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B cells arise via a precise developmental pathway. Goodnow and Beutler report that mice bearing mutations in Atp11c, which encodes a phosphatidylserine 'flippase', have defective B cell generation in the adult bone marrow.
B cells arise via a precise developmental pathway. Goodnow and Beutler report that mice bearing mutations in Atp11c, which encodes a phosphatidylserine 'flippase', have defective B cell generation in the adult bone marrow.
The NF-κB subunit RPS3 can contribute to the selection of nuclear targets by NF-κB. Lenardo and colleagues show that the kinase IκBβ phosphorylates RPS3 to promote its nuclear translocation, a process targeted by enteropathogenic Escherichia coli.
Regulatory T cells can adopt specialized differentiation programs in the periphery. Kallies and co-workers show that IRF4 and Blimp-1 control the acquisition of regulatory T cell effector functions, such as IL-10 production.
The kinase mTOR has emerged as an important regulator of helper T cell differentiation. Powell and co-workers show that the mTOR complex mTORC1 selectively regulates TH1 and TH17 differentiation, whereas mTORC2 signaling is required for TH2 differentiation.
Parasites use multifarious means to manipulate and avoid sterilizing immunity. Melendez and colleagues show that a nematode product triggers macrophage autophagocytosis to degrade the adaptor MyD88 and suppress inflammatory responses.
The transcription factor RORγt is expressed in many cell types. Eberl and colleagues show that intestinal homeostasis is regulated by an IL-25-dependent feedback pathway involving IL-22-expressing RORγt+ innate lymphoid cells.
The molecular mechanisms that direct the development of intestinal intraepithelial lymphocytes (IELs) remain unclear. Chen and co-workers demonstrate a role for TGF-β in the development of TCRαβ+CD8αα+ IELs.
CTLs can produce the regulatory cytokine IL-10 to prevent excess inflammation during clearance of viruses. Braciale and colleagues now unravel the molecular pathways involved in IL-10 expression by CTLs.
Although in vitro–generated cells of the TH17 helper T cell subset are highly plastic, it is unclear whether TH17 cells that develop in vivo retain their phenotype. To investigate this, Stockinger and colleagues have generated a TH17 reporter system to map the fate of these cells in vivo.
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.
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.
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.
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.
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.