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New study suggests benefit from chemotherapy depends on switching to B cells with antitumour activity. This switch is driven by complement signals, generated following chemotherapy-induced tumour cell death, that boost a distinct B cell subset that supports antitumour T cell immunity.
The first article in our Women in Immunology series pays tribute to Delphine Parrott, who conducted pioneering work in the fields of T cell biology, lymphoid tissue anatomy, lymphocyte trafficking and mucosal immunology.
Like bacteria, T cells are reported to communicate with each other and adapt their behaviour according to cell density. This quorum regulation supports T cell population expansion and contraction in response to infection.
Febrile temperature increases the differentiation of T helper 17 (TH17) cells with a more pro-inflammatory, pathogenic phenotype, which could have implications for the pathogenesis of autoimmunity.
McGinley et al. describe a new role for IL-17A in the induction phase of experimental autoimmune encephalomyelitis by indirectly recruiting IL-1β-producing myeloid cells.
Researchers identify a new population of cytotoxic T cells that recognize the non-polymorphic MHC class I-related molecule MR1 on multiple different cancer cells, raising the prospect of its use as T cell-based therapy for multiple cancers.
The ‘shock-and-kill’ strategy aims to eradicate HIV by luring the virus out of hiding, followed by killing of the virus and any infected cells. Two reports now demonstrate robust approaches to achieve the first step of such a strategy.
Jennifer Gommerman discusses a 2008 paper by Sidonia Fagarasan and colleagues showing that isolated lymphoid follicles (ILFs) in the gut can function as inductive sites for the generation of IgA-producing plasma cells in the absence of T cell help.
The host aryl hydrocarbon receptor can detect various quorum-sensing molecules produced by Pseudomonas aeruginosa, which may allow host immune cells to tune their response according to the bacterial density.
Rémy Bosselut describes a 2001 paper by Jordan et al. showing that CD25+ regulatory T cells can be selected on self-peptides, which provided important insights into mechanisms of thymic tolerance.
T cells expressing programmed cell death 1 (PD1) have been considered the main targets of immune checkpoint blockade therapy. But a new study shows that targeting PD1 on myeloid cells reprogrammes tumour-induced myelopoiesis to favour maturation of effector myeloid cells that promote antitumour immunity.
