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Tarlinton and colleagues show that the antiapoptotic protein Mcl1 is essential for plasma cell survival and is induced by BCMA signaling in bone marrow, but not spleen, plasma cells.

Chronic viral infection leads to a dysregulation of germinal center B cell responses. Di Pietro et al. show that the epigenetic modifier BMI-1 promotes this dysfunctional response and that targeting BMI-1 in B cells can restore humoral immunity and accelerate viral clearance.

Koala retroviruses are models of transposable element colonization of germlines. By mapping their integration sites in koala pedigrees, this study provides genetic risk scoring for breeding decisions and documents rates of acquisition and loss of retroviral integrations across generations.

Follicular helper T cells provide help to cognate B cells in germinal centers to boost humoral immunity. Nutt and colleagues generate IL-21–GFP reporter mice to track the fate of follicular helper T cells.

PRMT1 is an arginine methyltransferase involved in a variety of cell functions. Here the authors delete PRMT1 specifically in mature B cells to show the importance of arginine methylation for B cell proliferation, differentiation and survival, and thereby for humoral immunity.

How IL-21 functions during development of high affinity antibody in germinal centres (GC) is not fully known. Here using a cell cycle reporter mouse, the authors show that IL-21 promotes cell cycle progression within the GC light zone and enables release from the G1 cell cycle stage.

Tracking B cells in germinal centres — hotspots of B-cell proliferation and mutation during an immune response — reveals that those cells presenting the most antigen on their surface are programmed to dominate. See Letter p.637

Deep-sequencing analyses of immunoglobulin variable-segment genes from antibody-secreting cells have allowed comparisons of conventional immunization responses to disease flares experienced by patients with systemic lupus erythematosus. Such analyses provide insight into B cell recruitment and differentiation processes yielding expanded clones that contribute to this complex autoimmune disease.

The inflammatory cytokine interleukin 17, normally considered a T cell–associated factor, is now reported to be the central participant driving the development of germinal center–derived autoantibodies in a model disease setting.

Bronchus-associated lymphoid tissue (BALT), which develops in the lung during infancy before declining over childhood, supports localized immune reactions against airway infections in early life including the generation of germinal center-like B cells specific for respiratory pathogens.

B cell–T cell interactions in germinal centers are needed to generate high-affinity antibodies. PD-1 signaling is now shown to influence the quality of germinal center responses.

Effective vaccines elicit neutralizing antibodies and long-lasting memory, but this can be challenging with some pathogens, such as HIV. A new study shows how a slow-delivery protein immunization strategy administered in dose-escalation format over 12 days increased the durability of germinal centers and improved immunological outcomes.

The study of B cell biology is a mature field, but highlights from the past year remind us that there are still many exciting and unexpected things to be discovered in terms of B cell responses to antigen, germinal centres and plasma cells.

Expression of a competent Igh heavy chain initiates a pre-BCR checkpoint during B cell development. Reth and colleagues show that protein arginine methylation by a BTG2-PRMT1 complex is required to inactivate CDK4 and thereby establish pre-B cell arrest.

Certain bats species have previously been identified as ancestral sources of coronaviruses that infect humans but there is limited data on the genomic diversity or zoonotic potential of viruses infecting bats in the UK. Here, the authors use deep sequencing and in vitro assays to characterise coronaviruses recovered from 48 bat faecal samples.

B cells rewire complement for optimal germinal center responses. When B cell C3 activity is limited, germinal centers collapse and outputs are impaired.

B cells are thought to divide asymmetrically to generate distinct lineages required for adaptive immunity. Hawkins et al. find that surprisingly, mice lacking components of a complex required for asymmetric cell division display normal responses to vaccination and viral infection.

The terminal differentiation of antibody-secreting cells is controlled by a network of antagonistic transcription factors and, although it is highly complex, this process can be explained by a simple probabilistic differentiation process.

Koalas are susceptible to neoplasms, which are related to infection with the Koala retrovirus. Here, the authors use DNA sequencing to show that the retroviral insertion sites cluster near known cancer genes and demonstrate a high mutational load associated with the germline invasion of the virus.

In this Opinion article, a new model for the generation and the maintenance of memory B cells is proposed. The model involves these cells being continuously produced by the germinal centre throughout an immune response, with B cells that are produced later in the response being fitter and therefore having a survival advantage.

B cell development is tightly regulated in a stepwise manner to ensure proper generation of repertoire diversity via somatic gene rearrangements. Here, the authors show that a transcription factor, Erg, functions at the earliest stage to critically control two downstream factors, Ebf1 and Pax5, for modulating this gene rearrangement process.

Histone deaceytelase inhibitors are used in the treatment of haematological malignancies but can also act as modulators of the immune system. Here, the authors show that histone deaceytelase inhibitors are capable of modulating B-cell functions leading to improved outcome in autoimmune conditions.

Immune surveillance has been proposed to eliminate transformed cells and thereby limit tumor formation. Axel Kallies and colleagues now report that spontaneous B cell lymphoma development in Blimp1-deficient or Bcl6-overexpressing mice is accelerated by T cell deficiency and identify the Fas-Fas ligand pathway as a crucial mediator of T cell control of lymphoma growth.

Although important for early development, PU.1 is dispensable for mature B cell function, possibly owing to compensation by the related transcription factor SpiB. Here the authors show PU.1 and SpiB are collectively required for humoral immunity, through regulation of germinal centre formation and plasma cell differentiation.

Fas ligand (FasL) and its receptor Fas are critical for the shutdown of chronic immune responses and prevention of autoimmunity. FasL function is regulated by deposition in the plasma membrane and metalloprotease-mediated shedding, but it is unclear what the respective roles of these secreted and membrane-bound forms are. Gene-targeted mice that selectively lack either secreted FasL or membrane-bound FasL are now generated, shedding light on this problem.

The process of B cell differentiation into plasma cells involves dramatic cellular reprogramming. Corcoran and colleagues profile the transcriptome of all stages of B cell differentiation through to antibody-secreting plasma cells.