B-cell populations and sub-populations in Sjögren's syndrome

Hamza, Nishath; Bos, Nicolaas A.; Kallenberg, Cees G. M.

doi:10.1016/j.lpm.2012.05.021

Cited by 22 publications

(24 citation statements)

References 77 publications

(100 reference statements)

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“…Despite these uncertainties, a potential role of cells expressing CD38 in SS is supported by the study of peripheral blood B cells. Higher levels of mature CD38++ B cells are observed in the sera of SS patients [54], as well as a reduced number of memory B cells [55,56] and increased counts of activated T cells and plasmablasts [57]. Another recent study demonstrated that higher circulating levels of CD38+ B cells positively correlate with disease activity scores and serum levels of IgG and autoantibodies [58].…”

Section: Sjögren's Syndromementioning

confidence: 99%

Is There a Future for Anti-CD38 Antibody Therapy in Systemic Autoimmune Diseases?

Benfaremo

Gabrielli

2019

Cells

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CD38 is a type II glycoprotein highly expressed on plasmablasts, short-lived and long-lived plasma cells, but weakly expressed on other lymphoid cells, myeloid cells and non-hematopoietic cells. This expression pattern makes CD38 an interesting target for a targeted therapy aiming to deplete antibody-producing plasma cells. We present data suggesting that anti-CD38 therapy may be effective for the prevention at the preclinical stage and for the treatment of established autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, Sjögren’s syndrome and anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis. Given the high unmet need for efficacious disease-modifying treatment in these diseases, studies are warranted to determine if anti-CD38 antibody-based therapies may delay or prevent the disease progression of systemic autoimmune diseases.

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Section: Sjögren's Syndromementioning

confidence: 99%

Is There a Future for Anti-CD38 Antibody Therapy in Systemic Autoimmune Diseases?

Benfaremo

Gabrielli

2019

Cells

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“…As B cell signaling signature dis-appeared after a successful treatment with rituximab in Sjögren's syndrome, which is characterized by the B cell activation, [11,12], we sought to investigate whether TNF-α signature and B cell activation signaling were present in PBMCs of GPA.…”

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor-α Gene Signature Is Absent in Peripheral Blood Mononuclear Cells of Patients with Granulomatosis Polyangiitis

Koenig

Park

2015

J Rheum Dis

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Objective. Granulomatosis with polyangiitis (GPA), formally known as Wegener's granulomatosis, is a systemic vasculitis with necrotizing granulomatous inflammation. As treatment directed against tumor necrosis factor (TNF)-α failed in GPA, we investigated whether "TNF-α signature" (i.e. gene expression profile of TNF-α activation) was present in peripheral blood mononuclear cells (PBMCs) of patients with GPA. Methods. Gene expression profiling was performed using total RNA from PBMCs of 41 patients with GPA and 23 healthy control subjects using the Illumina microarray technique. Gene set enrichment analysis (GSEA) was performed to detect the presence of TNF-α signature using the curated list C2-V3.0 by the Broad Institute. False discovery rate＜0.05 was considered statistically significant. Results. GSEA did not show significant enrichment of any TNF-α associated gene sets in GPA. Expression levels of genes up-regulated by TNF-α did not differ between healthy control subjects, patients in remission (Birmingham Vasculitis Activity Score [BVAS]=0), and those with active disease (BVAS≥1). In addition, an unsupervised hierarchical clustering of those genes failed to cluster the samples into healthy control subjects and GPA in remission or with active disease. B cell activation signature was enriched in GPA patients. Conclusion. Absence of a TNF-α signature in PBMCs may suggest that TNF-α plays a less important role in the pathogenesis of GPA than previously accepted. (J Rheum Dis 2015;22:293-297)

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“…Como resultado, a patogênese da SSp foi, durante muitos anos, atribuída aos linfócitos T (Susan et al, 1994;Xanthou et al, 1999). No entanto, o surgimento de estratégias terapêuticas para diminuição da quantidade dos linfócitos B revelou-se notavelmente eficaz, inclusive quando comparadas à terapia contra linfócitos T, indicando um papel fundamental dos linfócitos B na imunopatogênese da SSp (Hamza et al, 2012).…”

Section: Proteína Cd20unclassified

“…Seguindo esta linha de pensamento, sabe-se que nesta síndrome exitem sinais clássicos de hipergamaglobulemia e aumento da produção de autoanticorpos como anti-Ro/SSA e anti-La/SSB que evidenciam a hiperativação dos linfócitos B (Lee et al, 2016;He et al, 2017) Theander et al, 2006;Hamza et al, 2012).…”

Section: Proteína Cd20unclassified

Xerostomia em doença autoimune com envolvimento glandular: estudo morfométrico das células dendríticas no mecanismo do comprometimento das glândulas salivares na Síndrome de Sjögren

Godoy¹

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B-cell populations and sub-populations in Sjögren's syndrome

Cited by 22 publications

References 77 publications

Is There a Future for Anti-CD38 Antibody Therapy in Systemic Autoimmune Diseases?

Is There a Future for Anti-CD38 Antibody Therapy in Systemic Autoimmune Diseases?

Tumor Necrosis Factor-α Gene Signature Is Absent in Peripheral Blood Mononuclear Cells of Patients with Granulomatosis Polyangiitis

Xerostomia em doença autoimune com envolvimento glandular: estudo morfométrico das células dendríticas no mecanismo do comprometimento das glândulas salivares na Síndrome de Sjögren

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