B cell–helper neutrophils stimulate the diversification and production of immunoglobulin in the marginal zone of the spleen

TL;DR: Primordial neutrophil functions are discussed, and more recent evidence that interactions between neutrophils and adaptive immune cells establish a feed-forward mechanism that amplifies pathologic inflammation is presented.

TL;DR: The concept of neutrophils phenotypic and functional heterogeneity is presented and several neutrophil subpopulations reported to date are described and the role these sub Populations seem to play in homeostasis and disease is discussed.

TL;DR: The emerging dual role played by neutrophils in the tumour microenvironment is discussed, while also mediating antitumour immune responses, and it is suggested that neutrophil function could be manipulated in myeloid cell-based therapeutic approaches to improve patient outcomes.

TL;DR: This Review examines in vivo observations of the recruitment of neutrophils from blood to tissues in models of blood-borne infections versus bacterial invasion through epithelial linings, and examines data on novel aspects of the activation of NADPH oxidase and the heterogeneity of phagosomes.

TL;DR: It is proposed that neutrophils regulate adaptive immunity through interactions with dendritic cells (DCs) and might function as danger sensors that communicate the presence of infection to DCs and instruct them to tailor ensuing immune responses to the type of pathogen.

TL;DR: It is demonstrated that development and induction of SHMs of human IgM+IgD+CD27+ B cells can occur in a T cell–independent manner.

TL;DR: These findings show that in addition to the muramyl form of peptidoglycan monomers, the anhydro murAmyl form, with no reducing end, is compatible with somnogenic activity, and amplify earlier observations with smaller synthetic molecules of the importance of amidation/deamidation in the structure-activity relationships of Muramyl peptides.

TL;DR: Overall systemic antibody responses to gut commensal bacteria were not affected during chronic HIV-1 infection, with titres decreasing when normalised to elevated plasma immunoglobulin G (IgG) levels found in patients with HIV, and HIV-associated hypergammaglobulinaemia is unlikely to be driven by induction of antimicrobiota antibodies.