B-1 cells

Intrarenal B cells are indicative of poor prognosis in human renal allografts. Here the authors use single cell RNA sequencing to examine how intrarenal B cells contribute to renal rejection and find a population of innate B cells reactive to renal-specific or inflammation-associated antigens.

CTLA-4 is an important co-inhibitory receptor for T cells. Here, the authors show that CTLA-4 also has a function on B-1a cells, as conditional deletion results in activation of these cells and knockout mice develop an autoimmune profile.

B-1a B cells are innate-like cells with biased reactivity to bacteria and self-antigens. Here the authors show that reduced interleukin-7 in developing fetal liver-derived pro-B cells induces premature immunoglobulin κ rearrangement, alleviating the requirement for a pre-BCR selection stage and allowing the generation of autoreactive B1-a B cells.

B cells are important for antigen presentation and antibody production in humoral immunity, but are also increasingly recognized for their immune regulatory functions. Here the authors show that HIF-1α, a hypoxia-induced transcription factor, is important for controlling IL-10 induction in and immune-suppressive activity of B cells.

Fat-associated lymphoid clusters (FALC) in the serous cavities house rapid IgM-producing B1 cells, but how the clusters are activated to respond to infection is unclear. Here the authors show that in response to lung inflammation or pleural nematode infection adipose stromal cell-derived IL-33 activates ILC2s to produce IL-5, thus driving the B1 response in the FALCs.