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Recent Advances in B Cells: Signal Transduction and Therapeutic Potential

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 2041

Special Issue Editor


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Guest Editor
Department of Immunology, Eötvös Loránd University, 1117 Budapest, Hungary
Interests: regulation of the immune response; B cells; signaling; receptor cross-talk; regulatory cells; autoimmunity; rheumatoid arthritis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

B cells play a critical role in the development of effective immune response; they differentiate into plasma cells or memory B cells, secrete high affinity antibodies and a variety of cytokines, provide long-lasting memory, present antigens to T cells and regulate immune responses. However, B cells can also cause diseases through recognizing and reacting to self. B cells must be educated to differentiate self from non-self; thus, they go through several developmental checkpoints where self-specific cells are eliminated. These checkpoints are under the control of B cell receptor (BCR) mediated signals, but also influenced by Toll-like receptor 7 (TLR-7) and TLR-9, the innate immune sensors. BCR, TLR-7, TLR-9 and possibly other receptors function together to regulate the pathogenesis of autoimmunity.

Dysregulated B cell signaling can be the primary driver of many human autoimmune diseases. Studying signaling and co-signaling molecules and pathways in B cells would help to elucidate the molecular mechanisms of autoimmune diseases and would lead to the discovery of novel therapeutic targets and to the development of new drugs for the treatment of autoimmune diseases.

This Special Issue, “Recent Advances in B Cells: Signal Transduction and Therapeutic Potential” in the International Journal of Molecular Sciences will comprise a selection of research papers and reviews that will contribute to defining proteins and signaling pathways that support atypical B cell response in autoimmune diseases. This will also help researchers to better understand disease mechanisms, to identify key immune regulatory processes, and eventually, provide new ideas for precision therapy.

 

Prof. Dr. Gabriella Sármay
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • Anergy
  • Autoimmune diseases
  • B cell signaling
  • Central tolerance
  • Extrafollicular response
  • Germinal center
  • Immune regulation
  • Peripheral tolerance
  • Signaling pathways and molecules
  • Toll-like receptors

Published Papers (1 paper)

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Research

10 pages, 1450 KiB  
Article
Ligation of TLR Homologue CD180 of B Cells Activates the PI3K/Akt/mTOR Pathway in Systemic Sclerosis and Induces a Pathological Shift in the Expression of BAFF Receptors
by Szabina Erdő-Bonyár, Judit Rapp, Dávid Szinger, Tünde Minier, Gábor Kumánovics, László Czirják, Timea Berki and Diána Simon
Int. J. Mol. Sci. 2022, 23(12), 6777; https://doi.org/10.3390/ijms23126777 - 17 Jun 2022
Cited by 1 | Viewed by 1446
Abstract
The phosphatidylinositol-3-kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) pathways are known to play a key role in B-cell activation and fibrosis in systemic sclerosis (SSc). Receptors of B-cell activator factor (BAFF) utilize these pathways, which can be influenced by Toll-like receptors [...] Read more.
The phosphatidylinositol-3-kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) pathways are known to play a key role in B-cell activation and fibrosis in systemic sclerosis (SSc). Receptors of B-cell activator factor (BAFF) utilize these pathways, which can be influenced by Toll-like receptors (TLRs), as TLRs can alter the expression of BAFF-binding receptors. Our results show that B-cell stimulation via TLR homologue CD180 phosphorylates Akt in diffuse cutaneous SSc (dcSSc) to a lower extent than in healthy controls (HCs). We found basal downregulated BAFF receptor (BAFF-R) and enhanced transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI) expression in dcSSc B cells, which might enhance the formation of autoantibody-secreting plasma cells. Moreover, this pathological shift was observed in naive B cells, emphasizing the importance of their increase in SSc. Additionally, we measured higher serum levels of autoantibodies to BAFF in dcSSc patients, suggesting that an imbalance in the complex system of BAFF/anti-BAFF autoantibodies/BAFF-binding receptors may contribute to the development of SSc. Anti-CD180 antibody treatment had opposite effects on the expression of BAFF-R and TACI in HC B cells, resulting in similar levels as observed in SSc B cells without stimulation, which argues against the usefulness of such therapy in SSc. Full article
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