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.
