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Plasma cells (PC) contribute to the pathogenesis of autoimmune diseases by secreting autoantibodies. Strategies to target pathogenic PCs are thus required. Here, the authors profile different PC subsets in naïve and lupus-prone mice and report the emergence and expansion of a CD19^– PC subset in diseased mice that could compromise the effectiveness of CD19-targeting therapies.

Although they are better known for their roles in antibody responses, B cells also contribute to immunity by secreting cytokines. Here, the authors discuss the various ways in which B cells can shape the immune response during infection and inflammatory disease by producing both pro-inflammatory and immunosuppressive cytokines.

Evidence from animal models indicates that B cells have both pathogenic and protective functions in autoimmune diseases. In this Review, the authors highlight recent insights into the suppressive functions of activated B cells in mice, describe the potential of B cells for use as cell-based therapy for experimental autoimmune diseases, and finally discuss the possibility of translating this cellular approach to treat human autoimmune diseases.

Accumulating evidence suggests that B cells can regulate immune responses. Here, the authors present a model to explain how B cells may regulate autoimmune pathology by secreting interleukin-10 in response to Toll-like receptor triggering and thereby mediate immune suppression.

The cellular components of the plasma cell niche in the bone marrow have remained elusive. Berek and co-workers show that eosinophils are key providers of plasma cell survival factors in the bone marrow.

Evidence of how functional Bregs develop in vivo has been lacking. Here the authors show that proB cells exposed in vivoto CpG differentiate into distinct Breg subsets that inhibit autoimmunity by arresting T cells in the lymph nodes via CCL19 and by producing IL-10 at the site of immunopathology.

Cognate antigen triggers B cells to undergo antibody maturation and terminal differentiation into antibody-secreting plasma cells. The transcription factor IRF4, which is essential for early B cell development, is also influential at these later stages of B cell development and function.

The mammalian aryl hydrocarbon receptor (known to sense environmental pollutants) is shown to also have a role as a pattern recognition receptor in sensing bacterial virulence factors, resulting in an antibacterial response and activation of innate and natural defences.

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.

The enzyme fructose-bisphosphate aldolase (FBA) plays central roles in glycolysis and gluconeogenesis. Here, Ziveri et al. show that FBA of the pathogen Francisella novicida acts, in addition, as a transcriptional regulator and is important for bacterial multiplication in macrophages.

Loss of B cell tolerance to autoantigens in systemic lupus erythematosus (SLE) is driven by TLR7, whereas TLR9 appears to protect against SLE by limiting the stimulatory activity of TLR7. The unique features of Toll-like receptor signalling in B cells implicate it as a therapeutic target in SLE.

B cells can secrete IL-35 upon activation, and subsequently contribute negatively to the regulation of immunity, such as T-cell-mediated autoimmunity or anti-microbial immunity, and a characterization of these cells raises new questions about possible independent roles for IL-10- and IL-35-expressing plasma cells as regulatory cells.

The authors identify in patients with rheumatoid arthritis a pathogenic subset of CD4+ T cells that augments B cell responses within inflamed tissues.