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Interleukin 23 is tightly associated with TH-17 cell–mediated inflammation and autoimmunity. A new study of mice deficient in its receptor shows that interleukin 23 is required for the terminal differentiation of TH-17 cells in vivo.
Autophagy has been linked to inflammatory bowel disease. Studies of two different mouse strains deficient in the autophagy-related gene product Atg16L1 now show that autophagy is important in regulating the secretory function of Paneth cells and the production of inflammatory cytokines in the intestine.
Compared with that of naive CD8+ T cells, the homeostatic population expansion of naive CD4+ T cells in a lymphopenic environment is limited. New data indicate that this difference is caused by high systemic concentrations of IL-7, which inhibit the function of dendritic cells.
The multifarious fates of CD4+ T helper cells mediate helpful and harmful immunity. An unexpected kinship between 'harmful' interleukin 17–producing T helper cells and 'helpful' follicular T helper cells has now been found.
The transcription factor Foxo1 regulates the homeostasis of naive peripheral T cells by 'translating' nutrient-availability signals into the expression of lymphoid tissue–homing molecules and the receptor for interleukin 7.
New findings show that a subpopulation of mucosal RORγt+ cells expresses natural killer cell receptors and produces interleukin 22. These innate immune cells may be pivotal in maintaining mucosal homeostasis.
Regulation of expression of the gene encoding interleukin 10 by the histone deacetylase HDAC11 emphasizes the ability of an antigen-presenting cell to induce immunity or tolerance in CD4+ T cells.
A systems biology approach provides correlates of successful vaccination, which allows a new method for measuring early vaccine efficiency and suggests hypotheses for the mechanisms that underlie immunogenicity.
ADAR1 catalyzes the deamination of adenosine to inosine in double-stranded RNA. This RNA-editing enzyme is now shown to be involved in hematopoiesis, where it acts to suppress interferon signaling and to block premature apoptosis.
On 24–27 September 2008, members of the scientific community gathered to discuss advances in innate immunity at the 'Toll meeting' in Cascais, Portugal. Before long, attendees noticed that 'Toll2008' might be a misnomer.
