Volume 11 Issue 3, March 2011

Retinoic acid and IL-15 drive inflammatory responses to dietary proteins.

Early exposure to UV rays promotes macrophage-driven melanoma development.

Pro-inflammatory macrophages induced by iron accumulation contribute to chronic lesions.

IL-7 suppresses the inhibitory networks that are established during chronic viral infection.

T_H17 cells adopt distinct functional fates during different inflammatory responses.

A new vaccine with mycobacterial antigens that are expressed throughout infection is effective against latent tuberculosis.

Memory B cells can be divided into short- and long-term populations according to immunoglobulin phenotype.

Mitochondrial ROS have an important role in pro-inflammatory cytokine production.

Neuroinflammation is driven by peptidoglycan-induced signalling in antigen-presenting cells.

Toll-like receptors (TLRs) are central to the induction of pro-inflammatory responses, but their signalling pathways must be tightly regulated. As discussed in this article, an emerging level of fine-tuning is mediated by microRNAs, several of which are induced by TLR signalling.

This Review focuses on how HIV infection affects the functions of dendritic cells and natural killer cells. The authors propose that a better understanding of the roles of these innate immune cells during HIV infection could lead to improved antiviral strategies.

Synergistic and antagonistic signalling crosstalk between receptors of the innate immune system maintains a fine balance between protective immunity and inflammatory pathology. This Review article looks at how pathogens can manipulate this signalling crosstalk to dysregulate the host immune response for their benefit.

Here, Wolfgang Junger discusses the importance of purinergic receptor signalling for fine-tuning immune cell responses. Autocrine signalling through purinergic receptors can both amplify and inhibit leukocyte functions; the author explains how this is important for sensing chemotactic gradients and detecting rare antigens.

Recent studies have shown that caspase 1 activation by inflammasomes controls a set of non-canonical effector mechanisms that might contribute to the immune response during infection and autoimmunity. These mechanisms include unconventional protein secretion, pyroptosis, regulation of metabolic pathways and restriction of bacterial replication.

In this Essay, the authors present a new perspective on how immune responses are regulated. They propose that the class of immune response is tailored to suit the tissue in which it is occurring rather than the invading pathogen.