Systemic Lupus Erithematosus Research Articles

Automated analysis of choroidal thickness in patients with systemic lupus erithematosus treated with hydroxychloroquine.

To evaluate the influence of hydroxychloroquine (HCQ) in choroidal thickness (CT) in patients with systemic lupus erythematous (SLE), considering the possible impact of disease activity on the choroid. Cross-sectional study comparing three groups: two groups of SLE patients treated with HCQ without HCQ-retinopathy (32 eyes/32 patients with < 5years of HCQ (group 1) and 44 eyes/44 patients with > 5years of HCQ (group 2)), and an age-matched healthy control group of 46 eyes/46 patients (group 3). A complete ophthalmic examination was performed, including swept-source optical coherence tomography (SS-OCT) Triton (Topcon). Data were correlated to systemic disease activity parameters. CT was thicker in group 1 compared to group 3 in central, nasal, and superior sectors, and to group 2 in inner superior and outer inferior sectors (p < 0.05). In the correlation analysis, disease activity and CT were inversely correlated in most sectors (p < 0.05). In the regression analysis, HCQ was related to thinner CT in temporal and inferior sectors and disease activity with variations in nasal sectors (p < 0.05). In SLE patients, HCQ is correlated to decreased CT, especially in the inferior and temporal areas. The choroid shows different responses to SLE activity and HCQ, and some sectors may be more sensitive than others.

Neuropsichiatric Manifestations of Systemic Lupus Erythematosus: Diagnosis and Treatment Approach

Abstract Neuropsychiatric involvement in systemic lupus erythematosus includes heterogeneous manifestations involving both the central and peripheral nervous system. A major issue in clinical evaluation is the attribution of neuropsychiatric symptoms to systemic lupus erithematosus. Antiphospholipid antibodies, immune complex, microangiopathy, early and accelerated arteriosclerosis are factors that have the main role in pathogenesis of neuropsychiatric manifestations of systemic lupus erithematosus. There are no neurological symptoms specific to systemic lupus erithematosus, but they can also occur very commonly in the general population. Lesions of nervous system can be focal or diffuse and may be due to systemic lupus erithematosus itself (primary lesions), but it also may be caused by other diseases or disbalances. Therapy of the neuropsychiatric manifestations depends on the nature of the pathological process (dominant inflammation or thrombosis). If it is result of an inflammatory neurotoxic process and in the presence of an increased activity of systemic lupus erithematosus, therapy includes glycocorticoids independently or in combination with immunosuppressives. Focal neuropsychiatric syndrome with antiphospholipid antibodies positivity should be treated with anticoagulant and/or antiplatelet therapy. In addition, control of classical cardiovascular risk factors, stop smoking, and treatment with hydroxychloroquine is recommended.

LESI NERVUS OKULOMOTOR INVOLVED PUPIL ET CAUSA ANEURISMA PADA PASIEN DENGAN STROKE SUBARACHNOID HEMORRHAGIC DAN SYSTEMIC LUPUS ERITHEMATOSUS

Introduction: Oculomotor nerve palsy is an pathological condition caused by microvascular injury, head injury, compression due to neoplasm or aneurysm, and also oculomotor nerve palsy can be caused by autoimmune prosses. Peripheral neuropathy is one of the clinical manifestations in patient with SLE, Oculomotor nerve palsy is one type of cranial neuropathy seen with SLE patient. Patient with SLE have a higher risk of serebrovascular event than general population. Case Illustration: Female 34 years old complained drop of the eyelid on the left eye and double vision when see with both eyes since 1 mounth before examination. Patient with history of headace and diagnosed with SLE since 2006 with regular treatment. From the examination, pupil anisocor, on the right eye pupil was 3 mm in diameter with positif direct and indirect reflex. On the left eye pupil was 6 mm with negative direct and indirect reflex. Extraocular movement on the left eye was limited except abduction movement. CT-Scan examination shows bilateral subarachnoid hemorrhage and from CT-Angiography shows dilatation of the left siphon carotid artery. Patient was diagnosed with oculomotor nerve palsy involving pupil caused by aneurysm with SAH and SLE. Discussion: Oculomotor nerve palsy mostly caused by aneurysm compression in posterior communicating artery (PCoA) and internal carotid artery (ICA). Cerebrovascular imaging, MRA and CTAngiography, can showing the aneurysm and its location. Risk of cerebrovascular event increased in patient with SLE than general population. Management patient with oculomotor nerve palsy with SLE nowadays is with pulse dose corticosteroid. Conclusion: SLE with oculomotor nerve palsy will increase risk of cerebrovascular event. Key Words : Oulomotor Nerve Palsy, Subarachnoid Hemorrhage, Systemic Lupus Erithematosus

Short Chain Fatty Acid (SCFA) Gut Biota and Interleukin 6 (IL-6) Related to the Severity of Systemic Lupus Erithematosus (SLE) at Dr. Mohammad Hoesin General Hospital Palembang

Background. SLE is an autoimmune disease characterized by the presence of autoantibodies in the nucleus, deposition of immune complexes, and can attack various body tissues. Gut biota in this case short-chain fatty acids (SCFA) play a role in the inflammatory process in the SLE, while the levels of IL- 6 can also be associated with a response to inflammation which will be seen in the degree of SLE activity. This study aims to determine the correlation of SCFA Gut biota and IL - 6 with SLE degree activity.&#x0D; Methods. This study is a cross-sectional study with a correlation test design, conducted from November 2021-January 2022 at RSMH Palembang with the research subjects being all SLE patients seeking treatment at the Allergy-Immunology Division of RSMH Palembang with categories of mild and moderate-severe SLE activity degree. Examination of SCFA Gut biota using stool samples and serum IL-6 levels were associated with SLE activity degree. Statistical analysis of the correlation test with Spearman for numerical data not normally distributed, and continued with linear regression test to assess the multivariate analysis in this study.&#x0D; Results. The sample consisted of 32 patients, every 16 patients with mild and moderate-severe SLE activity degrees. The correlation between SCFA Gut biota with SLE activity degree was found to have a correlation coefficient of r=-0.777 with p=0.000. Correlation between IL-6 with SLE activity degree obtained a correlation coefficient of r=0.910 with p=0.000, while the correlation test between IL-6 and SCFA Gut biota obtained r=-0.633 with a value of p=0.000. Multivariate analysis found that 70.5% of SCFA Gut biota and IL-6 affected SLE activity degree.&#x0D; Conclusion. SCFA Gut biota and IL-6 had a significant correlation in statistical tests with the SLE activity degree.

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

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: &amp;lt;0.005 Mu/L, FT4: &amp;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.

Optical Coherence Tomography Angiography findings in patients with Systemic Lupus Erithematosus

Optical Coherence Tomography Angiography findings in patients with Systemic Lupus Erithematosus

Polineuropatía desmielinizante inflamatoria crónica como forma de presentación de lupus eritematoso sistémico

We described a 35 years old female, who developed Chronic inflammatory demyelinating polyneuropathy as neurologic commitment during the early diagnosis in Systemic Lupus Erithematosus (SLE). While the neuropsychiatric commitment has a variable prevalence in SLE, the association that we describe is infrequent and it has important concerns during its treatment.

Application of Group Positive Psychotherapy(GPPT) to Increasing Well Being in Women with Systemic Lupus Erithematosus (SLE)

Systemic Lupus Erithematosus (SLE) is a chronic autoimmune disorder that can affect almost all organs of the body. SLE is part of the chronic illness disabilities (CID) with the highest number of women reproductive age. Not only the physical affects but also quite disturbing psychological conditions, for example increased negative emotions, depression, and suicidal ideation. Chronic illness disabilities (CID) patients often have low perception of life satisfaction and will affect a person's level of well-being. To achieve the condition of well-being, psychological interventions that can help increase the level of well-being in women with Systemic Lupus Erithematosus are needed. The intervention was a group positive psychotherapy by pleasent life, engaged life and meaning full life. The purpose of this research can help individuals to improve well-being especially for women with Systemic Lupus Erithematosus. In this research, Group Positive Psychotherapy was conducted in 14 sessions with pre-test and post-test. This research is a case study with a single case experimental design. The method used is mixed method with concurrent embedded strategy, using qualitative data as primary and quantitative data as secondary data. The measuring instrument used is The PERMA Profiler with a reliability value of 0,761 compared to Cronbach’s Alpha which is r 0,6 reliable. The participants in this study were 3 people. Based on qualitative results indicate that there is an increase in the level of wellbeing in the 3 participants and increasing score in 5 aspects of well-being after intervention.

Testing antinuclear antibodies in relatives of patients with systemic lupus erithematosus

Testing antinuclear antibodies in relatives of patients with systemic lupus erithematosus

Neuropsichyatric Manifestations of Systemic Lupus Erythematosus: Diagnosis and Treatment Approach

Abstract Neuropsychiatric involvement in systemic lupus erythematosus includes heterogeneous manifestations involving both the central and peripheral nervous system. A major issue in clinical evaluation is the attribution of neuropsychiatric symptoms to systemic lupus erithematosus. Antiphospholipid antibodies, immune complex, microangiopathy, early and accelerated arteriosclerosis are factors that have the main role in pathogenesis of neuropsychiatric manifestations of systemic lupus erithematosus. Th ere are no neurological symptoms specific to systemic lupus erithematosus, but they can also occur very commonly in the general population. Lesions of nervous system can be focal or diff use and may be due to systemic lupus erithematosus itself (primary lesions), but it also may be caused by other diseases or disbalances. Therapy of the neuropsychiatric manifestations depends on the nature of the pathological process (dominant inflammation or thrombosis). If it is result of an inflammatory neurotoxic process and in the presence of an increased activity of systemic lupus erithematosus, therapy includes glycocorticoids independently or in combination with immunosuppressives. Focal neuropsychiatric syndrome with antiphospholipid antibodies positivity should be treated with anticoagulant and/ or antiplatelet therapy. In addition, control of classical cardiovascular risk factors, stop smoking, and treatment with hydroxychloroquine is recommended.

Pro-inflammatory Ca++-activated K+ channels are inhibited by hydroxychloroquine

Antimalarials have demonstrated beneficial effects in Systemic Lupus Erithematosus and Rheumatoid Arthritis. However, the mechanisms and the molecular players targeted by these drugs remain obscure. Although hydroxychloroquine (HCQ) is a known ion channel inhibitor, this property has not been linked to its anti-inflammatory effects. We aimed to study whether HCQ inhibits pro-inflammatory ion channels. Electrophysiology experiments demonstrated that HCQ inhibited Ca++-activated K+ conductance in THP-1 macrophages in a dose-dependent manner. In macrophages, ATP-induced K+ efflux plays a key role in activating the NLRP3 inflammasome. ATP-induced IL-1beta secretion was controlled by the KCa1.1 inhibitor iberiotoxin. NS1619 and NS309 (KCa1.1 and KCa3.1 activators respectively) induced the secretion of IL-1beta. This effect was inhibited by HCQ and also by iberiotoxin and clotrimazol (KCa3.1 inhibitor), arguing against off-target effect. In vitro, HCQ inhibited IL-1beta and caspase 1 activation induced by ATP in a dose-dependent manner. HCQ impaired K+ efflux induced by ATP. In vivo, HCQ inhibited caspase 1-dependent ATP-induced neutrophil recruitment. Our results show that HCQ inhibits Ca++-activated K+ channels. This effect may lead to impaired inflammasome activation. These results are the basis for i) a novel anti-inflammatory mechanism for HCQ and ii) a new strategy to target pro-rheumatic Ca++-activated K+ channels.

A polymorphism upstream MIR1279 gene is associated with pericarditis development in Systemic Lupus Erythematosus and contributes to definition of a genetic risk profile for this complication.

Recently, a study has shown that a polymorphism in the region of MIR1279 modulates the expression of the TRAF3IP2 gene. Since polymorphisms in the TRAF3IP2 gene have been described in association with systemic lupus erithematosus (SLE) susceptibility and with the development of pericarditis, our aim is to verify if the MIR1279 gene variability could also be involved. The rs1463335 SNP, located upstream MIR1279 gene, was analyzed by allelic discrimination assay in 315 Italian SLE patients and 201 healthy controls. Moreover, the MIR1279 gene was full sequenced in 50 patients. A case/control association study and a genotype/phenotype correlation analysis were performed. We also constructed a pericarditis genetic risk profile for patients with SLE. The full sequencing of the MIR1279 gene in patients with SLE did not reveal any novel or known variation. The variant allele of the rs1463335 SNP was significantly associated with susceptibility to pericarditis ( P = 0.017 and OR = 1.67). A risk profile model for pericarditis considering the risk alleles of MIR1279 and three other genes (STAT4, PTPN2 and TRAF3IP2) showed that patients with 4 or 5 risk alleles have a higher risk of developing pericarditis ( OR = 4.09 with P = 0.001 and OR = 6.04 with P = 0.04 respectively). In conclusion, we describe for the first time the contribution of a MIR1279 SNP in pericarditis development in patients with SLE and a genetic risk profile model that could be useful to identify patients more susceptible to developing pericarditis in SLE. This approach could help to improve the prediction and the management of this complication.

Outcome of childhood-onset full-house nephropathy

Patients with full-house nephropathy (FHN) present renal lesions that are indistinguishable from those of lupus nephritis (LN) but lack the systemic features necessary to meet diagnostic criteria for systemic lupus erithematosus (SLE). Some have been reported to develop a delayed SLE with time. The clinical outcome of children having FHN without SLE has never been reported. Children with biopsy-proven FHN were selected after excluding SLE cases by the absence of America College of Rheumatology criteria. The proportion of patients with complete (proteinuria <0.5 g/day) or partial remission (proteinuria ≤50% from baseline), relapse (estimated glomerular filtration rate <25% and/or proteinuria ≥50% from baseline) and progression to Stage III chronic kidney disease (CKD) was described according to age and gender groups with the Kaplan-Meier curve and compared with the Log-rank test. Entity of treatment was summarized by a score at induction (0-6 months) and maintenance (6-18 months). Cox-regression model was performed to test predictors of remission, relapse and progression to CKD. Among 42 patients (28 pre-pubertal) who met the inclusion criteria, 39 (92.9%) achieved partial and 32 (76.2%) complete remission of nephropathy over 2.78 and 7.51 months of follow-up. At 10 years, the probability of progressing to CKD was 4.8%. Of those achieving remission, 18% had a renal flare mainly within 4 years after remission. Pre-pubertal males achieved complete remission more frequently than other patients but often relapsed; pre-pubertal females were treated more aggressively. Cox-regression analysis did not find independent predictors of remission or relapse. The outcome of the patients with FHN we investigated was encouraging. Recurrences are limited to the first 4 years following diagnosis, allowing progressive withdrawal of immunosuppression in patients achieving remission. Evaluation of risk factors for adverse outcome is necessary especially in pre-pubertal children.

P05.06: First trimester FMF algorithm screening for pre‐eclampsia applied in a Brazilian population: is the performance good enough?

To assess the performance of the first trimester FMF algorithm for PE in a Brazilian population. Patients attending for first trimester anomaly scan were recruited. Maternal characteristics (MC) were recorded and the following variables were obtained: maternal age, ethnicity, parity, PE in previous pregnancy, smoking status, medical conditions such as hypertension, diabetes, Systemic Lupus Erithematosus and Antiphospholipid Syndrome, weight, height and BMI. Arterial pressure was measured by manual sphygmo. Both uterine artery were insonated abdominally and mean PI calculated. Blood was collected and centrifuged, stored at −800 C for subsequent analysis. PAPP-A and PlGF were tested using Delfia Xpress machine (Perkin Elmer). MC, biochemical markers and Doppler measurements were inserted on FMF software in order to obtain an individual risk for PE. Perinatal outcome were obtained through medical chart review. PE diagnosis relied on traditional criteria (proteinuria > 300 mg/24 h and hypertension ≥ 140 × 90 mm Hg). Study involved 701 women. 84 were excluded mainly because of: no follow up (46), miscarriage or fetal death prior to 24 weeks (14), hypertensive disorder not classified (14). Of the remaining 617, 34 (5.5%) went on to develop PE, 7 (delivery before 34 weeks), 11 (between 34–37 weeks), 16 (after 37 weeks) while 12 (1.9%) had gestational hypertension. Control group was composed by 571 patients. Detection rate (DR) for early PE (before 34 weeks) was 28.6% and 100% for a false positive rate (FPR) of 5% and 10% respectively. DR for preterm PE (before 37 weeks) was 27.8% and 66.7%, for a FPR of 5% and 10% respectively. DR for PE at any gestational age was 23.5% and 52.9% for a FPR of 5% and 10% respectively. FMF algorithm performed very good in this Brazilian population. Performance should be viewed with caution though, since there was a small number of PE cases. Further and larger studies are warranted before implementing the test on a large scale.

Macroamylasemia; a Dilemma in Morbidity.

To the Editor, A one-year-old boy was referred for randomly detected hyperamylasemia. Physical examination was completely normal, including growth parameters. Medical history and family history were unremarkable. In laboratory, the repeated serum amylases were found elevated with the values of 280 IU/mL, 290 IU/mL and 310 IU/mL (N: 10–90 IU/mL) together with a lower urine amylase level of 10.5 IU/mL (N: 25–500 IU/mL). The complete blood count, acute-phase reactants, liver–renal–thyroid functional tests, serum lipase and immunoglobulins were normal. Antibodies against endomysium, gliadin, thyroglobulin, thyroid peroxidase, nucleus and dsDNA were negative. Abdominal ultrasonography and computed tomography (CT) scans were normal. According to these normal findings, hyperamylasemia due to macroamylasemia (MA) was found in patient. An informed consent form to research was obtained from parents. At analysis for MA, a precipitated activity was 87% at polyethylene glycol (PEG) precipitation (MA>60%) (1). Macroenzymes are complexes of serum enzymes commonly with immunoglobulins or lipoproteins that have a higher moleculer weight. Macroamylase is the most common macroenzyme, in which pancreatic or salivary amylase binds to plasma proteins and cannot be excreted by renal glomeruli. Macroamylasemia may be seen either isolated or associated with a variety of disorders, such as IgA deficiency, celiac disease, lymphoma, carcinoma, systemic lupus erithematosus, rheumatoid arthritis, liver disease and various autoimmune diseases (2–4). The pathogenesis of macroenzyme formation in these diseases is estimated by ‘antigen-driven’ theory: a self-antigen is altered or released from a sequestered site in the body and cross-reacts with an antibody initially formed against a foreign antigen. A second theory is the ‘dysregulation of immune tolerance, which is likely to occur in autoimmune disorders (4). The cross-reactivity to either gluten-related or other antigens resulting in autoantibody formation against pancreatic serum amylase at intestinal level is considered (5). The elevated serum amylase, low 24-hour urine amylase and reduced ratio of amylase clearance / creatinine clearance are important at diagnosis. It has been shown that PEG precipitation is also a precise method in the detection of MA by purifying protein from macromolecules more easily and quickly (1). Due to the problem at urine collection, PEG precipitation was preferred in this case. It was considered as isolated MA due to the absence of associated disorders. In conclusion, MA is generally a benign condition, but associated potential disorders should be considered at follow-up. The case highlights the dilemma of additional invasive explorations and unnecessary treatments by differentiating MA from other situations associated to hyperamylasemia.

Pentraxin 3 in Systemic Lupus Erithematosus: Questions to be Resolved

Systemic lupus erythematosus (SLE) is a autoimmune disorder with unpredictable course that involves polyclonal autoimmunity against multiple autoantigens and presents a broad spectrum of clinical manifestations (fever, skin rashes, arthralgia, inflammation of kidney, lungs, or brain). The pathogenesis of SLE is based on a combinations of genetic variants and environmental factor that promote loss-of-tolerance or tissue inflammation. In fact there is growing evidence to suggest that inflammation and related molecules plays a key role in the pathogenesis of SLE. The pentraxin superfamily (PTXs), divided into long and short PTXs, can induce by and a variety of inflammation-associated stimuli. Alongside the classical short pentraxins C-reactive protein (CRP) and serum amyloid P component (SAP), pentraxin 3 ( PTX3) is a prototypic of long pentraxin family, a multifunctional protein characterized by a cyclic multimeric structure and a conserved domain

The putative role of proteolytic pathways in the pathogenesis of Type 1 diabetes mellitus: The ‘autophagy’ hypothesis

Autoimmune diseases are a heterogeneous group of disorders affecting different organs and tissues. New tools, such as genome-wide association studies, have provided evidence for new susceptibility loci and candidate genes in the disease process including common susceptibility genes involved in the immunological synapse and T cell activation. Close linkages have been found in a number of diseases, including ankylosing spondylitis, multiple sclerosis, Crohn’s disease and insulin-dependent diabetes mellitus (Type 1 diabetes mellitus). Evidence for some association with Type 1 diabetes was previously found in the region containing 5q15/ERAP1 (endoplasmic reticulum aminopeptidase 1) (rs30187, ARTS1).Recent data suggest that in eukaryotic cells in addition to the ubiquitin/proteasome system another proteolytic pathway may have a significant role in the autoimmunity process, i.e. the autophagic pathway which constitutes the principal regulated catabolic process mediated by lysosomes. Autophagy could play a role in MHC class I and class II self-antigen presentation at the basis of the autoimmunity process. Furthermore cross-talk among different proteolytic pathways was recently highlighted i.e. components processed in the ubiquitin/proteasome system possibly engaged in autophagic pathways.T1D is an autoimmune disease characterised by the destruction of pancreatic beta cells by autoreactive T cells. Immunological abnormalities can precede months to years the initial symptoms and clinical diagnosis. Our hypothesis suggests that in the autoimmune process autophagy can intervene at different levels, during the thymic selection process of T lymphocytes causing escape of autoreactive T cells, at the initiation stage of the disease, in the preclinical period or subsequently to the disease onset having a role at the level of perpetuation of the autoimmunity process.Supporting evidence derives from the already reported discovery of polymorphisms in autophagy-related genes in patients affected by several autoimmune conditions such as Systemic Lupus Erithematosus. In addition deregulated autophagy was detected in T cells from lupus-prone mice and also found in T cells from patients. Autophagy was found activated in osteoclasts from RA patients as demonstrated by the increased expression of Atg7 and Beclin-1.Our hypothesis to be unraveled could have, if correct, relevant implications for the management of autoimmune conditions such as Type 1 diabetes. In principle, novel therapeutic approaches could be established by targeting deregulated autophagy offering novel opportunities to personalized medicine in patients affected by the disease.

The role of invariant NKT cells in organ-specific autoimmunity.

Invariant NKT cells (iNKT) represent a unique subset of innate lymphocytes that play a dual role and exert a pro-inflammatory function and also a tolerogenic function that is crucial to maintain T cell tolerance and prevent autoimmune diseases like Multiple Sclerosis, Type 1 Diabetes, Rheumatoid Arhritis and Systemic Lupus Erithematosus (SLE). Although a large body of evidence indicated that iNKT cells are instrumental to counter-regulate T cell-mediated autoimmune diseases, there is still some controversy on whether iNKT cells can actively induce immunosuppression and directly dampen T cell autoimmunity. Moreover, the recent discovery of a distinct iNKT cell subset, the iNKT17 cells, with strong adjuvant and pro-inflammatory function raised the question on what is the role of NKT17 cells in the pathogenesis of autoimmune diseases. Here, we review the current knowledge on iNKT cell biology and focus our attention on the possible mechanism of action and final effect of the different iNKT cell subsets in the pathogenesis of T cell-mediated autoimmune diseases.

Determinants of vascular damage in Systemic Lupus Erithematosus

Determinants of vascular damage in Systemic Lupus Erithematosus

PMS52 - Assessment of the Economic Impact of Belimumab for the Treatment of Systemic Lupus Erithematosus in the Italian Setting: A Cost-Effectiveness Analysis

PMS52 - Assessment of the Economic Impact of Belimumab for the Treatment of Systemic Lupus Erithematosus in the Italian Setting: A Cost-Effectiveness Analysis