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The transcription factor Ikaros is required for lymphopoiesis. Busslinger and colleagues show Ikaros positively regulates genes encoding pre-BCR signal transducers and thereby promotes pro-B to pre-B cell progression and proliferation.
Ikaros deletions are associated with certain human malignancies. Georgopoulos and colleagues show that loss of Ikaros arrests B lymphoid progenitors at an adherent and proliferative pre-B cell stage from which leukemia can arise.
Interactions of the TCR with self peptide–MHC are crucial to T cell development. Allen and colleagues show that the strength of such interactions also determines the intrinsic T cell functionality and responses to pathogens.
The transcriptional repressor DREAM is involved in pain sensing. Tiruppathi and colleagues show that it is also involved in innate signaling by regulating the anti-inflammatory deubiquitinase A20.
IL-1 triggers IRF1 signaling, but the biological importance of this has remained uncertain. Kordula and colleagues show that an IL-1–IRF1 pathway is necessary for the selective induction of chemokines and sterile inflammation.
The transcriptional regulator Aire is required for central tolerance, but how it manages to target tissue-specific genes is unclear. Anderson and colleagues show that Aire achieves such targeting by coopting the ATF7ip-MBD1 repressor complex.
Plasma cells must accommodate the cellular stress associated with antibody production. George and colleagues show that the survival of plasma cells requires inducible nitric oxide synthase (iNOS) to modulate the cellular ER stress response.
The role of the unfolded protein response in the immune system is poorly understood. Lambrecht and colleagues show that CD8α+ DCs have a constitutively active component of this response that is important for their homeostatic function.
Transcriptional complexes can polymerize and bind adjacent binding sites. Vinkemeier and colleagues show that STAT1 cooperativity is required downstream of type 2 interferonsignaling but not for type 1 interferon–induced immune responses.