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Cells
Special Issues
Emerging Mechanisms in B Cell Activation
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Emerging Mechanisms in B Cell Activation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 16137

Special Issue Editors

Dr. Pieta Mattila

E-Mail Website
Guest Editor
Faculty of Medicine, University of Turku, Abo, Finland
Interests: B cell activation; BCR signaling; antigen processing; cytoskeleton; cellular membranes
Dr. Maria-Isabel Yuseff

E-Mail Website
Guest Editor
Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile
Interests: B cells; membrane trafficking; antigen processing; proteostasis; cytoskeleton and cell polarity

Special Issue Information

Dear Colleagues,

B cells form a pivotal branch of adaptive immune system. Activation of B cells by specific antigens triggers a cell activation and differentiation cascade to mount high-affinity antibody responses. B cells can be activated by various forms of antigens as well as a cocktail of innate-type of signals but the molecular mechanisms of these processes still remain poorly understood. The technological advances in fields, such as microscopy, mechanobiology, molecular sensors, and proteomics, have recently opened new avenues in studying the cell biological events of B cell activation.

This Special Issue will focus on different aspects of B cell activation and its regulation, from the cell surface receptors to the various cell biological events and ultimately to the changes in the transcriptional profiling and cell fate. We welcome original manuscripts, reports on new technologies or methodologies used to study B cell activation, as well as reviews on this topic.

Dr. Pieta Mattila
Dr. Maria-Isabel Yuseff
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • B cells
  • infection
  • BCR signaling
  • antigen internalization
  • antigen presentation
  • Toll-like receptors
  • germinal center response
  • cytoskeleton and membrane trafficking

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Published Papers (6 papers)

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Research

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25 pages, 7058 KiB  
Article
WAVE2 Regulates Actin-Dependent Processes Induced by the B Cell Antigen Receptor and Integrins
by Abhishek Bedi, Kate Choi, Connor Keane, Madison Bolger-Munro, Ashley R. Ambrose and Michael R. Gold
Cells 2023, 12(23), 2704; https://doi.org/10.3390/cells12232704 - 25 Nov 2023
Cited by 1 | Viewed by 1949
Abstract
B cell antigen receptor (BCR) signaling induces actin cytoskeleton remodeling by stimulating actin severing, actin polymerization, and the nucleation of branched actin networks via the Arp2/3 complex. This enables B cells to spread on antigen-bearing surfaces in order to increase antigen encounters and [...] Read more.
B cell antigen receptor (BCR) signaling induces actin cytoskeleton remodeling by stimulating actin severing, actin polymerization, and the nucleation of branched actin networks via the Arp2/3 complex. This enables B cells to spread on antigen-bearing surfaces in order to increase antigen encounters and to form an immune synapse (IS) when interacting with antigen-presenting cells (APCs). Although the WASp, N-WASp, and WAVE nucleation-promoting factors activate the Arp2/3 complex, the role of WAVE2 in B cells has not been directly assessed. We now show that both WAVE2 and the Arp2/3 complex localize to the peripheral ring of branched F-actin when B cells spread on immobilized anti-Ig antibodies. The siRNA-mediated depletion of WAVE2 reduced and delayed B cell spreading on immobilized anti-Ig, and this was associated with a thinner peripheral F-actin ring and reduced actin retrograde flow compared to control cells. Depleting WAVE2 also impaired integrin-mediated B cell spreading on fibronectin and the LFA-1-induced formation of actomyosin arcs. Actin retrograde flow amplifies BCR signaling at the IS, and we found that depleting WAVE2 reduced microcluster-based BCR signaling and signal amplification at the IS, as well as B cell activation in response to antigen-bearing cells. Hence, WAVE2 contributes to multiple actin-dependent processes in B lymphocytes. Full article
(This article belongs to the Special Issue Emerging Mechanisms in B Cell Activation)
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20 pages, 8205 KiB  
Article
The Small GTPase Rab7 Regulates Antigen Processing in B Cells in a Possible Interplay with Autophagy Machinery
by Marika Runsala, Elina Kuokkanen, Eveliina Uski, Vid Šuštar, Meryem Özge Balci, Johanna Rajala, Vilma Paavola and Pieta K. Mattila
Cells 2023, 12(21), 2566; https://doi.org/10.3390/cells12212566 - 2 Nov 2023
Cited by 2 | Viewed by 1663
Abstract
In B cells, antigen processing and peptide-antigen (pAg) presentation is essential to ignite high-affinity antibody responses with the help of cognate T cells. B cells efficiently internalize and direct specific antigens for processing and loading onto MHCII. This critical step, which enables pAg [...] Read more.
In B cells, antigen processing and peptide-antigen (pAg) presentation is essential to ignite high-affinity antibody responses with the help of cognate T cells. B cells efficiently internalize and direct specific antigens for processing and loading onto MHCII. This critical step, which enables pAg presentation, occurs in MHCII compartments (MIICs) which possess the enzymatic machinery for pAg loading on MHCII. The intracellular transport systems that guide antigen and maintain this unique compartment remain enigmatic. Here, we probed the possible functional role of two known endosomal proteins, the Rab family small GTPases Rab7 and Rab9, that are both reported to colocalize with internalized antigen. As compared to Rab9, we found Rab7 to exhibit a higher overlap with antigen and MIIC components. Rab7 also showed a higher association with antigen degradation. The inhibition of Rab7 drastically decreased pAg presentation. Additionally, we detected the strong colocalization of perinuclearly clustered and presumably MIIC-associated antigen with autophagy protein LC3. When we pharmacologically inhibited autophagy, pAg presentation was inhibited. Together, our data promote Rab7 as an important regulator of antigen processing and, considering the previously reported functions of Rab7 in autophagy, this also raises the possibility of the involvement of autophagy-related machinery in this process. Full article
(This article belongs to the Special Issue Emerging Mechanisms in B Cell Activation)
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22 pages, 15775 KiB  
Article
Enhanced B Cell Receptor Signaling Partially Compensates for Impaired Toll-like Receptor 4 Responses in LPS-Stimulated IκBNS-Deficient B Cells
by Monika Adori, Sharesta Khoenkhoen, Jingdian Zhang, Xaquin Castro Dopico and Gunilla B. Karlsson Hedestam
Cells 2023, 12(9), 1229; https://doi.org/10.3390/cells12091229 - 24 Apr 2023
Cited by 2 | Viewed by 2729
Abstract
Lipopolysaccharide (LPS) stimulates dual receptor signaling by bridging the B cell receptor and Toll-like receptor 4 (BCR/TLR4). B cells from IκBNS-deficient bumble mice treated with LPS display reduced proliferative capacity and impaired plasma cell differentiation. To improve our understanding of the regulatory role [...] Read more.
Lipopolysaccharide (LPS) stimulates dual receptor signaling by bridging the B cell receptor and Toll-like receptor 4 (BCR/TLR4). B cells from IκBNS-deficient bumble mice treated with LPS display reduced proliferative capacity and impaired plasma cell differentiation. To improve our understanding of the regulatory role of IκBNS in B cell activation and differentiation, we investigated the BCR and TLR4 signaling pathways separately by using dimeric anti-IgM Fab (F(ab’)2) or lipid A, respectively. IκBNS-deficient B cells exhibited reduced survival and defective proliferative capacity in response to lipid A compared to B cells from wildtype (wt) control mice. In contrast, anti-IgM stimulation of bumble B cells resulted in enhanced viability and increased differentiation into CD138+ cells compared to control B cells. Anti-IgM-stimulated IκBNS-deficient B cells also showed enhanced cycle progression with increased levels of c-Myc and cyclin D2, and augmented levels of pCD79a, pSyk, and pERK compared to control B cells. These results suggest that IκBNS acts as a negative regulator of BCR signaling and a positive regulator of TLR4 signaling in mouse B cells. Full article
(This article belongs to the Special Issue Emerging Mechanisms in B Cell Activation)
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20 pages, 3676 KiB  
Article
Autophagy Induced by Toll-like Receptor Ligands Regulates Antigen Extraction and Presentation by B Cells
by Jonathan Lagos, Sara Sagadiev, Jheimmy Diaz, Juan Pablo Bozo, Fanny Guzman, Caroline Stefani, Silvana Zanlungo, Mridu Acharya and Maria Isabel Yuseff
Cells 2022, 11(23), 3883; https://doi.org/10.3390/cells11233883 - 1 Dec 2022
Cited by 2 | Viewed by 2653
Abstract
The engagement of B cells with surface-tethered antigens triggers the formation of an immune synapse (IS), where the local secretion of lysosomes can facilitate antigen uptake. Lysosomes intersect with other intracellular processes, such as Toll-like Receptor (TLR) signaling and autophagy coordinating immune responses. [...] Read more.
The engagement of B cells with surface-tethered antigens triggers the formation of an immune synapse (IS), where the local secretion of lysosomes can facilitate antigen uptake. Lysosomes intersect with other intracellular processes, such as Toll-like Receptor (TLR) signaling and autophagy coordinating immune responses. However, the crosstalk between these processes and antigen presentation remains unclear. Here, we show that TLR stimulation induces autophagy in B cells and decreases their capacity to extract and present immobilized antigens. We reveal that TLR stimulation restricts lysosome repositioning to the IS by triggering autophagy-dependent degradation of GEF-H1, a Rho GTP exchange factor required for stable lysosome recruitment at the synaptic membrane. GEF-H1 degradation is not observed in B cells that lack αV integrins and are deficient in TLR-induced autophagy. Accordingly, these cells show efficient antigen extraction in the presence of TLR stimulation, confirming the role of TLR-induced autophagy in limiting antigen extraction. Overall, our results suggest that resources associated with autophagy regulate TLR and BCR-dependent functions, which can finetune antigen uptake by B cells. This work helps to understand the mechanisms by which B cells are activated by surface-tethered antigens in contexts of subjacent inflammation before antigen recognition, such as sepsis. Full article
(This article belongs to the Special Issue Emerging Mechanisms in B Cell Activation)
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17 pages, 3735 KiB  
Article
Antibody Mediated Intercommunication of Germinal Centers
by Theinmozhi Arulraj, Sebastian C. Binder and Michael Meyer-Hermann
Cells 2022, 11(22), 3680; https://doi.org/10.3390/cells11223680 - 19 Nov 2022
Cited by 1 | Viewed by 1756
Abstract
Antibody diversification and selection of B cells occur in dynamic structures called germinal centers (GCs). Passively administered soluble antibodies regulate the GC response by masking the antigen displayed on follicular dendritic cells (FDCs). This suggests that GCs might intercommunicate via naturally produced soluble [...] Read more.
Antibody diversification and selection of B cells occur in dynamic structures called germinal centers (GCs). Passively administered soluble antibodies regulate the GC response by masking the antigen displayed on follicular dendritic cells (FDCs). This suggests that GCs might intercommunicate via naturally produced soluble antibodies, but the role of such GC–GC interactions is unknown. In this study, we performed in silico simulations of interacting GCs and predicted that intense interactions by soluble antibodies limit the magnitude and lifetime of GC responses. With asynchronous GC onset, we observed a higher inhibition of late formed GCs compared to early ones. We also predicted that GC–GC interactions can lead to a bias in the epitope recognition even in the presence of equally dominant epitopes due to differences in founder cell composition or initiation timing of GCs. We show that there exists an optimal range for GC–GC interaction strength that facilitates the affinity maturation towards an incoming antigenic variant during an ongoing GC reaction. These findings suggest that GC–GC interactions might be a contributing factor to the unexplained variability seen among individual GCs and a critical factor in the modulation of GC response to antigenic variants during viral infections. Full article
(This article belongs to the Special Issue Emerging Mechanisms in B Cell Activation)
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Review

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23 pages, 2222 KiB  
Review
Crosstalk of Transcriptional Regulators of Adaptive Immune System and microRNAs: An Insight into Differentiation and Development
by Maryam Boshtam, Ilnaz Rahimmanesh, Laleh Shariati, Malihe Najaflu, Hossein Khanahmad, Mina Mirian, Atefeh Zarepour, Ali Zarrabi and Shirin Kouhpayeh
Cells 2023, 12(4), 635; https://doi.org/10.3390/cells12040635 - 16 Feb 2023
Cited by 3 | Viewed by 2084
Abstract
MicroRNAs (miRNAs), as small regulatory RNA molecules, are involved in gene expression at the post-transcriptional level. Hence, miRNAs contribute to gene regulation of various steps of different cell subsets’ differentiation, maturation, and activation. The adaptive immune system arm, which exhibits the most specific [...] Read more.
MicroRNAs (miRNAs), as small regulatory RNA molecules, are involved in gene expression at the post-transcriptional level. Hence, miRNAs contribute to gene regulation of various steps of different cell subsets’ differentiation, maturation, and activation. The adaptive immune system arm, which exhibits the most specific immune responses, is also modulated by miRNAs. The generation and maturation of various T-cell subsets concomitant with B-cells is under precise regulation of miRNAs which function directly on the hallmark genes of each cell subset or indirectly through regulation of signaling pathway mediators and/or transcription factors involved in this maturation journey. In this review, we first discussed the origination process of common lymphocyte progenitors from hematopoietic stem cells, which further differentiate into various T-cell subsets under strict regulation of miRNAs and transcription factors. Subsequently, the differentiation of B-cells from common lymphocyte progenitors in bone marrow and periphery were discussed in association with a network of miRNAs and transcription factors. Full article
(This article belongs to the Special Issue Emerging Mechanisms in B Cell Activation)
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