Molecular Biology of B Cells

Molecular Biology of B Cells, 2nd Edition

Molecular Biology of B Cells, 2nd Edition,Tasuku Honjo,Michael Reth,Andreas Radbruch,Frederick Alt,ISBN9780123979339

Honjo   &   Reth   &   Radbruch   &   Alt   

Academic Press




A definitive reference on the molecular biology of B cells.

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Key Features

  • Covers signaling mechanisms regulating B cell differentiation
  • Provides information on the development of therapeutics using monoclonal antibodies and clinical application of Ab
  • Contains studies on B cell tumors from various stages of B lymphocytes
  • Offers an integrated view of all aspects of B cells to produce a normal immune response


Molecular Biology of B Cells, Second Edition is a comprehensive reference to how B cells are generated, selected, activated and engaged in antibody production. All of these developmental and stimulatory processes are described in molecular, immunological, and genetic terms to give a clear understanding of complex phenotypes.

Molecular Biology of B Cells, Second Edition offers an integrated view of all aspects of B cells to produce a normal immune response as a constant, and the molecular basis of numerous diseases due to B cell abnormality.  The new edition continues its success with updated research on microRNAs in B cell development and immunity, new developments in understanding lymphoma biology, and therapeutic targeting of B cells for clinical application.  With updated research and continued comprehensive coverage of all aspects of B cell biology, Molecular Biology of B Cells, Second Edition is the definitive resource, vital for researchers across molecular biology, immunology and genetics.


Research level immunologists, molecular biologists and geneticists

Tasuku Honjo

Dr. Tasuku Honjo graduated from Kyoto University Faculty of Medicine in 1966 (M.D.). After obtaining his Ph.D. in Biochimistry (Dr. O. Hayaishi), he spent 4 years in the U.S.A. as a postdoctoral fellow first in Carnegie Institution of Washington (Dr. D. Brown), and then in NIH (Dr. P. Leder) where he initiated studies on immunoglobulin genes. He returned to Tokyo University as an assistant professor in 1974, and then moved to Osaka University School of Medicine as Professor of Genetics in 1979. He succeeded to Dr. O. Hayaishi after his retirement at the Department of Medical Chemistry in Kyoto University. He also served as Dean of Medical School (1996-2000 and 2004-2005), and Executive Member of Council for Science and Technology Policy, Cabinet Office (2006-2012). Currently, he is Professor of Department of Immunology and Genomic Medicine, Kyoto University, and also Chairman of Board of Directors, Shizuoka Prefectural University Corporation. Dr. Honjo is well known for his discovery of activation-induced cytidine deaminase that is essential for class switch recombination and somatic hypermutation. He has established the basic conceptual framework of class switch recombination starting from discovery of DNA deletion (1978) and S regions (1980), followed by elucidation of the whole mouse immunoglobulin heavy-chain locus. His contribution further extended to cDNA cloning of IL-4 and IL-5 cytokines involved in class switching and IL-2 receptor alpha chain. Aside from class switching recombination, he discovered PD-1 (program cell death 1), a negative coreceptor at the effector phase of immune response and showed that PD-1 modulation contributes to treatments of viral infection, tumor and autoimmunity. In addition, he is known to be a discoverer of RBP-J, a nuclear protein that interacts with the intracellular domain of Notch in the nucleus. Notch/RBP-J signaling has been shown to regulate a variety of cell lineage commitment including T and B cells. For these contributions, Dr. Honjo has received many awards, including the Noguchi Hideyo Memorial Prize for Medicine (1981), Imperial Prize, Japan Academy Prize (1996), Robert Koch Prize (2012), and Order of Culture (2013). He is an honorary member of the American Association of Immunologists. He has been honored by the Japanese Government as a person of cultural merits (2000). He has also been elected as a foreign associate of National Academy of Sciences, USA in 2001, as a member of Leopoldina, the German Academy of Natural Scientists in 2003, and as a member of Japan Academy in 2005.

Affiliations and Expertise

Kyoto University, Japan

View additional works by Tasuku Honjo

Michael Reth

Prof. Dr Michael Reth has won the Paul Ehrlich and Ludwig Darmstaedter Prize, awarded by the Paul Ehrlich Foundation, for his research on the immune system. For the first time since 1996, the prize goes to a scientist working in Germany. Dr Reth is Professor for Molecular Immunology at the Institute of Biology III of the University of Freiburg and Scientific Director of the Cluster of Excellence BIOSS, Centre for Biological Signalling Studies. He is also head of the department for Molecular Immunology at the Max Planck Institute of Immunobiology and Epigenetics (MPI-IE). The prize is endowed with €100,000 and is one of the highest honours in science in Germany. By awarding the prize to Dr Reth, the Foundation has chosen to honour a scientist who, like Nobel laureate Paul Ehrlich, decodes how immunity operates at a molecular level, in order to find new therapies for cancer and infectious diseases. “This award is a great honour for me, because I deeply admire Paul Ehrlich’s work in immunology,” Dr Reth said. “He was one of the first scientists to consider the molecular level in this field.” Following Ehrlich’s scientific tradition, Dr Reth chose to focus his research on how the human body recognises foreign substances. “Due to the success of vaccinations, which was one of the greatest achievements in medicine, immunology has been an applied science from the beginning. However, we still do not fully understand the processes that underlie immunisation,” Dr Reth remarks. That is why his research revolves around the B cell component of the immune system. When activated, these blood cells produce antibodies to fight off infection. Dr Reth investigates the structure and organisation of the B cell antigen receptors. These molecules on the surface of B cells recognise foreign substances, so-called antigens, and trigger the activation of the immune system. Dr Reth was able to describe the basic structure of the antigen receptor of B cells for the first time in 1989. Together with his research group, he developed a new model for the activation of this receptor and recently provided further experimental evidence for this model. Furthermore Dr Reth has shown that receptors on the plasma membrane have a more complex structure than previously assumed. They are not freely diffusing on the cell surface but are organized in 50 to 150 nanometre sized membrane patches also called protein islands. The detailed analysis of the organization of receptors on the cellular membrane is a focus of research at the BIOSS Centre for Biological Signalling Studies, the cluster of excellence directed by Dr Reth since 2007. Located in the Signalhaus in Freiburg, BIOSS brings together engineers and biologists to investigate signalling processes using methods of synthetic biology. In the spirit of BIOSS’s motto “from analysis to synthesis”, researchers re-construct signalling cascades or develop new kinds of systems altogether - for example, hydrogels that release medication in a temporally controlled way, or signalling proteins that can be switched on and off with light. About Michael Reth: In 1989 Michael Reth joined Nobel laureate George Köhler’s laboratory at the MPI and later on was appointed Chair of Molecular Immunology at the University of Freiburg. He was awarded the Gottfried Willhelm Leibniz Prize of the German Research Foundation in 1995 and the EFIS-Schering-Plough European Immunology Prize in 2009. In 2012, Michael Reth was awarded an advanced grant by the European Research Council (ERC).

Affiliations and Expertise

Albert-Ludwigs University Freiburg, Germany

Andreas Radbruch

Andreas Radbruch did his PhD at the Genetics Institute of the Cologne University, Germany, with Klaus Rajewsky. He later became Associate Professor there and was a visiting scientist with Max Cooper and John Kearney at the University of Alabama, Birmingham. In 1996, he became Director of the German Rheumatism Research Centre Berlin, a Leibniz Institute, and in 1998, Professor of Rheumatology at the Charité, the Medical Faculty of the Humboldt University of Berlin. A biologist by education, Andreas Radbruch early on worked on somatic variants in myeloma and hybridoma cells lines, modeling antibody class switching and somatic hypermutation. In this context, his lab originally developed the MACS technology. Andreas Radbruch then showed that recombination is the physiological mechanism of class switching in vivo, in plasmablasts isolated ex vivo. Moreover, he could show that in vivo, class switch recombination is targeted to the same Ig class on both IgH loci of a cell, reflecting a tight control of targeting of recombination. An essential element of this control is transcription of recombinogenic sequences, and the processing of these switch (germline) transcripts, as became evident from targeted deletion of the control regions involved. The switch transcripts are induced by cytokines of T helper cells, e.g. interleukin-4. The Radbruch lab contributed essentially to our current understanding of the polarization and imprinting of T helper cells expressing interleukin-4 (Th2) versus those expressing interferon-? (Th1). The lab then addressed the organization of immunological memory as such. First they identified longlived (memory) plasma cells, mostly residing in bone marrow but also in secondary lymphoid organs and in inflamed tissues. They could show that these cells individually persist in dedicated survival niches, organized by CXCL12-expressing mesenchymal stroma cells. They identified different, dedicated niches for CD4+ and CD8+ memory T cells in the bone marrow, too, and could show that, at least in immune responses to vaccines, memory T cells are mostly maintained in bone marrow, resting in terms of proliferation and gene expression. Thus memory niches organize and maintain memory, and bone provides a privileged environment for resting memory cells. In chronic antibody-mediated diseases, Andreas Radbruch´s lab identified pathogenic antibody-secreting memory plasma cells as critical mediators of chronicity, refractory to conventional immunosuppression, and thus representing a novel therapeutic target. Similarly, in chronic T cell-mediated diseases, the pathogenic T cells induce and adapt to chronicity. Recently, the Radbruch group has identified Twist1, HopX and the microRNAs miR-182 and miR148a as molecular adaptations of proinflammatory T cells to chronicity, and innovative therapeutic targets. Andreas Radbruch´s work has been recognized by the Carol Nachman Prize for Rheumatology (2011), an Advanced Grant of the European Research Council (ERC, 2010), the Federal Cross of Merit (2008) and the Aronson Award (2000). He is a member of the Berlin-Brandenburg Academy of Sciences and Humanities (BBAW), the European Molecular Biology Organization (EMBO) and the German National Academy of Sciences Leopoldina.

Affiliations and Expertise

Deutsches Rheuma-Forschungszentrum, Germany

Frederick Alt

Frederick Alt received his Ph.D. in Biology from Stanford University in 1977 where he worked with Robert Schimke and discovered gene amplification and genomic instability in mammalian cancer cells. Alt moved to MIT for postdoctoral work with David Baltimore, where he helped elucidate basic principles of recombination in the immune system. His work with Baltimore included the discovery that production of membrane versus secreted immunoglobulin is achieved via differential RNA processing and the discovery that allelic exclusion of Immunoglobulin (Ig) gene rearrangements is controlled by feedback from protein products. With Baltimore, Alt also elucidated major aspects of the V(D)J recombination mechanism, including involvement of site-specific DNA double strand breaks (DSBs) that are end joined, and the discovery of ”N” regions, which represent a major source of antigen receptor diversity. Dr. Alt moved to Columbia University in 1982 as Assistant Professor of Biochemistry. He became Professor of Biochemistry and Molecular Biophysics in 1985 and HHMI Investigator in 1987. At Columbia, he established the role of Ig chains in regulating B cell development and discovered that antigen receptor genes are assembled by a common V(D)J recombinase. He then elucidated a role for non-coding gene transcription and "chromatin accessibility" as means to target the lineage, stage, and allele specific activity of the V(D)J recombinase. He extended that work to show that IgH class switch recombination (CSR) is B cells to particular IgH classes is directed by activation of non-coding transcription units that contain the CSR target sequences. At Columbia, he also discovered N-myc, based on its amplification in human neuroblastomas and he characterized the Myc cellular oncogene family. In 1991, Dr. Alt moved to Boston Children' Hospital (BCH) and Harvard Medical School as a Professor of Genetics and HHMI Investigator. He also became a Senior Investigator at the Immune Disease Institute (IDI). He was appointed Charles A. Janeway Professor of Pediatrics in 1993, Scientific Director of IDI in 2005, and Director of the Program in Cellular and Molecular Medicine (PCMM) at Children's Hospital in 2008. He also became President of IDI in 2010 and continues to serve as director since the merger of IDI with BCH where it remains the PCMM. At CHB and IDI, Dr. Alt's group confirmed his earlier proposal with Baltimore that N regions are added by terminal dexoynucleotidyl transferase, demonstrating that TdT is a V(D)J recombinase component. They also discovered that the joining activity of the V(D)J recombinase is carried out by a multi-component general cellular non-homologous DNA end joining (NHEJ) pathway. Subsequently, Dr. Alt was involved in the discovery of a number of the NHEJ factors and he then went on to discover the key role of NHEJ proteins in maintenance of genomic stability. Dr. Alt continues to elucidate many new aspects of the mechanism and control of V(D)J recombination and IgH CSR and also continues to elucidate mechanisms that generate and suppress genomic instability, most recently through development of high through-put methods to study DSBs and chromosomal translocations. In 1994, Dr. Alt was elected to the U.S. National Academy of Sciences, the American Academy of Arts and Sciences, and the American Academy of Microbiology; in 1999 he was elected to the European Molecular Biology Organization; in 2010 he was elected a Fellow of the American Association for Advancement of Sciences; and in 2011 he was elected to the Institute of Medicine. In 2004, Alt received the Clowes Memorial Award from AACR; in 2005 he received the Rabbi Shai Shacknai Prize from Hebrew University, the Pasarow Foundation Prize for Extraordinary Achievement in Cancer Research, the Leukemia & Lymphoma Society de Villiers International Achievemen

Affiliations and Expertise

Harvard Medical School, Boston, MA, USA

View additional works by Frederick Alt

Molecular Biology of B Cells, 2nd Edition

  • Dedication
  • Preface
  • Chapter 1. The Structure and Regulation of the Immunoglobulin Loci
    • 1. Introduction
    • 2. Genomic Organization of the Mouse Immunoglobulin Heavy Chain Locus
    • 3. Genomic Organization of the Mouse Immunoglobulin Kappa Light Chain Locus
    • 4. Genomic Organization of the Mouse Immunoglobulin Lambda Light Chain Locus
    • 5. B Cell Development and Regulation of V(D)J Recombination
    • 6. Junctional Diversity
    • 7. Combinatorial Diversity
    • 8. Noncoding Transcription and Immunoglobulin Locus Rearrangement
    • 9. The Process of Dh-Jh Recombination
    • 10. Epigenetics and Immunoglobulin Locus Rearrangement
    • 11. Insulators and Immunoglobulin Locus Rearrangement
    • 12. 3D Structure and Compaction of the Immunoglobulin Heavy Chain Locus
    • 13. Conclusion
  • Chapter 2. The Mechanism of V(D)J Recombination
    • 1. Overview
    • 2. Antigen Receptor Gene Assembly
    • 3. Recombination Signal Sequences
    • 4. Biochemistry of V(D)J Cleavage
    • 5. RAG1 and RAG2
    • 6. A Role for HMGB1 in V(D)J Recombination
    • 7. Recombination Complexes: Analysis of Stoichiometry and Organization
    • 8. V(D)J Recombination Is Tightly Regulated during Lymphocyte Development
    • 9. Accessibility Model of Regulation
    • 10. Overview of Chromatin Structure
    • 11. Regulation by Nucleosome Structure and Histone Acetylation
    • 12. Regulation by Histone Methylation
    • 13. How Is the Chromatin Structure of Antigen Receptor Loci Developmentally Regulated?
    • 14. Additional Layers of Regulation
    • 15. Regulation of V(D)J Recombination: Summary
    • 16. Oncogenic Lesions in Lymphoid Neoplasms: The Price of a Diverse Antigen Receptor Repertoire
    • 17. Proposed Mechanisms Underlying RAG-Mediated Genomic Lesions
    • 18. Regulatory Controls Proposed to Suppress RAG-Mediated Genomic Instability
    • 19. V(D)J Recombination Errors as Pathogenic Lesions in Lymphoid Neoplasms: Summary
  • Chapter 3. Transcriptional Regulation of Early B Cell Development
    • 1. PU.1 Sets the Stage for Lymphoid and Myeloid Development
    • 2. Lineage Priming in Lymphoid Progenitors by Ikaros
    • 3. E2A Regulates the Chromatin Landscape to Promote Gene Expression in B Cell Development
    • 4. E2A Is Inhibited by Id Proteins
    • 5. Interleukin-7/Stat5 Signaling Provides an Early Signal for B Cell Lineage Specification
    • 6. Early B Cell Factor: Central Coordinator of B Cell Development
    • 7. Collaboration between EBF1 and Foxo1
    • 8. Regulation of the B Cell-Specific Program by Pax5
    • 9. Regulation of B Lineage Commitment
    • 10. Conclusion
  • Chapter 4. Relationships among B Cell Populations Revealed by Global Gene Analysis
    • 1. Introduction
    • 2. Gene Profile Changes with B Cell Maturation Suggest an Ordering of Transitional Stages
    • 3. Distinctions in Gene Networks Activated in Mature B Cell Populations
    • 4. Fo/B2 B Cells in Different Tissues are Similar, but Specialization with Location Emerges
    • 5. Conclusions
  • Chapter 5. Roles of MicroRNAs in B Lymphocyte Physiology and Oncogenesis
    • 1. Introduction
    • 2. Control of Cell Survival and Proliferation by Mir-17~92 in B Cell Development and Lymphomagenesis
    • 3. The Problem of MiRNA Target Identification and Validation
    • 4. Mir-155 in Germinal Center B Cells and Lymphomagenesis
    • 5. Discovery of an Elusive Tumor Suppressor: Mir-15a~16-1 Cluster
    • 6. Lin28b Regulates the Fetal-Adult B Cell Development Switch
    • 7. To Be Further Determined
    • 8. Concluding Remarks
  • Chapter 6. Proliferation and Differentiation Programs of Developing B Cells
    • 1. Proliferation and Differentiation Programs at the Pro-B Cell Stage
    • 2. Proliferation and Differentiation Programs at the Pre-B Cell Stage
    • 3. Selection Mechanisms at the Immature B Cell Stage
  • Chapter 7. Development and Function of B Cell Subsets
    • 1. Introduction
    • 2. B-1, Marginal Zone and Follicular B Cells
    • 3. Mechanisms for the Compartmentalization of B-Cell Subsets
    • 4. Selection and Differential Survival Mechanisms: BCR Signaling, Composition, and Specificity
    • 5. Other Factors Involved in the Formation of B-Cell Subsets
    • 6. Homeostasis of B-Cell Subsets and Repertoires
    • 7. Conclusion
  • Chapter 8. B Cells and Antibodies in Jawless Vertebrates
    • 1. Introduction
    • 2. Lampreys and Hagfish Have Three Types of VLR Genes
    • 3. VLR Gene Assembly Mechanism and Sequence Diversity
    • 4. Lamprey CDA1 and CDA2
    • 5. VLRA, VLRB, and VLRC Are Expressed by Different Lymphocyte Populations
    • 6. Characterization of B-Like and Two T-Like Lymphocyte Populations in Cyclostomes
    • 7. VLRA+, VLRB+, and VLRC+ Cells Have Distinct Gene Expression Profiles
    • 8. Generation of the T-Like and B-Like Cells in Lampreys
    • 9. The Unique Structure of VLRB Antibodies
    • 10. VLRB Monoclonal Antibodies
    • 11. Structure of VLR Antigen-Binding Domains
    • 12. Structures of VLRB Antibody-Antigen Complexes
    • 13. Conclusion
  • Chapter 9. The Origin of V(D)J Diversification
    • 1. The Alien Seed
    • 2. The Evolution of BCR and TCR Loci
    • 3. Considerations on the ur-V Gene
    • 4. Concluding Remarks
  • Chapter 10. Structure and Signaling Function of the B-Cell Antigen Receptor and Its Coreceptors
    • 1. Introduction
    • 2. Basic Structure of the BCR Complex
    • 3. BCR Activation Models
    • 4. The Resting State of the BCR
    • 5. Interaction of the BCR with Signal-Transducing Kinases and Adaptors
    • 6. BCR Coreceptors CD19 and CD22
    • 7. CD19 Functions in a Complex with CD21 and CD81
    • 8. Signaling by the CD19 Tail
    • 9. Human Mutations in the CD19/Cd21/Cd81 Complex
    • 10. CD22: An Inhibitory Receptor
    • 11. Regulation of CD22 Signaling by Ligand Interactions
    • 12. The Role of CD22 in Preventing Autoimmunity
    • 13. BCR-Controlled Signaling Processes
    • 14. BCR-Mediated Adaptor and PLCy2 Activation
    • 15. IP3 Promotes Calcium Release and Activation of Nuclear Factor of Activated T Cells
    • 16. DAG and Nuclear Factor-?B Activation
    • 17. Activation of the PI3K Pathway
    • 18. Akt and Foxo Regulation
  • Chapter 11. Fc and Complement Receptors
    • 1. Consequences of FCyRIIB Deficiency
    • 2. Consequences of Complement and Complement Receptor Deficiencies
    • 3. FC Receptors
    • 4. Complement Receptors
    • 5. Coreceptor Signaling versus Antigen Localization to FDCs
    • 6. Frontiers: Complement versus FC Receptors
  • Chapter 12. B Cell Localization and Migration in Health and Disease
    • 1. Introduction
    • 2. Migration of B Cells in the Bone Marrow
    • 3. Migration of B Cells into and within SLOs
    • 4. Location and Migration of Antibody-Secreting Cells
    • 5. Body Cavity B-1 B Cell Trafficking
    • 6. Mucosal B Cell Migration
    • 7. Homing of B Cells during Chronic Inflammation and Tertiary Lymphoid Organ Formation
    • 8. Migration of Neoplastic B Cells
    • 9. Conclusion
  • Chapter 13. B Cells as Regulators
    • 1. Introduction
    • 2. Regulatory Role of B Cells in UC
    • 3. Protective Function of B Cells in EAE
    • 4. Regulatory Roles of B Cells in Systemic Lupus Erythematosus
    • 5. Regulatory Role of B Cells in Bacterial Infections
    • 6. Characterization and Function of IL-10-Producing B Cells in Humans
    • 7. Concluding Remarks
    • Conflict of Interest
  • Chapter 14. B Cell Memory and Plasma Cell Development
    • Chapter 14a. Generation of Memory B Cells
    • Chapter 14b. Plasma Cell Biology
    • Chapter 14c. Memory Plasma Cells
  • Chapter 15. The Role of the BAFF and Lymphotoxin Pathways in B Cell Biology
    • 1. BAFF/APRIL: Important Regulators of B Cell Survival, Homeostasis, and Function
    • 2. The Lymphotoxin Pathway: Shaping B Cell Environments
    • 3. Conclusions and Perspectives
  • Chapter 16. The Mucosal Immune System: Host-Bacteria Interaction and Regulation of Immunoglobulin A Synthesis
    • 1. Introduction
    • 2. Geography, Regulation, and Properties of Gut Immunoglobulin A
    • 3. Synthesis of Gut Immunoglobulin A
    • 4. T Cell-Dependent Immunoglobulin A Induction
    • 5. T Cell-Independent Immunoglobulin A Induction
    • 6. Function of Immunoglobulin A
    • 7. Clinical Relevance
    • 8. Conclusions
  • Chapter 17. Gut Microbiota and Their Regulation
    • 1. Microbiota
    • 2. Microbes, Primary Ig Diversification, and Early Life B Cell Selection
    • 3. Microbial Influence on IgA Production
    • 4. Microbial Influence on IgE Production
    • 5. B-Lineage Cell Influence on Commensal Microbes
    • 6. Concluding Remarks
  • Chapter 18. Molecular Mechanisms of AID Function
    • 1. Introduction
    • 2. AID Structure and Function
    • 3. AID’s Molecular Mechanism of DNA Cleavage and Recombination
    • 4. The Mechanism of AID’s Specificity Determination for DNA Cleavage
    • 5. Regulation of AID Expression
    • 6. Concluding Remarks
  • Chapter 19. The Mechanism of IgH Class Switch Recombination
    • 1. Antibody Class
    • 2. Organization of Mouse IgH Locus
    • 3. A Two-Step Model of CSR
    • 4. Mechanisms by Which AID Initiates CSR and SHM
    • 5. Germline S Region Transcription Targets AID Activity during CSR
    • 6. Role of Transcription Stalling in AID Targeting
    • 7. AID Cofactors Facilitate AID Access to Its ssDNA Substrates
    • 8. Differential AID Targeting and Outcomes during CSR and SHM
    • 9. Long-Range Joining of S Region Breaks
    • 10. Classical Nonhomologous End Joining
    • 11. Alternative End Joining
    • 12. Chromosomal Translocation in Lymphomas Caused by Aberrant CSR
    • 13. Evolution of the IgH CSR Mechanism
  • Chapter 20. Somatic Hypermutation: The Molecular Mechanisms Underlying the Production of Effective High-Affinity Antibodies
    • 1. Introduction
    • 2. Activation-Induced Cytidine Deaminase in Somatic Hypermutation
    • 3. Targeting of the SHM
    • 4. Activation-Induced Cytidine Deaminase and Downstream Repair Pathways
    • 5. Mismatch Repair in Somatic Hypermutation
    • 6. Base Excision Repair in Somatic Hypermutation
    • 7. Conclusion
  • Chapter 21. Aberrant AID Expression by Pathogen Infection
    • 1. Introduction
    • 2. Physiologic Role of Activation-Induced Cytidine Deaminase
    • 3. AID Induction in B Cells
    • 4. Regulation of AID Expression in B Cells
    • 5. Aberrant AID Expression by Pathogen Infection and Tumorigenesis
    • 6. Conclusion
  • Chapter 22. Molecular Pathogenesis of B Cell Lymphomas
    • 1. Introduction
    • 2. The Cell of Origin of Lymphomas
    • 3. Mechanisms of Genetic Lesion in Lymphoma
    • 4. Molecular Pathogenesis of Most Common Lymphoma Types
  • Chapter 23. B Cells Producing Pathogenic Autoantibodies
    • 1. Origin of Autoantibodies
    • 2. Immunodeficiency, B Cell Malignancy, and Autoreactivity
    • 3. Features of Pathogenic Autoantibodies
    • 4. Effector Mechanisms of Pathogenic Autoantibodies
    • 5. B Cells as the Therapeutic Target in Autoimmune Disease
    • 6. Conclusion
  • Chapter 24. The Cellular and Molecular Biology of HIV-1 Broadly Neutralizing Antibodies
    • 1. Introduction
    • 2. Highly Conserved Structures on HIV-1 Env
    • 3. Mechanisms of HIV-1 Neutralization by Antibodies
    • 4. Role of Neutralizing Antibodies in Protection from HIV-1 Transmission
    • 5. Biology of Broad Neutralizing Antibody Development
    • 6. Characteristics of HIV-1 Env Neutralizing Antibodies
    • 7. HIV-1 Env Antibodies Induced by Current HIV Vaccine Candidates
    • 8. New Strategies for Induction of HIV-1 bnAbs
    • 9. Summary
  • Chapter 25. Immune Deficiencies Caused by B Cell Defects
    • 1. Defects in B Cell Development
    • 2. Defects in B Cell Migration
    • 3. Defects in B Cell Survival
    • 4. Defects in B Cell Activation
    • 5. PADs with Unknown Etiology
    • 6. Therapeutic Approaches
    • 7. Conclusion
  • Chapter 26. IMGT® Immunoglobulin Repertoire Analysis and Antibody Humanization
    • 1. IMGT® and the Birth of Immunoinformatics
    • 2. Fundamental Information from IMGT-ONTOLOGY Concepts
    • 3. IMGT® Immunoglobulin Repertoire Analysis
    • 4. IMGT® Antibody Engineering and Humanization
    • 5. Conclusion
    • 6. Availability and Citation
  • Chapter 27. Anti-Interleukin-6 Receptor Antibody Therapy Against Autoimmune Inflammatory Diseases
    • 1. Interleukin-6 and Its Receptor System
    • 2. Pleiotropic Activity of IL-6
    • 3. Regulation of IL-6 Synthesis
    • 4. Dysregulated Persistent IL-6 Synthesis Has a Pathologic Role in the Development of Various Diseases
    • 5. A Humanized Anti-IL-6 Receptor Antibody for Treatment of Autoimmune Inflammatory Diseases
    • 6. Interleukin-6 Blockade Affects B- and T-Cell Function In Vivo; Lessons from Tocilizumab Treatment
    • 7. Concluding Remarks
    • 8. Conflict of Interest
  • Chapter 28. Targeting the IL-17/IL-23 Axis in Chronic Inflammatory Immune-Mediated Diseases
    • 1. Introduction
    • 2. The IL-17 Family
    • 3. IL-17 Receptor/Pathway
    • 4. TH17 Cell Differentiation
    • 5. Cellular Sources and Targets
    • 6. the role of the il-17/23 axis in immune-mediated inflammatory diseases
    • 7. Crohn’s Disease
    • 8. Psoriasis
    • 9. Psoriatic Arthritis
    • 10. Ankylosing Spondylitis
    • 11. Summary
  • Chapter 29. Discovery and Development of Anti-TNF Therapy: Pillar of a Therapeutic Revolution
    • 1. Introduction
    • 2. How Was TNF Defined as a Therapeutic Target?
    • 3. Establishing the Clinical Utility of Anti-TNF Therapy
    • 4. Proof of Efficacy
    • 5. Optimizing Long-term Use
    • 6. Phase III Clinical Trials
    • 7. Conclusions
  • Index

Quotes and reviews

"...comprehensively describes how B cells are generated, selected, activated, and engaged in antibody production and the normal immune response...This field has seen rapid advances...and it is an excellent resource. Score: 83 - 3 Stars" --Doody's
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