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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.
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.
The cellular components of the plasma cell niche in the bone marrow have remained elusive. Berek and co-workers show that eosinophils are key providers of plasma cell survival factors in the bone marrow.
The biological role of 2′-O-methylation of host and viral mRNA has remained elusive. Thiel and co-workers show that this modification modulates the induction of type I interferon and sensitivity to interferon.
TH2 cells are important for allergic and antiparasitic responses. Sun and colleagues demonstrate highly selective expression of the ECM1 protein in TH2 cells and a key role for it in regulating migration.
The function of the chemokine CCL8 has remained unknown. Luster and colleagues show that CCL8 has high expression in allergic skin, where it recruits CCR8+ TH2 cells with abundant IL-5 expression.
The cytidine deaminase AID is essential for the immunoglobulin-diversification processes. Chaudhuri and colleagues identify the splicing factor PTBP2, which promotes the binding of AID to switch-region DNA.
Ldb1 functions as a core component of various multiprotein transcription complexes. Love and co-workers show a continuous requirement for Ldb1 in the maintenance of both fetal and adult HSC.
Pathways dependent on the transcription factor NF-κB provide innate immunity against microbes. Karin and colleagues show that mice lacking the kinase IKKβ have IL-1-dependent neutrophilia. Loss of IL-1 signaling restores blood cellularity but severely compromises antimicrobial defense.
Against a backdrop of some of the most savage spending cuts in the developed world, the UK science budget has emerged relatively unscathed, but funding priorities may yet prove problematic.
NF-κB is a critical transcription factor that is regulated by several post-transcriptional modifications. The characterization of their roles would help in the design of new therapeutic targets in cancer and inflammation.