Volume 9 Issue 9, September 2008

Natural killer T cells acquire their unique phenotype and characteristics during development in the thymus. Evidence suggests that the transcription factor PLZF has a unique function in the development of these cells and their acquisition of 'innate-like' characteristics.

Excessive lung inflammation in response to infection or allergens can lead to tissue damage and potentially loss of organ function. The CD200-CD200R interaction acts to limit such destructive immune responses in the lung.

New findings show that cellular microRNAs 'calibrate' the baseline expression of mRNAs encoding stress-inducible ligands of the activating NKG2D receptor. This regulation serves to protect innocent cells but may be exploited by tumors and viruses to thwart immune attack.

Definitive new data solidify and clarify the function of the adaptor TRADD in tumor necrosis factor receptor 1 signaling and show that in some situations, TRADD is also required for the transmission of Toll-like receptor signals.

The function of the kinase p38α in inflammation is unclear. Park and colleagues show that p38α exerts pro- or anti-inflammatory effects depending on the cell type in which it is expressed and the stimulus eliciting its activation.

Uncontrolled TLR signaling results in excessive inflammation. Arthur and colleagues show that the kinases MSK1 and MSK2 orchestrate a feedback loop involving interleukin 10 and the phosphatase DUSP1 to control TLR4 signaling.

The function of the adaptor protein TRADD is uncertain. Teams led by Pasparakis and Liu solidify TRADD's function in TNF receptor signaling and extend its influence to TRIF-dependent Toll-like receptor pathways.

The function of the adaptor protein TRADD is uncertain. Teams led by Pasparakis and Liu solidify TRADD's function in TNF receptor signaling and extend its influence to TRIF-dependent Toll-like receptor pathways.

Invariant natural killer cells recognize glycolipids presented by CD1d molecules and can mediate rapid innate responses. Sant'Angelo and colleagues show that these cells express the transcription factor PLZF, which is required for their innate effector function.

The mechanisms controlling expression of the stress-induced NKG2D ligands MICA and MICB are not fully understood. Mandelboim and colleagues suggest that microRNAs maintain low MICA and MICB expression in the absence of cell stress.

Lungs are continually challenged by exposure to airborne particles and microbes, yet they resist overt inflammatory responses. Hussell and colleagues show that this 'quiescent' state requires CD200-CD200R interactions between alveolar macrophages and lung tissues.

Immune cells are constantly in motion in surveillance for potential microbial threats. Here we present a collection of reviews that describe the trafficking patterns, cues and means by which immune cells transit tissues in health and in response to infections.