Trial reportEuropean journal of immunology2014
Exacerbated experimental arthritis in Wiskott-Aldrich syndrome protein deficiency: modulatory role of regulatory B cells.
Trial report in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.Nature reviews. Immunology · 2026Review
- Autoimmunity and inborn errors of immunity: a complex coexistence.Frontiers in immunology · 2026Review
- B cell development: transcriptional regulation and immunological mechanisms in homeostasis.Frontiers in immunology · 2025Review
- Article
- Autoimmunity in Wiskott-Aldrich Syndrome: Updated Perspectives.The application of clinical genetics · 2021Review
- Immunosuppressive Mechanisms of Regulatory B Cells.Frontiers in immunology · 2021Review
- From Anti-EBV Immune Responses to the EBV Diseasome via Cross-reactivity.Global medical genetics · 2020Article
- Treatment of primary immunodeficiency with allogeneic transplant and gene therapy.Hematology. American Society of Hematology. Education Program · 2019Review
- Congenital Defects in Actin Dynamics of Germinal Center B Cells.Frontiers in immunology · 2019Review
- Clinical Manifestations and Pathophysiological Mechanisms of the Wiskott-Aldrich Syndrome.Journal of clinical immunology · 2018Review
- Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells.Nature communications · 2017Article
- Wiskott-Aldrich syndrome protein: Emerging mechanisms in immunity.European journal of immunology · 2017Review
- Abnormalities of follicular helper T-cell number and function in Wiskott-Aldrich syndrome.Blood · 2016Article
- B10 cells induced by Schistosoma japonicum soluble egg antigens modulated regulatory T cells and cytokine production of T cells.Parasitology research · 2015Article
- Age-Dependent Defects of Regulatory B Cells in Wiskott-Aldrich Syndrome Gene Knockout Mice.PloS one · 2015Article
- Signal Integration during T Lymphocyte Activation and Function: Lessons from the Wiskott-Aldrich Syndrome.Frontiers in immunology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
Patients deficient in the cytoskeletal regulator Wiskott-Aldrich syndrome protein (WASp) are predisposed to varied autoimmunity, suggesting it has an important controlling role in participating cells. IL-10-producing regulatory B (Breg) cells are emerging as important mediators of immunosuppressive activity. In experimental, antigen-induced arthritis WASp-deficient (WASp knockout [WAS KO]) mice developed exacerbated disease associated with decreased Breg cells and regulatory T (Treg) cells, but increased Th17 cells in knee-draining LNs. Arthritic WAS KO mice showed increased serum levels of B-cell-activating factor, while their B cells were unresponsive in terms of B-cell-activating factor induced survival and IL-10 production. Adoptive transfer of WT Breg cells ameliorated arthritis in WAS KO recipients and restored a normal balance of Treg and Th17 cells. Mice with B-cell-restricted WASp deficiency, however, did not develop exacerbated arthritis, despite exhibiting reduced Breg- and Treg-cell numbers during active disease, and Th17 cells were not increased over equivalent WT levels. These findings support a contributory role for defective Breg cells in the development of WAS-related autoimmunity, but demonstrate that functional competence in other regulatory populations can be compensatory. A properly regulated cytoskeleton is therefore important for normal Breg-cell activity and complementation of defects in this lineage is likely to have important therapeutic benefits.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.