Germinal centers: programmed for affinity maturation and antibody diversification

Bannard, Oliver; Cyster, Jason G.

doi:10.1016/j.coi.2016.12.004

Cited by 170 publications

(185 citation statements)

References 72 publications

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“…Helper T cells shape and orchestrate immune responses through direct cellular interactions and soluble factors. For example, direct TCR:MHC‐II interactions result in the selection of high‐affinity B cell clones in germinal centers via CD40‐CD40L interactions 3 . As APC, B cells can engage in this direct communication with CD4 + T cells.…”

Section: T Helper Immunity In the Context Of Cancer Immunotherapymentioning

confidence: 99%

Harnessing neoantigen specific CD4 T cells for cancer immunotherapy

Brightman

Naradikian

Miller

et al. 2020

Journal of Leukocyte Biology

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The goal of precision immunotherapy is to direct a patient's T cell response against the immunogenic mutations expressed on their tumors. Most immunotherapy approaches to‐date have focused on MHC class I‐restricted peptide epitopes by which cytotoxic CD8+ T lymphocytes (CTL) can directly recognize tumor cells. This strategy largely overlooks the critical role of MHC class II‐restricted CD4+ T cells as both positive regulators of CTL and other effector cell types, and as direct effectors of antitumor immunity. In this review, we will discuss the role of neoantigen specific CD4+ T cells in cancer immunotherapy and how existing treatment modalities may be leveraged to engage this important T cell subset.

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Section: T Helper Immunity In the Context Of Cancer Immunotherapymentioning

confidence: 99%

Harnessing neoantigen specific CD4 T cells for cancer immunotherapy

Brightman

Naradikian

Miller

et al. 2020

Journal of Leukocyte Biology

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“…80 GC B cells harboring this BCR are actively deleted, but they can be While receptor editing in the bone marrow takes place via Ragmediated VJl recombination, 86,87 such Rag reexpression is unlikely to occur in the GC. 80 GC B cells harboring this BCR are actively deleted, but they can be While receptor editing in the bone marrow takes place via Ragmediated VJl recombination, 86,87 such Rag reexpression is unlikely to occur in the GC.…”

Section: Autore Ac Tivit Y In the G Cmentioning

confidence: 99%

Plasma cell differentiation during the germinal center reaction

Ise

Kurosaki

2019

Immunological Reviews

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Summary Germinal centers (GCs) are formed in secondary lymphoid tissues upon immunization with T‐dependent antigens. In GCs, somatic hypermutation generates B cells with increased antibody affinity and these high‐affinity B cells preferentially differentiate into plasma cells, which home to bone marrow and confer long‐lived humoral immunity. Recent studies have shed new light on the cellular and molecular basis for initiating the transition from a GC B cell to a plasma cell. Here, we review recent progress in our understanding of how plasma cell generation during the GC reaction is regulated for inducing effective long‐term protective immunity and for preventing harmful autoimmunity.

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“…We now understand that MBCs develop in secondary lymphoid organs such as the spleen and lymph nodes (2–5) (Figure 1). Naïve B cells encounter antigens in the follicles in many cases as immune complexes or complement fixed antigens bound to Fc receptors, complement receptors or scavenger receptors on the surface of dendritic cells (DC).…”

Section: Introductionmentioning

confidence: 99%

Atypical memory B cells in human chronic infectious diseases: An interim report

Portugal

Obeng-Adjei

Moir

et al. 2017

Cellular Immunology

165

177

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Immunological memory is a remarkable phenomenon in which survival of an initial infection by a pathogen leads to life-long protection from disease upon subsequent exposure to that same pathogen. For many infectious diseases, long-lived protective humoral immunity is induced after only a single infection in a process that depends on the generation of memory B cells (MBCs) and long-lived plasma cells. However, over the past decade it has become increasingly evident that many chronic human infectious diseases to which immunity is not readily established, including HIV-AIDS, malaria and TB, are associated with fundamental alterations in the composition and functionality of MBC compartments. A common feature of these diseases appears to be a large expansion of what have been termed exhausted B cells, tissue-like memory B cells or atypical memory B cells (aMBCs) that, for simplicity’s sake, we refer to here as aMBCs. It has been suggested that chronic immune activation and inflammation drive the expansion of aMBCs and that in some way aMBCs contribute to deficiencies in the acquisition of immunity in chronic infectious diseases. Although aMBCs are heterogeneous both within individuals and between diseases, they have several features in common including low expression of the cell surface markers that define classical MBCs in humans including CD21 and CD27 and high expression of genes not usually expressed by classical MBCs including T-bet, CD11c and a variety of inhibitory receptors, notably members of the FcRL family. Another distinguishing feature is their greatly diminished ability to be stimulated through their B cell receptors to proliferate, secrete cytokines or produce antibodies. In this review, we describe our current understanding of the phenotypic markers of aMBCs, their specificity in relation to the disease-causing pathogen, their functionality, the drivers of their expansion in chronic infections and their life span. We briefly summarize the features of aMBCs in healthy individuals and in autoimmune disease. We also comment on the possible relationship of human aMBCs and T-bet+, CD11c+ age/autoimmune-associated B cells, also a topic of this review volume.

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Germinal centers: programmed for affinity maturation and antibody diversification

Cited by 170 publications

References 72 publications

Harnessing neoantigen specific CD4 T cells for cancer immunotherapy

Harnessing neoantigen specific CD4 T cells for cancer immunotherapy

Plasma cell differentiation during the germinal center reaction

Atypical memory B cells in human chronic infectious diseases: An interim report

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