scholarly journals Detection of islet cell surface antibody in the thyroid disease and systemic lupus erythematosus

1983 ◽  
Vol 6 (6) ◽  
pp. 550-554
Author(s):  
Kiyoshi Kunihiro ◽  
Yasushi Yokogawa ◽  
Junko Ono ◽  
Ryosaburo Takaki ◽  
Shiro Noguchi ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Surface ◽  
Lupus Erythematosus ◽  
Thyroid Disease ◽  
Islet Cell ◽  
Systemic Lupus ◽  
Islet Cell Surface Antibody ◽  
Surface Antibody

Increased Expression of Phospholipid Scramblase 1 in Monocytes from Patients with Systemic Lupus Erythematosus

2010 ◽  
Vol 37 (8) ◽  
pp. 1639-1645 ◽  
Author(s):  
ERIKO SUZUKI ◽  
OLGA AMENGUAL ◽  
TATSUYA ATSUMI ◽  
KENJI OKU ◽  
TOKO HASHIMOTO ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Flow Cytometry ◽  
Cell Surface ◽  
Lupus Erythematosus ◽  
Splice Variants ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Phospholipid Scramblase ◽  
Phospholipid Scramblase 1 ◽  
D Dimer

Objective.A high incidence of thromboembolic events has been reported in patients with systemic lupus erythematosus (SLE). Phosphatidylserine (PS) is normally sequestered in the inner leaflet of cell membranes. Externalization of PS during cell activation is mediated by phospholipid scramblase 1 (PLSCR1) and has a central role in promoting blood coagulation. We investigated the underlying pathogenic status of thrombophilia in SLE by analyzing PLSCR1 expression on monocytes from patients with SLE.Methods.Sixty patients with SLE were evaluated. Twenty-three patients had antiphospholipid syndrome (APS/SLE). Plasma D-dimer levels were measured as a marker of fibrin turnover. The cDNA encoding human PLSCR1 was cloned from the total RNA extract from monocytes, and independent clones were sequenced. PLSCR1 mRNA expression in CD14+ cells was determined by real-time polymerase chain reaction. PS exposure on CD14+ cell surface was analyzed by flow cytometry.Results.Elevated D-dimer levels were found in plasma from SLE patients. Three splice variants of PLSCR1 mRNA were identified in all subjects, and levels of full-length PLSCR1 mRNA were significantly increased in SLE compared to healthy controls (2.9 ± 1.5 vs 1.3 ± 0.4, respectively; p < 0.0001). Flow-cytometry analysis showed relative enhancement of PS exposure in the surface of CD14+ cells in SLE patients compared to healthy controls.Conclusion.Novel PLSCR1 splice variants were identified. Monocytes in SLE patients had enhanced PLSCR1 mRNA expression, as well as increased fibrin turnover and cell-surface PS exposure, indicating that PLSCR1 may, in part, contribute to the prothrombotic tendency in SLE.

scholarly journals Altered Cell Surface N-Glycosylation of Resting and Activated T Cells in Systemic Lupus Erythematosus

2019 ◽  
Vol 20 (18) ◽  
pp. 4455 ◽  
Author(s):  
Enikő Szabó ◽  
Ákos Hornung ◽  
Éva Monostori ◽  
Márta Bocskai ◽  
Ágnes Czibula ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
T Cell ◽  
Cell Surface ◽  
Lupus Erythematosus ◽  
Lectin Binding ◽  
Systemic Lupus ◽  
Activated T Cells ◽  
Neuraminidase Treatment ◽  
Altered Cell

Altered cell surface glycosylation in congenital and acquired diseases has been shown to affect cell differentiation and cellular responses to external signals. Hence, it may have an important role in immune regulation; however, T cell surface glycosylation has not been studied in systemic lupus erythematosus (SLE), a prototype of autoimmune diseases. Analysis of the glycosylation of T cells from patients suffering from SLE was performed by lectin-binding assay, flow cytometry, and quantitative real-time PCR. The results showed that resting SLE T cells presented an activated-like phenotype in terms of their glycosylation pattern. Additionally, activated SLE T cells bound significantly less galectin-1 (Gal-1), an important immunoregulatory lectin, while other lectins bound similarly to the controls. Differential lectin binding, specifically Gal-1, to SLE T cells was explained by the increased gene expression ratio of sialyltransferases and neuraminidase 1 (NEU1), particularly by elevated ST6 beta-galactosamide alpha-2,6-sialyltranferase 1 (ST6GAL1)/NEU1 and ST3 beta-galactoside alpha-2,3-sialyltransferase 6 (ST3GAL6)/NEU1 ratios. These findings indicated an increased terminal sialylation. Indeed, neuraminidase treatment of cells resulted in the increase of Gal-1 binding. Altered T cell surface glycosylation may predispose the cells to resistance to the immunoregulatory effects of Gal-1, and may thus contribute to the pathomechanism of SLE.

scholarly journals Graves’ Disease and Evans’ Syndrome as First Manifestation of Systemic Lupus Erithematosus

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A930-A930
Author(s):  
Andrés Alberto Gómez-Noronha ◽  
Eddy López-Huamanrayme ◽  
Carmen Cecilia Quiroa-Alfaro
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Heart Rate ◽  
Autoimmune Disease ◽  
Thyroid Hormones ◽  
Lupus Erythematosus ◽  
Thyroid Disease ◽  
Hellp Syndrome ◽  
Graves Disease ◽  
Evans Syndrome ◽  
Systemic Lupus

Abstract Background: Graves’ disease is the most common cause of hyperthyroidism triggered by antibodies called thyroid-stimulating immunoglobulin (TSI) which stimulates an overproduction of thyroid hormones. Evans’ syndrome is a rare condition characterized by autoimmune hemolytic anemia and immune thrombocytopenic purpura. Systemic lupus erythematosus (SLE) is also an autoimmune disease with extreme heterogeneity and potentially involvement of any organ or system. It is well known when a patient is diagnosed with an autoimmune disease, it is about time to show up other manifestations of another one, just as it happened in this case report. Clinical Case: A 31-year-old pregnant woman (22 weeks) was admitted to the obstetric emergency room due to headaches, weakness and tinnitus. During anamnesis, she said she was diagnosed with hypertension several weeks before she was pregnant. At physical examination, a 160/100 mm/Hg blood pressure and a heart rate over 100 bpm were found. Initial tests were solicited congruent with severe thrombocytopenia (20 000/mm3) and severe anemia (6 gr/dl), there was also a modest increase in transaminases levels. Transfusion support was needed and a “HELLP syndrome” was diagnosed. Gynecologists decided to perform an emergency hysterotomy and the end of pregnancy. During the post-operative care and the following days, the patient persisted with an average of 100 bpm heart rate and hypertension despite of the use of antihypertensive medication. Physicians also noticed the presence of malar rash and goiter. Thyroid hormones levels where requested and the results were consistent with primary hyperthyroidism (TSH: &lt;0.005 Mu/L, FT4: &gt;100 pmol/L). Further tests were required such as TSI (positive), a thyroid scintigraphy (high thyroid uptake), antinuclear antibodies (ANA: + 1/160 speckled pattern, anti- Smith: +) and extractable nuclear antigen antibodies (ENA) panel. Grave’s disease and SLE were diagnosed. Rheumatologists suggested that the diagnosis of HELLP Syndrome was unclear and they strongly believed that thrombocytopenia and anemia during pregnancy were part of Evans’s syndrome and at the same time of SLE. Antithyroid drugs (thiamazol), beta blockers (propranolol) hydroxychloroquine and corticoids (prednisone) were given to the patient with an excellent clinical and biochemical response. Conclusion: A 25% of patients with SLE can be diagnosed with an autoimmune thyroid disease, such as Graves’ disease (1). Frequent evaluation of thyroid hormones and antithyroid antibodies should be performed in patients with SLE, especially when there are related symptoms of a thyroid disorder. References: 1.Chan AT, Al-Saffar Z, Bucknall RC. Thyroid disease in systemic lupus erythematosus and rheumatoid arthritis. Rheumatology (Oxford). 2001;40:353---4.

scholarly journals Autoimmune thyroid disease and associated rheumatic disorders

2005 ◽  
Vol 133 (Suppl. 1) ◽  
pp. 55-60 ◽  
Author(s):  
Djunajdar Kerimovic-Morina
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Systemic Sclerosis ◽  
Rheumatic Diseases ◽  
Lupus Erythematosus ◽  
Thyroid Disease ◽  
Autoimmune Thyroid Disease ◽  
Systemic Lupus ◽  
Autoimmune Thyroid ◽  
Antithyroid Antibodies

Musculosceletal manifestations were found in patients with hyperthyroidism as well as hypothyroidism. This article will review the available evidence that autoimmune thyroid disease is associated with: Sj?gren?s sydrome (SS), systemic lupus erythematosus (SLE), systemic sclerosis, rheumatoid arthritis (RA) and spondyloarthropathies. Possible pathogenesis of these manifestations has not been completely established. Sj?gren?s syndrome occurs in about 1/10 of patients with autoimmune thyroid disease; patients with SLE and antithyroid antibodies were significantly older than those pattiens without antibodies. Patients with systemic sclerosis and thyroid disease were significantly younger than those without antibodies. Thyroid disfunction was found three times more often in women with RA than in women with noninflammatory rheumatic diseases, and those with thyroid disease tended to have a shorter duration of arthritis.

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