scholarly journals Regulatory T-Cell-Associated Cytokines in Systemic Lupus Erythematosus

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Akiko Okamoto ◽  
Keishi Fujio ◽  
Tomohisa Okamura ◽  
Kazuhiko Yamamoto
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Organ Damage ◽  
Interleukin 10 ◽  
Peripheral Tolerance ◽  
Systemic Lupus ◽  
Autoantibody Production ◽  
Inflammatory Processes ◽  
Complex Deposition

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production, complement activation, and immune complex deposition, resulting in tissue and organ damage. An understanding of the mechanisms responsible for homeostatic control of inflammation, which involve both innate and adoptive immune responses, will enable the development of novel therapies for SLE. Regulatory T cells (Treg) play critical roles in the induction of peripheral tolerance to self- and foreign antigens. Naturally occurring CD4+CD25+Treg, which characteristically express the transcription factor forkhead box protein P3 (Foxp3), have been intensively studied because their deficiency abrogates self-tolerance and causes autoimmune disease. Moreover, regulatory cytokines such as interleukin-10 (IL-10) also play a central role in controlling inflammatory processes. This paper focuses on Tregs and Treg-associated cytokines which might regulate the pathogenesis of SLE and, hence, have clinical applications.

scholarly journals Cytokines and Their Roles in the Pathogenesis of Systemic Lupus Erythematosus: From Basics to Recent Advances

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Desmond Yat Hin Yap ◽  
Kar Neng Lai
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Critical Role ◽  
Type I Interferons ◽  
Type I ◽  
Systemic Lupus ◽  
Immune Disorder ◽  
Autoantibody Production ◽  
Inflammatory Processes ◽  
Complex Deposition

Systemic lupus erythematosus (SLE) is a complex auto-immune disorder which involves various facets of the immune system. In addition to autoantibody production and immune complex deposition, emerging evidences suggest that cytokines may act as key players in the immunopathogenesis of SLE. These cytokines assume a critical role in the differentiation, maturation and activation of cells and also participate in the local inflammatory processes that mediate tissue insults in SLE. Certain cytokines such as the IL-6, IL-10, IL-17, BLys, type I interferons (IFN) and tumor necrosis factor-α(TNF-α) are closely linked to pathogenesis of SLE. The delineation of the role played by these cytokines not only fosters our understanding of this disease but also provides a sound rationale for various therapeutic approaches. In this context, this review focuses on selected cytokines which exert significant effect in the pathogenesis of SLE and their possible clinical applications.

scholarly journals Constrictive Pericarditis as the First Presentation of Systemic Lupus Erythematosus

2019 ◽  
pp. 9-11
Author(s):  
Hannah Jethwa ◽  
Maaz Rana ◽  
Jamie Kitt ◽  
Sarah Menzies ◽  
Alan Steuer ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Immune Complexes ◽  
Constrictive Pericarditis ◽  
Organ Damage ◽  
Differential Diagnoses ◽  
Chronic Infections ◽  
Systemic Lupus ◽  
Wide Range

Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by multi-organ damage mediated by immune complexes and autoantibodies. It often presents with patients being non-specifically unwell and there is a wide range of differential diagnoses, one of which includes chronic infections such as Tuberculosis (TB). Exudative pericarditis is a relatively common feature in SLE and is present in up to 62% of patients on autopsy, although only a quarter of patients are symptomatic; constrictive pericarditis is a very rare feature of SLE. We report a 49 year old gentleman who was diagnosed with SLE which presented with features of constrictive pericarditis following an extensive period of investigations for TB.

Autoantibodies persist in relatives to systemic lupus erythematosus patients during 12 years follow-up

Lupus ◽  
2016 ◽  
Vol 26 (7) ◽  
pp. 723-728 ◽  
Author(s):  
H Langkilde ◽  
A Voss ◽  
N Heegaard ◽  
H Laustrup
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Population Based ◽  
Systemic Lupus ◽  
Autoantibody Production ◽  
Increased Risk ◽  
Reported Health

Background Systemic lupus erythematosus (SLE) is an autoimmune disease with presence of autoantibodies and characteristic multi-organ involvement. Relatives of SLE patients have an increased risk of autoantibody production and autoimmune diseases. Methods In 2001, 226 first degree relatives (FDRs) of a population-based cohort of SLE patients were examined for the prevalence of autoantibodies and self-reported health complaints. In 2013, 143 FDRs were re-investigated and deceased’s medical records were examined. Results Participants and non-participants were comparable regarding baseline characteristics, while deceased FDRs were older than participants, but with comparable ANA status. ANA status at baseline correlated to ANA status at follow-up. At follow-up, two FDRs reported SLE and 15 FDRs other autoimmune diseases. No observation at baseline alone could predict self-reported health. During follow-up 33 died at median age 76 years. Three deceased FDRs were diagnosed with an autoimmune disease. Conclusion The study showed that FDRs of SLE patients have an increased prevalence of ANA compared to healthy controls. The prevalence increased during follow-up, and ANA positive FDRs at baseline were prone to be ANA positive at follow-up. ANA positive FDRs had more self-reported autoimmune diseases, including SLE and rheumatoid arthritis, than reported from other population-based investigations.

scholarly journals Role of interleukin 10 in the B lymphocyte hyperactivity and autoantibody production of human systemic lupus erythematosus.

1995 ◽  
Vol 181 (3) ◽  
pp. 839-844 ◽  
Author(s):  
L Llorente ◽  
W Zou ◽  
Y Levy ◽  
Y Richaud-Patin ◽  
J Wijdenes ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
B Lymphocytes ◽  
Lupus Erythematosus ◽  
Mononuclear Cells ◽  
Severe Combined Immunodeficiency ◽  
Interleukin 10 ◽  
Systemic Lupus ◽  
Human Igg ◽  
Autoantibody Production

Interleukin-10 (IL-10) is produced at a high level by B lymphocytes and monocytes of patients with systemic lupus erythematosus (SLE). In the present work, we analyzed whether this increased production of IL-10 contributed to the abnormal production of immunoglobulins (Ig) and of autoantibodies in SLE. The role of IL-10 was compared with that of IL-6, another cytokine suspected to play a role in these abnormalities. The spontaneous in vitro production of IgM, IgG, and IgA by peripheral blood mononuclear cells from SLE patients was weakly increased by recombinant IL (rIL)-6, but strongly by rIL-10. This production was not significantly affected by an anti-IL-6 mAb but was decreased by an anti-IL-10 mAb. We then tested the in vivo effect of these antibodies in severe combined immunodeficiency mice injected with PBMC from SLE patients. The anti-IL-6 mAb did not significantly affect the serum concentration of total human IgG and of anti-double-stranded DNA IgG in the mice. In contrast, the anti-IL-10 mAb strongly inhibited the production of autoantibodies, and, to a lesser extent, that of total human IgG. These results indicate that the Ig production by SLE B lymphocytes is largely IL-10 dependent, and that the increased production of IL-10 by SLE B lymphocytes and monocytes may represent a critical mechanism in the emergence of the autoimmune manifestations of the disease.

Multisystem diseases

2012 ◽  
Author(s):  
James Carton
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Systemic Sclerosis ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Women Of Childbearing Age ◽  
Childbearing Age ◽  
Systemic Lupus ◽  
Autoantibody Production

Systemic lupus erythematosus 346Systemic sclerosis 348Sarcoidosis 349Vasculitis 350• A multisystem autoimmune disease characterized by autoantibody production against a number of nuclear and cytoplasmic autoantigens.• Incidence of 4 per 100,000 people per year.• Most cases occur in women of childbearing age....

scholarly journals SAT0232 PERCEPTION OF THE DISEASE IN PATIENTS WITH EARLY SYSTEMIC LUPUS ERYTHEMATOSUS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1059.3-1059
Author(s):  
M. Garabajiu ◽  
L. Mazur-Nicorici ◽  
T. Rotaru ◽  
V. Salaru ◽  
S. B. Victoria ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Systemic Lupus Erythematosus ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Disease Duration ◽  
Activity Index ◽  
Damage Index ◽  
Organ Damage ◽  
Systemic Lupus

Background:Systemic lupus erythematosus is an autoimmune disease with a major impact on patient’s quality of life.Objectives:To evaluate patient’s attitude toward early disease and factors that influence it.Methods:Performed case-control study included SLE patients that fulfilled SLICC, 2012 classification criteria. The research included two groups of patients: early SLE – 1stgroup (disease duration ≤24 months) and non-early SLE – 2ndgroup control (disease duration >24 months). The pattern of the disease activity was assessed by patient global assessment (PGA), Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) and Systemic Lupus Activity Measure (SLAM), for SLE activity, SLICC/ACR Damage Index (DI) for disease irreversible changes and SF-8 for the Quality of Life (QoL).Results:A total of 101 SLE patients with 34 in the 1stgroup (early SLE) and 67 in the 2ndgroup (non-early SLE) was analyzed. The disease activity showed high disease activity in both groups by SLEDAI (7,02±4,16 and 6,26±4,43 points, p>0,05) and SLAM (7,47±4,40 and 7,31±4,10 points, p>0,05) such as (46,97±19,39 vs 47,98±22,41 points). The QoL was appreciated as low, by both components (mental and physical), in groups. The damage index was higher in the 2nd group (0,23±0,43 and 1,07±1,29, p<0,001), which can be explained by the development of irreversible changes with the increase of disease duration.The PGA in early SLE was influenced by subjective symptoms contained in SLAM index (r=0,48, p<0,05), such as fatigue and depression, and the level of the quality of life (r=0,65, p<0,001). Meantime, PGA in patients with longer disease duration (>2 years), was influenced by the presence of organ damage by SLICC/ACR DI (0,23, p<0,05) and objective findings of the disease activity contained in SLEDAI (r=0,33, p<0,005) and SLAM (0,44, p<0,001).Conclusion:The disease recognition in patients with early SLE was determined by subjective and psycho-emotional signs, while in patients with longer disease duration it was influenced by organ damage and complications.References:no referencesDisclosure of Interests:None declared

scholarly journals Leptin promotes systemic lupus erythematosus by increasing autoantibody production and inhibiting immune regulation

2016 ◽  
Vol 113 (38) ◽  
pp. 10637-10642 ◽  
Author(s):  
Elaine V. Lourenço ◽  
Aijing Liu ◽  
Giuseppe Matarese ◽  
Antonio La Cava
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
New Zealand ◽  
Renal Disease ◽  
Lupus Erythematosus ◽  
Cellular Level ◽  
Presentation Of Self ◽  
Systemic Lupus ◽  
Autoantibody Production

Leptin is an adipocytokine that plays a key role in the modulation of immune responses and the development and maintenance of inflammation. Circulating levels of leptin are elevated in systemic lupus erythematosus (SLE) patients, but it is not clear whether this association can reflect a direct influence of leptin on the propathogenic events that lead to SLE. To investigate this possibility, we compared the extent of susceptibility to SLE and lupus manifestations between leptin-deficient (ob/ob) and H2-matched leptin-sufficient (wild-type, WT) mice that had been treated with the lupus-inducing agent pristane. Leptin deficiency protected ob/ob mice from the development of autoantibodies and renal disease and increased the frequency of immunoregulatory T cells (Tregs) compared with leptin-sufficient WT mice. The role of leptin in the development of SLE was confirmed in the New Zealand Black (NZB) × New Zealand White (NZW)F1 (NZB/W) mouse model of spontaneous SLE, where elevated leptin levels correlated with disease manifestations and the administration of leptin accelerated development of autoantibodies and renal disease. Conversely, leptin antagonism delayed disease progression and increased survival of severely nephritic NZB/W mice. At the cellular level, leptin promoted effector T-cell responses and facilitated the presentation of self-antigens to T cells, whereas it inhibited the activity of regulatory CD4 T cells. The understanding of the role of leptin in modulating autoimmune responses in SLE can open possibilities of leptin-targeted therapeutic intervention in the disease.

scholarly journals MiR-410 Down-Regulates the Expression of Interleukin-10 by Targeting STAT3 in the Pathogenesis of Systemic Lupus Erythematosus

2016 ◽  
Vol 39 (1) ◽  
pp. 303-315 ◽  
Author(s):  
Dongmei Liu ◽  
Na Zhang ◽  
Xiaomei Zhang ◽  
Muting Qin ◽  
Youdan Dong ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Autoimmune Disorder ◽  
Interleukin 10 ◽  
Luciferase Assay ◽  
Mrna Levels ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Targeting Effect

Background/Aims: Systemic lupus erythematosus (SLE) is a heterogeneous chronic inflammatory autoimmune disorder, in the pathogenesis of which miRNAs play a versatile function. The purpose of this study was to investigate the effect of miRNA-410 on the pathogenesis of SLE in T cells of SLE patients. Methods: Real-time PCR was used to test the mRNA levels of miRNA-410 in SLE patients and healthy controls. ELISA analysis was performed to examine the production levels of IL-10. Luciferase Assay was used to confirm the targeting effect of miRNA-410 on 3'UTR of STAT3 mRNA. Results: We found that the expression level of miR-410 in T cells of SLE patients was decreased comparing to that in healthy controls, whereas overexpression of miR-410 significantly reduced the expression levels of IL-10. Furthermore, miR-410 suppresses the transcription activity of STAT3 by binding directly to the 3 'UTR of STAT3 mRNA. Moreover, silence of STAT3 down regulated IL-10 expression in CD3+ T cells. Conclusion: Our results demonstrate that miR-410 is the key regulatory factor in the pathogenesis of SLE by regulating the expression of IL-10 through targeting STAT3. These data suggest a novel function of miR-410 and bring new insight into understanding the complex mechanisms involved in SLE.

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