Tuft cells constitutively express IL-25 to sustain ILC2 homeostasis in the intestine, but mechanisms driving IL-25 secretion have been unclear. Here, Feng et al. find that tuft cells express IL-17RB, which is required to regulate the bioavailability of IL-25 and to restrain the activation of ILC2s during homeostasis.

Panzer and colleagues show that the integrated stress response pathway regulates cytokine translation in CD4⁺ T_RM cells during homeostasis and inflammation.

Strategies to advance the field of neuroimmunology by embracing its complexity via inclusion of its multidisciplinary properties were discussed at a meeting in Cold Spring Harbor. Attendees proposed fostering of open communications and funding of collaborations across disciplines, and the recognition that our understanding of the neuroimmune system requires interdisciplinary science.

In this broad Review, the authors describe how the immune response to leukemias develops, how these cancer cells avoid it and how various immunotherapies have been designed to overcome resistance.

Tuft cells constitutively express IL-25 to sustain ILC2 homeostasis in the intestine, but mechanisms driving IL-25 secretion have been unclear. Here, Feng et al. find that tuft cells express IL-17RB, which is required to regulate the bioavailability of IL-25 and to restrain the activation of ILC2s during homeostasis.

Panzer and colleagues show that the integrated stress response pathway regulates cytokine translation in CD4⁺ T_RM cells during homeostasis and inflammation.

The authors show that NAT10 is upregulated with T cell antigen receptor signaling and that T cell-specific NAT10 deficiency results in diminished numbers of naive T cells, translating to an inability to mount a significant antiviral T cell response.

Fan and colleagues show that the neurotransmitter GABA signals in intestinal ILC3s to suppress IL-17A production through a regulatory loop that involves suppression of C/EBP-β and induction of Igfb7.

Sinclair et al. combine quantitative proteomics and an autophagy flux reporter to map autophagy substrates and triggers during CD8 T cell differentiation. Proteins degraded and fueled by autophagy in naïve and effector T cells are identified and it is revealed that the regulation of amino acid transport allows antigen receptors and inflammatory cytokines to repress autophagy flux to shape T cell differentiation.

Itkin et al. identify a role for Fli-1 in hematopoietic stem cell activation during regenerative hematopoiesis. They show that Fli-1 coordinates hematopoietic stem cells to stimulate niche-derived Notch1 feedback signals for demand-needed hematopoietic cell output.

Strategies to advance the field of neuroimmunology by embracing its complexity via inclusion of its multidisciplinary properties were discussed at a meeting in Cold Spring Harbor. Attendees proposed fostering of open communications and funding of collaborations across disciplines, and the recognition that our understanding of the neuroimmune system requires interdisciplinary science.