ArticleArthritis research & therapy2016
Regulatory and effector B cell cytokine production in patients with relapsing granulomatosis with polyangiitis.
Article in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- BAFF and APRIL signaling in the B-cell lineage: implications for the pathogenesis of ANCA-associated vasculitis.Frontiers in immunology · 2026Review
- Impaired humoral and T helper cell responses to toxic shock syndrome toxin-1 (TSST-1) in granulomatosis with polyangiitis.Rheumatology (Oxford, England) · 2025Article
- Regulatory B cells are reduced in the blood in patients with granulomatosis with polyangiitis, and fail to regulate T-cell IFN-γ production.Clinical and experimental immunology · 2023Article
- Soluble markers of B cell activation suggest a role of B cells in the pathogenesis of systemic sclerosis-associated pulmonary arterial hypertension.Frontiers in immunology · 2022Article
- Investigation of type I interferon responses in ANCA-associated vasculitis.Scientific reports · 2021Article
- Article
- Evidence for enhanced Bruton's tyrosine kinase activity in transitional and naïve B cells of patients with granulomatosis with polyangiitis.Rheumatology (Oxford, England) · 2019Article
- Could Lymphocyte Profiling be Useful to Diagnose Systemic Autoimmune Diseases?Clinical reviews in allergy & immunology · 2017Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundB cells are capable of producing regulatory and effector cytokines. In patients with granulomatosis with polyangiitis (GPA), skewing of the pro- and anti-inflammatory cytokine balance may affect the risk of relapse. This study aimed to investigate differences in B cell cytokine production in patients with relapsing GPA and in controls, and determine whether this can aid in relapse prediction.
methodsThirteen GPA patients with an upcoming relapse were matched with non-relapsing patients and healthy controls in a retrospective design. The B cell subset distribution was determined from peripheral blood. Cryopreserved peripheral blood mononuclear cells were cultured and intracellular B cell production of regulatory (IL10) and effector (TNFα, IFNγ, IL2, IL6) cytokines was assessed. Finally, serum markers associated with B cell activation (sCD27) and migration (CCL19) were determined.
resultsGPA patient samples exhibited significantly lower percentages of TNFα+ B cells than controls, an effect that was most pronounced in patients about to relapse. B cell capacity for IL10 production was similar in patients and controls. No significant differences were observed for cytokine production in relapsing and non-relapsing GPA patients. TNFα production correlated strongly with IL2, IFNγ and the percentage of memory B cells. No change in effector cytokines occurred before relapse, while the percentage of IL10+ B cells significantly decreased. GPA patients in remission had increased serum levels of CCL19 and sCD27, and sCD27 levels increased upon active disease.
conclusionsWhile differences in effector B cell cytokine production were observed between patients and controls, monitoring this in GPA did not clearly distinguish patients about to relapse. Prospective measurements of the regulatory cytokine IL10 may have potential for relapse prediction. Memory B cells appear mainly responsible for effector cytokine production. Increased migration of these cells could explain the decreased presence of TNFα+ B cells in the circulation.
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