Volume 12 Issue 3, March 2011

Infections in infants continue to be an important cause of morbidity and mortality worldwide. Understanding the immune mechanisms that operate in infants is necessary for the development of new approaches to improve the health of infants around the world.

MicroRNAs regulate many biological functions. Research now indicates that intestinal epithelial microRNAs might also regulate the differentiation of goblet cells and promote T helper type 2 immune responses to parasite infection.

Direct evaluation of the contribution of somatic hypermutation (SHM) to mucosal immunity has been hampered by the lack of models able to dissociate SHM from class-switch recombination, which are both dependent on the cytidine deaminase AID. A new mouse AID model now demonstrates the critical role of SHM in the control of gut bacteria.

During the past few decades, the vital and lethal functions of mitochondria have been investigated extensively. Data now demonstrate that these organelles also regulate the innate immune response by modulating inflammasome-mediated generation of proinflammatory cytokines.

The NADPH oxidase of professional phagocytes has an important role in host defense against certain microbes, including tuberculous mycobacteria. The identification of patients with rare inherited hypomorphic mutations in genes encoding components of this enzyme complex could produce new mechanistic insights.

Mendelian susceptibility to mycobacterial disease (MSMD) is a rare syndrome. Casanova and colleagues characterize MSMD in two kindreds and find macrophage-tropic mutations in genes encoding the respiratory burst machinery predispose these kindreds to mycobacterial diseases.

Autophagy is a physiological process that involves the engulfment and degradation of organelles. Choi and colleagues demonstrate that autophagy is important for the removal of damaged mitochondria and thus the control of inflammation.

Macrophages are functionally highly plastic, but the transcriptional control of this process is only partially understood. Udalova and colleagues demonstrate that the transcription factor IRF5 controls the plasticity of M1 macrophages in both mice and humans.

Normal gut–immune system homeostasis requires interactions among epithelial cells, lymphocytes and host microflora. Ben-Neriah and colleagues show that defined microRNA expression in the gut mucosa is also important for maintaining gut integrity and homeostasis.

Loss of IL-2 signaling results in autoimmunity. Laurence and colleagues show that the IL-2–STAT5 axis counteracts STAT3 activation of Il17 to dampen IL-17 production independently of Foxp3.

Although in vitro–generated cells of the T_H17 helper T cell subset are highly plastic, it is unclear whether T_H17 cells that develop in vivo retain their phenotype. To investigate this, Stockinger and colleagues have generated a T_H17 reporter system to map the fate of these cells in vivo.

Secretory IgA protects mucosal surfaces. Honjo and colleagues show that somatic hypermutation of IgA dependent on the cytidine deaminase AID is necessary to maintain gut immune homeostasis and shapes the intestinal microflora population.