High BAFF expression associated with active disease in systemic lupus erythematosus and relationship with rs9514828C&gt;T polymorphism in TNFSF13B gene

Marín‐Rosales, Miguel; Cruz, Álvaro; Salazar-Camarena, Diana Celeste; Santillán-López, Enrique; Espinoza-García, Noemí; Muñoz‐Valle, José Francisco; Ramírez‐Dueñas, Maria Guadalupe; Edith, Oregon-Romero; Orozco‐Barocio, Gerardo; Palafox‐Sánchez, Claudia Azucena

doi:10.1007/s10238-019-00549-8

Cited by 36 publications

(26 citation statements)

References 52 publications

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“…These mechanisms contribute to the increased dependency on BAFF/APRIL-mediated survival mechanisms to promote apoptosis in autoreactive B cells in SLE. On the other hand, sBAFF and sAPRIL levels were increased in SLE patients in concordance with previous studies [6][7][8][9][10][11] , and both correlated with disease activity evaluated by the SLEDAI-2K. It is important to note that sAPRIL displayed a stronger correlation than did sBAFF.…”

Section: Discussionsupporting

confidence: 90%

“…It is important to note that sAPRIL displayed a stronger correlation than did sBAFF. Previous reports have shown the associations of sBAFF and sAPRIL levels with disease activity and musculoskeletal, haematological and renal manifestations in SLE 6,[8][9][10]33 . Nevertheless, the controversy regarding the utility of both cytokines as disease activity biomarkers remains, since other authors have reported a lack of associations 11,[41][42][43][44] .…”

Section: Discussionmentioning

confidence: 90%

“…At the time of sampling in all SLE patients, the rheumatologist determined scores for the Mexican version of the Systemic Lupus Erythematosus Disease Activity Index (Mex-SLEDAI) 51 and Systemic Lupus International Collaborating Clinics index (SLICC) 52 . A Mex-SLEDAI score >2 was considered a marker of active disease 53 . Patients who showed only mild manifestations, such as leukopenia (1 pt), lymphopenia (1 pt), or fever and fatigue (1 pt), and did not require adjusted treatment were classified as having LDA.…”

Section: Methods Patients and Healthy Controlsmentioning

confidence: 99%

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Analysis of the receptor BCMA as a biomarker in systemic lupus erythematosus patients

Salazar-Camarena

Palafox‐Sánchez

Cruz

et al. 2020

Sci Rep

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B cell activating factor (BAff) and a proliferation-inducing ligand (ApRiL) play central roles in B cell development and maturation. Soluble forms of their receptors can be generated by proteolytic cleavage; however, their physiological and clinical roles are unknown. this study aimed to assess the relationships between the receptor soluble B cell maturation antigen (sBcMA) and clinical variables in systemic lupus erythematosus (SLe) patients. Serum cytokine concentrations were measured by ELISA for 129 SLE patients and 34 healthy controls (HCs), and the expression of the receptor BCMA was evaluated on B and plasma cells from 40 subjects. SLE patients showed aberrant expression of the receptor BcMA on B and plasma cells. Soluble levels of the receptor sBcMA and its ligands sApRiL and sBAFF were increased in SLE patients compared with HCs. Additionally, sBCMA (r s = 0.6177) and sAPRIL (r s = 0.4952) correlated strongly with disease activity. Active SLE patients who achieved low disease activity showed decreased sBCMA (53.30 vs 35.30 ng/mL; p < 0.05) and sBAFF (4.48 vs 2.27 ng/mL; p < 0.05) serum levels after treatment, while sAPRIL expression remained unchanged. At a cutoff value of 22.40 ng/mL, sAPRIL showed high sensitivity (96.12%) and specificity (94.12%) for discrimination between HCs and SLE patients, while sBAFF showed lower sensitivity (82.2%) but higher specificity (94.1%) at a cutoff of 1.195 ng/mL. Relatively high levels of sAPRIL and sBCMA clustered active SLE patients. the receptor sBcMA could be a potential biomarker of disease activity in SLe.Systemic lupus erythematosus (SLE) is a chronic autoimmune disease caused by perturbations in the immune system. The extreme heterogeneity of this disease is primarily explained because genetic background confers susceptibility and environmental factors act as triggers that contribute to disease initiation and progression 1 . A key point in SLE pathogenesis is an imbalance between apoptotic cell numbers and apoptotic material disposal that leads to activation of the humoural response. The serological hallmark of SLE is the production of autoantibodies, which target antigens located in the nucleus or destined for the cell surface in the cytoplasm and are secreted by cells 2 . As T and B cell abnormalities are thought to be central to the disease process 3 , the cytokines that promote B cell differentiation and loss of tolerance have emerged as essential players in the pathophysiology of SLE 1,4 . In the regulation of B cell activation, several members of the tumour necrosis factor (TNF) superfamily participate, including B cell activating factor (BAFF) and A Proliferation-Inducing Ligand (APRIL). These stimulating factors play central roles in B cell development and maturation 5 . Altered serum levels of these cytokines have been found in autoimmune diseases such as SLE 6-11 , rheumatoid arthritis 12,13

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 90%

Section: Methods Patients and Healthy Controlsmentioning

confidence: 99%

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Analysis of the receptor BCMA as a biomarker in systemic lupus erythematosus patients

Salazar-Camarena

Palafox‐Sánchez

Cruz

et al. 2020

Sci Rep

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“…As result there is increased production of soluble BAFF and a higher number of B lymphocytes and immunoglobulins, predisposing to autoimmunity. High BAFF expression is related to active disease, renal and hematological involvement in SLE patients [145].…”

Section: Tnfsf13b/baffmentioning

confidence: 99%

New Horizons in the Genetic Etiology of Systemic Lupus Erythematosus and Lupus-Like Disease: Monogenic Lupus and Beyond

Demirkaya

Şahin

Romano

et al. 2020

JCM

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Systemic lupus erythematosus (SLE) is a clinically and genetically heterogeneous autoimmune disease. The etiology of lupus and the contribution of genetic, environmental, infectious and hormonal factors to this phenotype have yet to be elucidated. The most straightforward approach to unravel the molecular pathogenesis of lupus may rely on studies of patients who present with early-onset severe phenotypes. Typically, they have at least one of the following clinical features: childhood onset of severe disease (<5 years), parental consanguinity, and presence of family history for autoimmune diseases in a first-degree relative. These patients account for a small proportion of patients with lupus but they inform considerable knowledge about cellular pathways contributing to this inflammatory phenotype. In recent years with the aid of new sequencing technologies, novel or rare pathogenic variants have been reported in over 30 genes predisposing to SLE and SLE-like diseases. Future studies will likely discover many more genes with private variants associated to lupus-like phenotypes. In addition, genome-wide association studies (GWAS) have identified a number of common alleles (SNPs), which increase the risk of developing lupus in adult age. Discovery of a possible shared immune pathway in SLE patients, either with rare or common variants, can provide important clues to better understand this complex disorder, it’s prognosis and can help guide new therapeutic approaches. The aim of this review is to summarize the current knowledge of the clinical presentation, genetic diagnosis and mechanisms of disease in patents with lupus and lupus-related phenotypes.

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“…У человека ген, кодирующий BAFF, расположен на 13-й хромосоме в участке 13g32-34 [7]. Опубликованы данные о связи гена BAFF с рядом аутоиммунных заболеваний -ревматоидным артритом, синдром Шёгрена, системной красной волчанкой и др.…”

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Association of BAFF gene polymorphisms with multiple sclerosis progression

Смагина

Ельчанинова

Palashchenko

2020

RJTAO

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Рассеянный склероз (РС)-хроническое аутоиммунное заболевание, которое развивается при сложном взаимодействии внешних и генетических факторов [1, 2]. Влияние генетических факторов на предрасположенность к РС давно известно. Наиболее значимым генетическим фа-ктором риска РС, выявленным еще в 70-е годы прошлого столетия, является носительство определенных аллелей гена главного комплекса гистосовместимости HLА DRB1. Позже в полногеномном исследовании (gеnоmе-widе аssосiаtiоn studiеs, GWАS) с участием нескольких тысяч

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High BAFF expression associated with active disease in systemic lupus erythematosus and relationship with rs9514828C>T polymorphism in TNFSF13B gene

Cited by 36 publications

References 52 publications

Analysis of the receptor BCMA as a biomarker in systemic lupus erythematosus patients

Analysis of the receptor BCMA as a biomarker in systemic lupus erythematosus patients

New Horizons in the Genetic Etiology of Systemic Lupus Erythematosus and Lupus-Like Disease: Monogenic Lupus and Beyond

Association of BAFF gene polymorphisms with multiple sclerosis progression

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