scholarly journals Salivary Cytokines as Potential Diagnostic Biomarkers for Systemic Lupus Erythematosus Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zeineb Zian ◽  
Assia Bouhoudan ◽  
Nadira Mourabit ◽  
Gholamreza Azizi ◽  
Mohcine Bennani Mechita
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Unknown Etiology ◽  
Systemic Lupus ◽  
Diagnostic Biomarkers ◽  
Additional Information ◽  
Autoimmune Inflammatory Disease ◽  
Cytokine Levels ◽  
Variable Clinical Presentation ◽  
Significant Attention

Systemic lupus erythematosus (SLE) is a complex autoimmune inflammatory disease characterized by an unknown etiology and a highly variable clinical presentation. This clinical heterogeneity might be explained by dysregulation of tolerance to self and apoptotic mechanisms, overproduction of autoantibodies, and abnormal cytokine levels. Cytokine imbalance levels have been associated with disease activity and severity in SLE patients. In the last years, salivary cytokines related to SLE have gained significant attention and researchers have begun to focus on the identification of cytokines in the saliva of SLE patients using it as a diagnostic fluid for the inflammatory process underlying SLE. This review highlights and summarizes recent studies revealing the cytokines that have been identified in the saliva of individuals with SLE. Data reported and discussed in this report may provide useful additional information to better understand the mechanisms associated with the disease.

scholarly journals Correlations of Expression Levels of a Panel of Genes (IRF5, STAT4, TNFSF4, MECP2, and TLR7) and Cytokine Levels (IL-2, IL-6, IL-10, IL-12, IFN-γ, and TNF-α) with Systemic Lupus Erythematosus Outcomes in Jordanian Patients

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Amal H. Uzrail ◽  
Areej M. Assaf ◽  
Shtaywy S. Abdalla
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Renal Damage ◽  
Organ Damage ◽  
Systemic Lupus ◽  
Expression Levels ◽  
Cardiovascular Damage ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Ifn Γ

Systemic lupus erythematosus (SLE) is characterized by systemic end-organ damage. We investigated the involvement of IRF5, TLR-7, MECP2, STAT4, and TNFSF4 genes and TNF-α, IFN-γ, IL-2, IL-12, IL-6, and IL-10 cytokines in SLE pathogenesis and in organ damage in Jordanian patients. Blood was collected from 51 patients and 50 controls. Expression levels of SLE genes in PBMCs and cytokine levels were determined using RT-PCR and ELISA, respectively. Expression levels of all genes and levels of TNF-α, IL-12, IL-6, and IL-10 were higher in SLE patients than those in controls (p<0.05), whereas IL-2 level was lower. High STAT4 (α), TNFSF4, and IL-10 levels correlated with cardiovascular damage, and high MECP2 (α) and TNF-α correlated with renal damage. Pulmonary and musculoskeletal damages correlated with high levels of TNFSF4. We concluded that STAT4 and TNFSF4 genes with TNF-α and IL-10 cytokines could be used as biomarkers to assess SLE activity and manage treatment.

scholarly journals Cytokine Networks in Systemic Lupus Erythematosus

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Hooi-Ming Lee ◽  
Hidehiko Sugino ◽  
Norihiro Nishimoto
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Cytokine Production ◽  
Organ Damage ◽  
Multiple Organ ◽  
Serum Cytokine ◽  
Systemic Lupus ◽  
Pathological Conditions ◽  
Cytokine Levels ◽  
Cytokine Networks

Systemic lupus erythematosus (SLE) is an autoimmune disease more prominent in women and characterized by multiple organ damage. Imbalance in cytokine production and cytokine levels correlates with SLE progression, making the understanding of SLE cytokine networks very important for SLE treatment strategy and drug development. In this article, we review cytokine networks that may be involved in the pathogenesis of SLE by briefly describing abnormal cytokine production and serum cytokine levels in SLE patients. We also focus on the pathological roles of cytokines and their interactions in immunoregulatory networks and suggest how their disturbances may implicate in pathological conditions in SLE. Finally, we further discuss the influence of estrogen on these cytokine networks.

scholarly journals FcγRIIA expression accelerates nephritis and increases platelet activation in systemic lupus erythematosus

Blood ◽  
2020 ◽  
Vol 136 (25) ◽  
pp. 2933-2945
Author(s):  
Imene Melki ◽  
Isabelle Allaeys ◽  
Nicolas Tessandier ◽  
Benoit Mailhot ◽  
Nathalie Cloutier ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Mouse Model ◽  
Platelet Activation ◽  
Lupus Erythematosus ◽  
Bone Marrow Cells ◽  
Human Platelets ◽  
Interferon Response ◽  
Type I ◽  
Systemic Lupus ◽  
Autoimmune Inflammatory Disease

Abstract Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by deposits of immune complexes (ICs) in organs and tissues. The expression of FcγRIIA by human platelets, which is their unique receptor for immunoglobulin G antibodies, positions them to ideally respond to circulating ICs. Whereas chronic platelet activation and thrombosis are well-recognized features of human SLE, the exact mechanisms underlying platelet activation in SLE remain unknown. Here, we evaluated the involvement of FcγRIIA in the course of SLE and platelet activation. In patients with SLE, levels of ICs are associated with platelet activation. Because FcγRIIA is absent in mice, and murine platelets do not respond to ICs in any existing mouse model of SLE, we introduced the FcγRIIA (FCGR2A) transgene into the NZB/NZWF1 mouse model of SLE. In mice, FcγRIIA expression by bone marrow cells severely aggravated lupus nephritis and accelerated death. Lupus onset initiated major changes to the platelet transcriptome, both in FcγRIIA-expressing and nonexpressing mice, but enrichment for type I interferon response gene changes was specifically observed in the FcγRIIA mice. Moreover, circulating platelets were degranulated and were found to interact with neutrophils in FcγRIIA-expressing lupus mice. FcγRIIA expression in lupus mice also led to thrombosis in lungs and kidneys. The model recapitulates hallmarks of human SLE and can be used to identify contributions of different cellular lineages in the manifestations of SLE. The study further reveals a role for FcγRIIA in nephritis and in platelet activation in SLE.

scholarly journals IKZF1 polymorphisms are associated with susceptibility, cytokine levels, and clinical features in systemic lupus erythematosus

Medicine ◽  
2020 ◽  
Vol 99 (41) ◽  
pp. e22607
Author(s):  
Lin Chen ◽  
Qian Niu ◽  
Zhuochun Huang ◽  
Bin Yang ◽  
Yongkang Wu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Clinical Features ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Cytokine Levels

Chloroquine treatment influences proinflammatory cytokine levels in systemic lupus erythematosus patients

Lupus ◽  
2006 ◽  
Vol 15 (5) ◽  
pp. 268-275 ◽  
Author(s):  
A Wozniacka ◽  
A Lesiak ◽  
J Narbutt ◽  
D P McCauliffe ◽  
A Sysa-Jedrzejowska
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Proinflammatory Cytokine ◽  
Systemic Lupus ◽  
Chloroquine Treatment ◽  
Cytokine Levels

scholarly journals Immunopathological Roles of Cytokines, Chemokines, Signaling Molecules, and Pattern-Recognition Receptors in Systemic Lupus Erythematosus

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Shui-Lian Yu ◽  
Woon-Pang Kuan ◽  
Chun-Kwok Wong ◽  
Edmund K. Li ◽  
Lai-Shan Tam
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Pattern Recognition ◽  
Lupus Erythematosus ◽  
Pattern Recognition Receptors ◽  
Signaling Molecules ◽  
Unknown Etiology ◽  
Systemic Lupus ◽  
Pathological Conditions ◽  
Complex Process ◽  
Immune Pathways

Systemic lupus erythematosus (SLE) is an autoimmune disease with unknown etiology affecting more than one million individuals each year. It is characterized by B- and T-cell hyperactivity and by defects in the clearance of apoptotic cells and immune complexes. Understanding the complex process involved and the interaction between various cytokines, chemokines, signaling molecules, and pattern-recognition receptors (PRRs) in the immune pathways will provide valuable information on the development of novel therapeutic targets for treating SLE. In this paper, we review the immunopathological roles of novel cytokines, chemokines, signaling molecules, PRRs, and their interactions in immunoregulatory networks and suggest how their disturbances may implicate pathological conditions in SLE.

scholarly journals Problems of early diagnosis of systemic lupus erythematosus during the COVID-19 pandemic

2021 ◽  
Vol 59 (2) ◽  
pp. 119-128
Author(s):  
E. L. Nasonov ◽  
T. V. Popkova ◽  
T. A. Panafidina
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Early Diagnosis ◽  
Lupus Erythematosus ◽  
Clinical Symptoms ◽  
Clinical Signs ◽  
Immunological Tolerance ◽  
Unknown Etiology ◽  
Systemic Lupus ◽  
Stress Effects ◽  
Autoimmune Rheumatic Disease

Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease of unknown etiology, characterized by overproduction of organ-nonspecific autoantibodies to various components of the cell nucleus and cytoplasm and the development of immune-inflammatory damage to internal organs. The debut of SLE is preceded by an asymptomatic period, characterized by impaired immunological tolerance to its own autoantigens, determined by the multifaceted interaction of external, genetic and epigenetic factors, hormonal disorders, microbiome pathology, stress effects, etc. Development of a certain spectrum of clinical symptoms characteristic of SLE along with the detection of a reflects the progression of the immunopathological process in SLE, however, there is no generally accepted term that defines the patient’s condition, which has individual serological and clinical signs characteristic of this disease. In rheumatology, the concept of «incomplete» SLE is currently most often used. The problems of early diagnosis of SLE, clinical and laboratory predictors of the transformation of “incomplete” SLE into “reliable” SLE, difficulties in diagnosing SLE during the COVID-19 pandemic are considered. Particular attention is paid to the comparative characteristics of the immunopathological mechanisms of SLE and COVID-19.

scholarly journals Systemic Lupus Erythematosus with Unusual Manifestations

2020 ◽  
Vol 17 (6) ◽  
pp. 43-53
Author(s):  
Lorena Manea ◽  
Cătălin Mihai Popescu ◽  
Raluca Popescu ◽  
Daniela Adriana Ion ◽  
Andreea Alexandra Nicola ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Nasal Septum ◽  
Disease Patient ◽  
Clinical Manifestations ◽  
Unknown Etiology ◽  
Septal Perforation ◽  
Systemic Lupus ◽  
Extended Defect ◽  
Nasal Septal Perforation

Abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown etiology, presenting with variable clinical picture. Having a high heterogeneity and lacking pathognomonic features, very often the diagnosis poses a great challenge for the clinician. Several unusual clinical manifestations such as nasal septal perforation and digital gangrene can occur in LES patients. Case report. We report the case of a 42-year-old woman, known with SLE, hospitalized in our department for a clinical presentation consisting of a recent major epistaxis, physical asthenia and acral necrosis of the upper limbs. Physical examination revealed an afebrile patient, with a cushingoid facies, facial telangiectasias, and necrotic scars localized on the distal phalanges, bilaterally. A diagnostic nasal endoscopy showed a large septal perforation with the absence of the cartilaginous nasal septum. CT highlighted an extended defect at the level of the cartilaginous part of the nasal septum. Conclusion. Nasal septal perforation remains an underdiagnosed invalidating complication of lupus and treated and discovered early could have an important impact on the general health of an already burdened by disease patient.

scholarly journals Case of a Сombination of Lupus Erythematosus, Antiphospholipid Syndrome and Myocardial Infarction

Kardiologiia ◽  
2019 ◽  
Vol 59 (12) ◽  
pp. 92-96
Author(s):  
N. A. Kosheleva ◽  
N. M. Nikitina ◽  
E. U. Andreeva
Keyword(s):  
Myocardial Infarction ◽  
Systemic Lupus Erythematosus ◽  
Antiphospholipid Syndrome ◽  
Lupus Erythematosus ◽  
Clinical Manifestations ◽  
The Body ◽  
Systemic Autoimmune Disease ◽  
Unknown Etiology ◽  
Systemic Lupus ◽  
Wide Range

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease of unknown etiology characterized by a wide range of clinical manifestations with damage to various organs and systems of the body. There are bad prognostic factors for SLE: damage to the heart, kidney, central nervous system, the development of hematological crises and secondary antiphospholipid syndrome. A number of authors consider systemic lupus erythematosus a “new” risk factor for atherosclerosis. The overall risk of myocardial infarction (MI) in patients with SLE is 10 times higher than in the general population. The article presents clinical case report of the development of myocardial infarction in a woman with SLE, receiving therapy for secondary antiphospholipid syndrome.

scholarly journals Cellular Mechanism of Immunology in Systemic Lupus Erythematosus

2021 ◽  
Author(s):  
Tianhong Xie ◽  
Ping Li
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Plasma Cells ◽  
Suppressor Cells ◽  
T Helper 1 ◽  
Systemic Lupus ◽  
Autoantibody Production ◽  
Autoreactive T Cells ◽  
Cytokine Levels

To date, the mechanism of systemic lupus erythematosus (SLE) has not been thoroughly deciphered. Recent research demonstrated that CD138+ T cells accumulate in an SLE murine model, indicating that they are autoreactive T cells that significantly promote autoantibody production. Double negative (DN) T cells have been demonstrated to participate in the progression of SLE, but their detailed mechanism and the role in SLE remain unclear. Importantly, the expression of CD138 in CD3+ T cells plays a key role in the progression of lupus; it causes the accumulation of autoreactive T cells, including DN T cells, by significantly preventing their apoptosis. T helper 1 cells and interferon gamma both prevail in SLE; they may play essential roles in building the inflammatory condition of SLE. Defects occur in regulatory B (Breg) cells during their expansion in SLE, resulting in more differentiation of activated B cells into plasma cells; this subsequently increases antibody production. Myeloid-derived suppressor cells (MDSCs) enhance the expansion of Breg cells. However, the sustained increase of cytokine levels in SLE promotes the differentiation of more MDSCs into macrophage and dendritic cells, resulting in the defective expansion of MDSCs. The defective expansion of Breg cells and MDSCs breaks the immune-tolerance milieu in SLE, resulting in increased autoantibody secretion from those abnormal plasma cells. This review discusses recent advances regarding the detailed roles and mechanisms of these immunocytes in SLE.

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