Function and regulation of self-reactive marginal zone B cells in autoimmune arthritis
Open accessAbstract
Polyreactive innate-type B cells account for many B cells expressing self-reactivity in the periphery. Improper regulation of these B cells may be an important factor that underlies autoimmune disease. Here we have explored the influence of self-reactive innate B cells in the development of collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis. We show that splenic marginal zone (MZ), but not B-1 B cells exhibit spontaneous IgM reactivity to autologous collagen II in naı¨ve mice. Upon immunization with heterologous collagen II in complete Freund's adjuvant the collagen-reactive MZ B cells expanded rapidly, while the B-1 B cells showed a modest anti-collagen response. The MZ B cells were easily activated by toll-like receptor (TLR) 4 and 9-ligands in vitro, inducing proliferation and cytokine secretion, implying that dual engagement of the B-cell receptor and TLRs may promote the immune response to self-antigen. Furthermore, collagen-primed MZ B cells showed significant antigen-presenting capacity as reflected by cognate T-cell proliferation in vitro and induction of IgG anti-collagen antibodies in vivo. MZ B cells that were deficient in complement receptors 1 and 2 demonstrated increased proliferation and cytokine production, while Fcγ receptor IIb deficiency of the cells lead to increased cytokine production and antigen presentation. In conclusion, our data highlight self-reactive MZ B cells as initiators of the autoimmune response in CIA, where complement and Fc receptors are relevant in controlling the self-reactivity in the cells.
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The time point of lowest TBX3 activity corresponds to the time point reported for the highest B cell activation and proliferation of CII-specific IgM-positive B cells in the CIA model.
“which corresponds to the time point reported for the highest B cell activation and proliferation of CII-specific IgM-positive B cells in the CIA model [64].”
From The oncoprotein TBX3 is controlling severity in experimental arthritis (2019) · cites this paper as [64]
The Results (page unavailable) report that CII-reactive IgM-positive marginal-zone B cells expanded after immunization and peaked in number on day 12. That supports a peak in the B-cell response, but the paper does not report that activation and proliferation themselves were highest at that time point. The comparison with TBX3 activity is the citing authors’ own framing, not a finding attributed to this source. (LLM, conf=0.83)
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- Authors
- Palm, A.-K. E., Friedrich, H. C., Mezger, A., Salomonsson, M., Myers, L. K., & Kleinau, S.
- Affiliations
- Uppsala University (SE)
- University of Tennessee Health Science Center (US)
- Corresponding author
- Kleinau, Sandra
- Venue
- Cellular & Molecular Immunology
- Published
- 2015-05-11
- Volume
- 12
- Issue
- 4
- Pages
- 493-504
- ISSN
- 1672-7681 (ISSN-L)
- 2042-0226
- PMC
- PMC4496548
- OpenAlex
- W1480811716
- Cited by
- 30
- References
- 50
- Citations by year
- 2025: 4 · 2024: 6 · 2023: 2 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 2 · 2017: 2 · 2016: 5
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Cellular and Molecular Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR064825)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Keywords
- marginal zone B cells, autoreactive B cells, collagen-induced arthritis, rheumatoid arthritis, B-1 cells, type II collagen, TLR4, TLR9, B cell receptor, antigen presentation, complement receptors, autoantibodies, B cell activation
- MeSH terms
- Animals, Arthritis, Rheumatoid, Collagen, Mice, Mutant Strains, Spleen, B-Lymphocyte Subsets, Receptors, IgG, Cell Proliferation, Toll-Like Receptor 4, Toll-Like Receptor 9, Mice
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