Volume 14 Issue 11, November 2014

CD4⁺T cells in newborn babies show increased production of CXCL8, which could be important for defence against infections.

Distinct subsets of thymic antigen-presenting cells contribute to the generation of a diverse and self-tolerant T cell repertoire.

Fucosylation of intestinal epithelial cells in response to commensal or systemic bacterial stimulation promotes disease resistance and tolerance through the metabolic support of the gut microbiota.

Recombination-activating gene (RAG) proteins determine functional specialization and cellular fitness in natural killer cells.

Whether neutrophils kill a pathogen by phagocytosis or NETosis is determined by pathogen size.

LOX1 activates dendritic cells and B cells to boost humoral immune responses.

Although the MHC class II-mediated modulation of CD4⁺ T cell responses is typically associated with dendritic cells, macrophages and B cells, other cell populations are also suggested to show such behaviour. The authors discuss these atypical antigen-presenting cells and question their relevance to immune responses in vivo.

The closely related oxysterols, 25-hydroxycholesterol and 7α,25-dihydroxycholesterol, have important functions in innate and adaptive immune responses, ranging from antiviral and inflammation-regulatory effects to a role as a guidance cue for B cells and dendritic cells.

Malaria infections can result in deleterious activation of innate immune cells. In this Review, the authors summarize how thePlasmodiumparasite is recognized by innate immune receptors, and discuss the role of these receptors in host resistance to infection and in the pathogenesis of malaria.

In this Opinion article, the authors discuss how the induction of regulated cell death and inflammatory pathways may lead to an auto-amplification loop that causes tissue damage and organ failure. They propose that targeting both processes could be useful for treating a broad range of clinical conditions with an inflammatory basis.

Chronic viral infections and malignant tumours are associated with the development of T cells that have an 'exhausted' phenotype and that are thought to be severely functionally impaired. In this Opinion article, the authors propose that the exhausted phenotype is actually a functional adaptation to cause minimal tissue damage while still mediating a critical level of pathogen control.