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Regulatory T cells adopt specialized differentiation programs controlled by transcription factors. The transcription factors Blimp-1 and IRF4 are now shown to be pivotal in the maturation of effector regulatory T cells.
Helminth parasites are adept at dampening immunity. New data showing that intracellular degradative pathways are manipulated have important implications for therapy.
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.
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 migration of TH2 cells into allergy-affected tissue is key to maintaining the inflammatory response. CCR8-CCL8, a newly identified chemokine receptor–ligand pair, mediates the skin accumulation of TH2 cells with the specific potential to drive chronic eosinophilic inflammation.
Maintenance of hematopoietic stem cells depends on a fine-tuned transcriptional network. A detailed study of the nuclear adaptor Ldb1 provides additional clues as to how hematopoietic stem cell homeostasis is controlled.
Long-lived plasma cells require a specialized bone marrow microenvironment in order to survive and produce antibody. Eosinophils make an important contribution to maintaining this survival niche.
