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The nuclear factor-κB (NF-κB) family of regulators is well known for mediating dendritic cell (DC) maturation—that is, the acquisition of the functions required for full activation of T cells. Paradoxically, a key member of this family, NF-κB1, is now also implicated in maintaining DCs in an immature state (pages 1663–1667).
IgA regulates intestinal homeostasis by maintaining appropriate communities of bacteria within the gut. A new study shows that intestinal bacteria regulate metabolism via IgA (pages 1585–1593).
The path to drug approval is long, hard and often perplexing. In recent months, the US Food and Drug Administration (FDA) has promised to bolster 'regulatory science', which aims to transform its decision-making process to be more efficient, transparent and accountable. However, diverse stakeholders, including patients, drug developers and the US Congress, will have to rise to the challenge of coordinating their priorities if this endeavor is to succeed.
Retracting a paper is perhaps the most unpleasant task a journal has to face, particularly if the retraction involves scientific misconduct. With the number of retractions on the rise, an improved mechanism to deal with misconduct is necessary.
Although protein-polysaccharide conjugate vaccines provide notable clinical benefits, it is still not fully understood how they work. A new mechanism of action for these vaccines has been identified in which T cells can recognize sugar epitopes in the context of the major histocompatibility complex (MHC) provided they are bound to a protein 'anchor', which allows binding of the sugar epitope to the MHC (pages 1602–1609).
Cellular production of nitric oxide (NO) by nitric oxide synthase (NOS) in the face of limiting pools of arginine requires the intracellular citrulline-to-NO pathway, catalyzed by the enzyme argininosuccinate lyase (ASL). People with the urea cycle disorder argininosuccinic aciduria, caused by a deficiency of ASL, have systemic NO deficiency, which can be rescued by the use of an alternative, NOS-independent, nitrite-to-NO pathway.