Balic et al. describe a new role for STAT3 in TLR4 signalling in macrophages, linking LPS mediated activation of this innate immune receptor to phosphorylation of mitochondrial STAT3, resulting in distinct metabolic reprogramming.

We discuss the study by McNamara et al., who report that low levels of antigen-specific antibodies in serum can limit the boosting of antibody and B-cell responses following immunization with live attenuated malaria sporozoites.

Coronavirus disease 2019 (COVID-19) results from a virus making an interspecies leap that tests genetic resistance to viral disease, like most of the great plagues sculpting human history. Here I set out known unknowns for tackling COVID-19, taking advantage of progress understanding how viral disease is countered by fundamentally different genetic mechanisms for resistance: resistance to virus transmission primarily by activation of immune responses; and resistance to pathology primarily by tolerance checkpoints to limit immune responses.

Here, we address the immunologic role of renin–angiotensin–aldosterone system and renin–angiotensin–aldosterone system inhibitor based on current and previous evidence aiming to improve the current knowledge regarding this system and its inhibition from molecular and immunologic perspectives.

In this study, we found that neuropeptides released from pulmonary C-fiber endings could enhance airway hypersensitivity in asthma by increasing the number of ILC2s and iILC2s and type 2 cytokines [interleukin (IL)-4, IL-5 and IL-13] production. However, α7 nicotinic acetylcholine receptor signaling activated by acetylcholine could suppress allergic inflammation or facilitate oral ovalbumin feeding-induced asthmatic tolerance by reducing ILC2 or iILC2 responses and sphingosine-1-phosphate-dependent iILC2 recruitment into the lung.

TANK-binding kinase 1 (TBK1) knockdown inhibits the receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-induced osteoclast (OC) differentiation and function. Downregulation of TBK1 greatly suppresses RANKL-induced gene expressions correlated with OC differentiation. TBK1 mediates the OC differentiation and function by regulating NF-κB, mitogen-activated protein kinases and protein kinase B signals.

Marginal zone B cells express the short-chain fatty acid receptor GPR43. Mice lacking GPR43 have heightened responses to T-cell-independent antigens and have elevated levels of immunoglobulin M specific for double-stranded DNA and phosphatidylcholine. Thus, short-chain fatty acids may regulate marginal zone B-cell responses to several antigens.