Metabolic control of the Treg/Th17 axis.

Publication Type:

Journal Article

Source:

Immunological reviews, Volume 252, Issue 1, p.52-77 (2013)

Keywords:

Autoimmunitydigestive disease, digestive deseases Cell Differentiationdigestive disease, digestive deseases Gene Expression Regulationdigestive disease, digestive deseases Humansdigestive disease, digestive deseases Hypoxia-Inducible Factor 1digestive disease, digestive deseases Immune Tolerancedigestive disease, digestive deseases Inflammationdigestive disease, digestive deseases Lymphocyte Activationdigestive disease, digestive deseases Metabolic Networks and Pathwaysdigestive disease, digestive deseases Signal Transductiondigestive disease, digestive deseases T-Lymphocyte Subsetsdigestive disease, digestive deseases T-Lymphocytes, Helper-Inducerdigestive disease, digestive deseases T-Lymphocytes, Regulatory

Abstract:

The interplay of the immune system with other aspects of physiology is continually being revealed and in some cases studied in considerable mechanistic detail. A prime example is the influence of metabolic cues on immune responses. It is well appreciated that upon activation, T cells take on a metabolic profile profoundly distinct from that of their quiescent and anergic counterparts; however, a number of recent breakthroughs have greatly expanded our knowledge of how aspects of cellular metabolism can shape a T-cell response. Particularly important are findings that certain environmental cues can tilt the delicate balance between inflammation and immune tolerance by skewing T-cell fate decisions toward either the T-helper 17 (Th17) or T-regulatory (Treg) cell lineage. Recognizing the unappreciated immune-modifying potential of metabolic factors and particularly those involved in the generation of these functionally opposing T-cell subsets will likely add new and potent therapies to our repertoire for treating immune mediated pathologies. In this review, we summarize and discuss recent findings linking certain metabolic pathways, enzymes, and by-products to shifts in the balance between Th17 and Treg cell populations. These advances highlight numerous opportunities for immune modulation.