and anti-IgG linear fluorescence on the continuous dermal side of the cleavage. Indirect immunofluorescence of the skin showed conjugated anti-IgA, was anti-IgM negative, and displayed pemphigus in conjunction with anti-IgG fluorescence in the nucleus of keratinocytes, consistent with a diagnosis of bullous lupus erythematosus. DISCUSSION: BSLE is an acquired autoimmune bullous disease caused by autoantibodies against type VII collagen or other components of the junctional zone, epidermis, and dermis. It must be differentiated from the secondary bubbles and vacuolar degeneration of the basement membrane that may occur in acute and subacute cutaneous lupus erythematosus.
| S-EPMC4423270 | biostudies-other
Project description:Autoimmune diseases such as psoriasis, rheumatoid arthritis, and systemic lupus erythematosus (SLE) have high rates of hypertension and cardiovascular disease. Systemic lupus erythematosus is a prototypic autoimmune disorder that primarily affects women of childbearing age and is associated with a loss of self-tolerance, autoreactive B and T lymphocytes, and the production of autoantibodies, especially to nuclear components. In this study, we hypothesized that the pristane-inducible model of SLE would develop hypertension and vascular dysfunction as the disease progressed. To test this hypothesis, female C57BL/6 mice were administered PBS or pristane. Seven months after pristane administration, mice developed various autoantibodies, including anti-dsDNA IgG, anti-ssDNA IgG, and anti-nRNP IgG, as well as hypergammaglobulinemia. Several other immunological changes, including increased circulating neutrophils and increased CD4- CD8- (double negative) thymocytes were also detected. Mean arterial pressure (MAP) was elevated in pristane-treated mice when compared to PBS-treated mice. In addition, second-order mesenteric arteries from pristine-treated mice had impaired relaxation to the endothelium-dependent vasodilator acetylcholine compared to PBS-treated mice. These data suggest that the immune system dysfunction present in the pristane model of lupus contributes to the development of hypertension and vascular dysfunction.
| S-EPMC7851437 | biostudies-literature