| First Author | Zhu Y | Year | 2024 |
| Journal | Science | Volume | 385 |
| Issue | 6708 | Pages | eadk1679 |
| PubMed ID | 39088603 | Mgi Jnum | J:358540 |
| Mgi Id | MGI:7714789 | Doi | 10.1126/science.adk1679 |
| Citation | Zhu Y, et al. (2024) A chemogenetic screen reveals that Trpv1-expressing neurons control regulatory T cells in the gut. Science 385(6708):eadk1679 |
| abstractText | Neuroimmune cross-talk participates in intestinal tissue homeostasis and host defense. However, the matrix of interactions between arrays of molecularly defined neuron subsets and of immunocyte lineages remains unclear. We used a chemogenetic approach to activate eight distinct neuronal subsets, assessing effects by deep immunophenotyping, microbiome profiling, and immunocyte transcriptomics in intestinal organs. Distinct immune perturbations followed neuronal activation: Nitrergic neurons regulated T helper 17 (T(H)17)-like cells, and cholinergic neurons regulated neutrophils. Nociceptor neurons, expressing Trpv1, elicited the broadest immunomodulation, inducing changes in innate lymphocytes, macrophages, and RORgamma(+) regulatory T (T(reg)) cells. Neuroanatomical, genetic, and pharmacological follow-up showed that Trpv1(+) neurons in dorsal root ganglia decreased T(reg) cell numbers via the neuropeptide calcitonin gene-related peptide (CGRP). Given the role of these neurons in nociception, these data potentially link pain signaling with gut T(reg) cell function. |
