Follicular B cells articles from across Nature Portfolio

CREBBP and KMT2D mutations frequently co-occur in B cell lymphomas with unclear significance. Here the authors show that they cooperate to skew B cell fate decisions and induce a CD8-depleted immune-evasive microenvironment to facilitate lymphomagenesis.

An antigen-specific in vitro germinal center system based on the use of just two cell types, B cells and CD4+ T cells, is developed to study antigen-specific germinal center reactions and T cell help to cognate versus bystander B cells.

COVID-19 booster immunizations aimed at spike protein from new SARS-CoV-2 variants induce robust germinal centre B cell responses against the original spike protein, as well as de novo B cell responses against the variant spike protein.

Follicular and marginal zone B (FoB and MZB, respectively) cells have divergent metabolic characteristics. Here the authors show that deficiency of glutamate cysteine ligase (Gclc), the enzyme for glutathione synthesis, differentially impacts FoB and MZB homeostasis, while specifically impeding FoB activation and downstream antiviral immunity.

Pathways of glycan-mediated B cell suppression during pregnancy are important for promoting fetomaternal tolerance.

Elemento, Melnick and colleagues examine the chromatin and transcriptional changes that occur during differentiation of human primary B cells into antibody-secreting cells. In naive B cells, the transcription factor OCT2 is preloaded at high-affinity super-enhancer sites present in repressed ‘silent’ chromatin; upon activation, OCAB is recruited to these regions, where it facilitates arrays of OCT2 binding to lower-affinity octamer motifs, leading to active formation of germinal center B cell-specific super-enhancers.

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

To trigger an adequate humoral immune response while ensuring self-tolerance, B cell activation is tightly controlled. A new study indicates that an NR4A-enforced built-in brake fine-tunes the early phase of transcriptional reprogramming induced by BCR stimulation.

Follicular helper T cells (T_FH cells) sequentially acquire the potential to secrete interleukin 21 (IL-21) and IL-4. The shift from secretion of IL-21 to that of IL-4 modifies the nature of the 'help' signals delivered by T_FH cells to germinal center (GC) B cells.

Inflammation disrupts the organization of subcapsular sinus macrophages, impairing the B cell response to secondary infections.