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Complement provides costimulatory signals to T cells. Medof and colleagues demonstrate that an absence of complement signaling in naive T cells generates an autoinductive loop to drive induced regulatory T cells.
Immune responses can cause immunopathology. Yarovinsky and colleagues show that IFN-γ induced by T cell–intrinsic TLR signaling in CD4+ TH1 cells during Toxoplasma gondii infection causes dysbiosis and loss of Paneth cells.
Interleukin 7 (IL-7) signaling is essential during early lymphocyte development. Patra and colleagues identify a distinct IL-7–kinase Jak3–dependent pathway that activates the transcription factor NFATc1 in DN1 thymocytes to promote their survival.
Hacohen and colleagues use an integrative approach that combines quantitative proteomics, genomics and small molecule perturbations to identify new genes involved in DNA sensing and type I interferon production.
Why signaling via both the receptor for interleukin 7 (IL-7R) and the T cell antigen receptor (TCR) is required for T cell homeostasis has been unclear. Singer and colleagues show that engagement of the TCR interrupts IL-7R signals to prevent a mechanism of cytokine-induced cell death.
Follicular regulatory T cells control humoral immune responses, but how these cells are in turn controlled has been unclear. Sharpe and colleagues demonstrate that signaling via PD-1 regulates number and function of these cells.
During sterile inflammation, emigrating leukocytes sequentially engage subsets of pericytes associated with blood vessels and acquire adhesive, migratory and survival signals.
Feedback inhibition by interferon-γ blocks the NLRP3 inflammasome by triggering inducible nitric oxide synthase (iNOS), and the resulting nitric oxide (NO) thio-nitrosylates NLRP3, shutting it down. This prevents excessive immunopathology during chronic infection with Mycobacterium tuberculosis.
The mechanisms by which cells detect and fight foreign organisms is crucial for the host defense against infection. The sensing of cytosolic DNA is pivotal in this process, is kept in check by the exonuclease Trex1 and has been linked to lysosomal biogenesis via the transcription factor TFEB in an interferon-independent manner.
Psoriasis is associated with the TH17 subset of helper T cells. Dysregulation of interleukin 17 (IL-17) signaling leads to enhanced TH17 differentiation, more production of IL-22 and IL-22-dependent skin inflammation.
The intracellular sensor DDX41 is important for generating innate responses to DNA viruses. Liu et al. demonstrate that the ubiquitin ligase TRIM21 degrades and thereby regulates DDX41-dependent responses.