BCR Signaling and B Cell Activation

159K

views

70

authors

13

articles

Editorial

28 January 2020

Editorial: BCR Signaling and B Cell Activation

Wanli Liu

,

Pavel Tolar

,

Wenxia Song

and

Tae Jin Kim

23,175 views

20 citations

Editors

4

Tsinghua University

The Francis Crick Institute

University of Maryland, College Park

Sungkyunkwan University

Impact

T-bet+ cells induced in vitro also express malaria-associated atypical MBC markers. Tonsil B cells were cultured in vitro for 40 h unstimulated or stimulated with antigen on PLB in the presence of CpG and IFN-γ. naïve (IgD+CD10−) and memory (IgD−CD10−) B cells were analyzed by flow cytometry for the expression of T-bet and FcRL5, CD11c, CXCR3, CD86, and CD95. (A) Representative flow cytometry plots indicating expression of FcRL5, CD11c, CXCR3, CD86, or CD95 by T-bet+ naïve and memory B cells. (B) Comparison of expression of FcRL5, CD11c, CXCR3, CD86, or CD95 by unstimulated or stimulated T-bet+ and T-bet− naïve and memory B cells (n = 7). Data for expression of these surface markers by T-bet+ naïve and memory B cells stimulated in vitro on all the stimulation conditions is provided in Supplementary Table 2. Data were analyzed using one-way analysis of variance (ANOVA) with Tukey's adjustment. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, not significant.

Original Research

24 April 2019

The Differentiation in vitro of Human Tonsil B Cells With the Phenotypic and Functional Characteristics of T-bet+ Atypical Memory B Cells in Malaria

Abhijit A. Ambegaonkar

, 2 more and

Haewon Sohn

8,495 views

36 citations

CD22 is necessary for galectin-9 mediated inhibition of BCR signaling in human Daudi B cells. WT and CD22-KO Daudi B cells treated with rGal9 were stimulated with 5 μg/ml anti-IgM F(ab')2 for indicated times, lysed, and subjected to SDS-PAGE followed by immunoblotting with (A) anti-phosphotyrosine and (B) phospho-CD19 and phospho-ERK. Quantifications (shown below) normalized to β-tubulin loading control. Blots and quantification representative of at least three independent experiments.

Original Research

04 April 2019

N-Linked Glycosylation Regulates CD22 Organization and Function

Laabiah Wasim

, 5 more and

Bebhinn Treanor

9,279 views

25 citations

Predicted role of actin regulators during the GC response of B cells. (Upper left): Schematics of the lymph node structure. (Lower left): Immunohistochemistry of a single GC. Red: GL7; Green: CD21/35; Blue: B220. (Right): Schematic of a GC. Antigen-engaged B cells meet antigen experienced Tfh cells and enter the B cell follicle to initiate a GC response. B cells in dark zone express AID (activation-induced cytidine deaminase) and undergo somatic hypermutation. B cell clones that successfully mutate the BCR migrate to light zone, capture antigens deposit on the surface of FDC (follicular dendric cells), and present the antigen to Tfh (T follicular helper) cells. The positive selected B cell clones can differentiate into plasma cells, memory cells or migrate back to dark zone for further mutations and selection.

Review

06 March 2019

Congenital Defects in Actin Dynamics of Germinal Center B Cells

Minghui He

and

Lisa S. Westerberg

6,335 views

13 citations

Review

27 February 2019

B Cell Dysfunction Associated With Aging and Autoimmune Diseases

Shiliang Ma

, 2 more and

Yi Hao

Impaired humoral responses, as well as an increased propensity for autoimmunity, play an important role in the development of immune system dysfunction associated with aging. Accumulation of a subset of atypical B cells, termed age-associated B cells (ABCs), is one of the key age-related changes in B cell compartments. ABCs are characterized by their distinct phenotypes, gene expression profiles, special survival requirements, variations in B cell receptor repertoires, and unique functions. Here, we summarize recent progress in the knowledge base related to the features of ABCs, their potential role in immune senescence, and their relationship with autoimmune diseases.

29,737 views

137 citations

Overview of BCR signaling molecules involved in actin remodeling. CD19, PIP2, PLCγ2,PKC, the Rho family, and Rap GTPase, Btk, calcium, and WASP are major BCR signaling molecules involved in actin remodeling. These signaling molecules as well as their regulators form a network to participate in actin-cytoskeleton reorganization during B-cell activation.

Review

09 January 2019

The Coordination Between B Cell Receptor Signaling and the Actin Cytoskeleton During B Cell Activation

Jingwen Li

, 11 more and

Chaohong Liu

20,609 views

61 citations

Graphical summary of altered peripheral B cell subsets and immune response in IgM KO and IgD KO animals. Schematic representation of B cell development in WT (left), IgM KO (middle), and IgD KO (right) animals highlighting the defect in preBCR signaling, increased follicular (FO) B cell compartment and decreased B1/ MZ B cell compartment in IgM KO animals. In contrast, follicular (FO) B cell compartment is reduced and B1/ MZ B cell compartment is increased in IgD KO animals. In response to antigen, IgD KO animals show a time delay and decreased serum antibody titer compared to WT animals.

Review

18 December 2018

Isotype Specific Assembly of B Cell Antigen Receptors and Synergism With Chemokine Receptor CXCR4

Palash C. Maity

, 2 more and

Hassan Jumaa

22,151 views

16 citations

Original Research

30 January 2019

Toll-Like Receptor Signaling Drives Btk-Mediated Autoimmune Disease

Jasper Rip

, 4 more and

Odilia B. J. Corneth

7,950 views

63 citations

Original Research

19 February 2019

Proteasome Dependent Actin Remodeling Facilitates Antigen Extraction at the Immune Synapse of B Cells

Jorge Ibañez-Vega

, 3 more and

Maria-Isabel Yuseff

7,235 views

38 citations

CD22 dependent regulation of the B-cell receptor (BCR) signal. (A) In resting B cells the conformation of the BCR is closed and CD22 is forming homooligomers (cis-interaction) distinct from the BCR. (B) Specific antigen binding induces conformational opening of the BCR, followed by activation and phosphorylation of ITAMs of the Igα/Igβ-complex. Increased SYK recruitment and activation of the BTK-BLNK-PLCγ2-complex leads to more Ca2+-release out of the endoplasmatic reticulum. Additionally, CD22 clusters are recruited to the BCR. (C) After BCR activation, CD22 recruitment inhibits the BCR signaling. Additionally, CD22 can also be recruited to the BCR by bind its ligands on other cells (trans-interaction). Due to vicinity of CD22 to BCR, ITIMs of CD22 get phosphorylated by LYN. SHP-1 binds to CD22 and inhibits further Ca2+ release. In addition, through the formed CD22-Grb2-PMCA complex, Ca2+ is transported out of the cell into the extracellular space by PMCA.

Review

03 December 2018

B Cell Siglecs–News on Signaling and Its Interplay With Ligand Binding

Sarah J. Meyer

, 2 more and

Lars Nitschke

12,311 views

83 citations

Article Cover Image

Original Research

20 September 2018

Systemic ST6Gal-1 Is a Pro-survival Factor for Murine Transitional B Cells

Eric E. Irons

and

Joseph T. Y. Lau

4,827 views

27 citations

Original Research

17 October 2018

The Mst1 Kinase Is Required for Follicular B Cell Homing and B-1 B Cell Development

Faisal Alsufyani

, 6 more and

Shiv Pillai

3,775 views

13 citations

Original Research

18 December 2018

Hypomorphic Mutations in the BCR Signalosome Lead to Selective Immunoglobulin M Deficiency and Impaired B-cell Homeostasis

Christoph B. Geier

, 5 more and

Hermann M. Wolf

3,875 views

11 citations

Open for submission

Frontiers in Immunology

Unveiling Innate B Cells: Redefining B Lymphocyte Roles in Immunity

Edited by Chaim A Schramm, Kyeong-Hee Lee, Föger Niko

Deadline

30 April 2025

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About

B cells are critical mediators of the adaptive immune system and are responsible for the production of protective antibodies against a diverse range of pathogens. Antigen recognition by B cell receptors (BCRs) triggers the initiation of B cell activation and subsequent responses including proliferation and differentiation, leading to the formation of plasma cells and of memory B cells. Upon antigen encounter, BCRs form clusters and initiate multiple signaling pathways that are essential for cell survival, proliferation and differentiation. It is well documented that B cell signaling controls a diverse range of responses in B cells, including (i) the formation of the immunological synapse; (ii) cytoskeletal re-organization; (iii) changes in cell morphology and (iv) cell migration. These pathways also modulate multiple functions of B cells, such as (i) antigen affinity discrimination and (ii) antigen internalization and presentation. Deregulation of BCR signaling can result in B cell disorders and related diseases, including B cell malignancies, immunodeficiency and autoimmune diseases.

Recent advancements in cell imaging and biophysical techniques have provided good opportunities for observing and analyzing the fundamental aspects of B cell responses following antigen recognition. Through the advent of these new technologies, one can define the precise molecular mechanisms underlying the deregulation of BCR signaling in different immune disorders. However, B cell biologists are still working to address the following questions:

1. To what extent antigen binding to the BCR can trigger effective BCR signaling?
2. How can binding between antigen and the BCR be converted across the plasma membrane into chemical changes that initiate B cell signaling cascades?
3. How do co-receptors, lipid species, cortical cytoskeletons, and signaling molecules participate in BCR signaling?
4. How can different B cell subsets maintain distinct BCR signaling?
5. What is the nature of deregulated BCR signaling in immune diseases?
6. How do tissue microenvironments regulate BCR signaling in vivo?
7. How B-1 cells maintain their cellular homeostasis in spite of their constitutive activation via the BCR.

In this Research Topic, we aim to cover the recent advances and remaining questions in the field of BCR signaling. We welcome the submission of Review, Mini-Review, Original Research and Opinion articles that address, but are not limited to the following topics:

1. Orchestration and characterization of BCR signaling in steady state and during antigen exposure.
2. The role of lipids and metabolism in BCR signaling.
3. The functions of the cytoskeleton in BCR signaling.
4. BCR signaling in autoimmune disease.
5. Microenvironmental cues of antigens in BCR signaling.
6. Alternative pathway for BCR signaling induced by cytokines.
7. Biophysical studies of BCR signaling.
8. Application of cutting edge technologies to investigate BCR signaling.

B cells are critical mediators of the adaptive immune system and are responsible for the production of protective antibodies against a diverse range of pathogens. Antigen recognition by B cell receptors (BCRs) triggers the initiation of B cell activation and subsequent responses including proliferation and differentiation, leading to the formation of plasma cells and of memory B cells. Upon antigen encounter, BCRs form clusters and initiate multiple signaling pathways that are essential for cell survival, proliferation and differentiation. It is well documented that B cell signaling controls a diverse range of responses in B cells, including (i) the formation of the immunological synapse; (ii) cytoskeletal re-organization; (iii) changes in cell morphology and (iv) cell migration. These pathways also modulate multiple functions of B cells, such as (i) antigen affinity discrimination and (ii) antigen internalization and presentation. Deregulation of BCR signaling can result in B cell disorders and related diseases, including B cell malignancies, immunodeficiency and autoimmune diseases.

Recent advancements in cell imaging and biophysical techniques have provided good opportunities for observing and analyzing the fundamental aspects of B cell responses following antigen recognition. Through the advent of these new technologies, one can define the precise molecular mechanisms underlying the deregulation of BCR signaling in different immune disorders. However, B cell biologists are still working to address the following questions:

1. To what extent antigen binding to the BCR can trigger effective BCR signaling?
2. How can binding between antigen and the BCR be converted across the plasma membrane into chemical changes that initiate B cell signaling cascades?
3. How do co-receptors, lipid species, cortical cytoskeletons, and signaling molecules participate in BCR signaling?
4. How can different B cell subsets maintain distinct BCR signaling?
5. What is the nature of deregulated BCR signaling in immune diseases?
6. How do tissue microenvironments regulate BCR signaling in vivo?
7. How B-1 cells maintain their cellular homeostasis in spite of their constitutive activation via the BCR.

In this Research Topic, we aim to cover the recent advances and remaining questions in the field of BCR signaling. We welcome the submission of Review, Mini-Review, Original Research and Opinion articles that address, but are not limited to the following topics:

1. Orchestration and characterization of BCR signaling in steady state and during antigen exposure.
2. The role of lipids and metabolism in BCR signaling.
3. The functions of the cytoskeleton in BCR signaling.
4. BCR signaling in autoimmune disease.
5. Microenvironmental cues of antigens in BCR signaling.
6. Alternative pathway for BCR signaling induced by cytokines.
7. Biophysical studies of BCR signaling.
8. Application of cutting edge technologies to investigate BCR signaling.

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Editors

Tsinghua University

The Francis Crick Institute

University of Maryland, College Park

Sungkyunkwan University

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