Neuropeptide regulation of non-redundant ILC2 responses at barrier surfaces

Tsou, Amy M.; Yano, Hiroshi; Parkhurst, Christopher N.; Mahlakõiv, Tanel; Chu, Coco; Zhang, Wen; He, Zhengxiang; Jarick, Katja J.; Zhong, Connie; Putzel, Gregory G.; Hatazaki, Mai; Longman, Randy S.; Sonnenberg, Gregory F.; Scherl, Ellen; Lukin, Dana J.; Battat, Robert; Sockolow, Robbyn; Ciecierega, Thomas; Solomon, Aliza; Barfield, Elaine; Chien, Kimberley; Ferreira, Johanna; Williams, Jasmin; Khan, Shaira; Chong, Peik Sean; Mozumder, Samah; Chou, Li-Shan; Zhou, Wenqing; Ahmed, Aquil; Joseph, Ann Mary; Lorenz, Ivo C.; David, Andrew; Balderes, Paul; Klose, Christoph S. N.; Lira, Sérgio A.; Artis, David

doi:10.1038/s41586-022-05297-6

Cited by 39 publications

(28 citation statements)

References 59 publications

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“…New tools, such as mice with an ILC2-specific Il4 gene deficiency or mice specifically lacking the IL-4 + ILC2 population, need to be developed to examine the specific role of IL-4 + ILC2s. Since it has been reported that ILC2s selectively express the neuromedin U receptor 1 (Nmur1; Klose et al, 2017 ; Wallrapp et al, 2017 ) and ILC2-specific Cre strains (Nmur1-Cre mice) have recently been developed ( Jarick et al, 2022 ; Tsou et al, 2022 ), the role of IL-4 + ILC2s can be investigated by creating ILC2-specific Il4 -deficient mice in the future.…”

Section: Discussionmentioning

confidence: 99%

“…In response to IL-33 stimulation, nILC2s moderately proliferate locally at mucosal tissues and play critical roles in immune protection by producing IL-5 and IL-13. In addition, nILC2s express amphiregulin and contribute to tissue repair ( Monticelli et al, 2015 ; Tsou et al, 2022 ). On the other hand, iILC2s express high levels of KLRG1 (a C-type lectin receptor) and IL-17RB (an IL-25 receptor component), and expand and transiently appear after helminth infection and recombinant IL-25 administration ( Huang et al, 2015 ; Huang et al, 2018 ; Ricardo-Gonzalez et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

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Diet-mediated constitutive induction of novel IL-4+ ILC2 cells maintains intestinal homeostasis in mice

Cui

Nagano

Morita

et al. 2023

Journal of Experimental Medicine

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Group 2 innate lymphoid cells (ILC2s) expressing IL-5 and IL-13 are localized at various mucosal tissues and play critical roles in the induction of type 2 inflammation, response to helminth infection, and tissue repair. Here, we reveal a unique ILC2 subset in the mouse intestine that constitutively expresses IL-4 together with GATA3, ST2, KLRG1, IL-17RB, and IL-5. In this subset, IL-4 expression is regulated by mechanisms similar to but distinct from those observed in T cells and is partly affected by IL-25 signaling. Although the absence of the microbiota had marginal effects, feeding mice with a vitamin B1-deficient diet compromised the number of intestinal IL-4+ ILC2s. The decrease in the number of IL-4+ ILC2s caused by the vitamin B1 deficiency was accompanied by a reduction in IL-25–producing tuft cells. Our findings reveal that dietary vitamin B1 plays a critical role in maintaining interaction between tuft cells and IL-4+ ILC2s, a previously uncharacterized immune cell population that may contribute to maintaining intestinal homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Diet-mediated constitutive induction of novel IL-4+ ILC2 cells maintains intestinal homeostasis in mice

Cui

Nagano

Morita

et al. 2023

Journal of Experimental Medicine

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“…Amphiregulin is reported to control inflammation in the periphery (38)(39)(40)(41)(42) and in the CNS during stroke (43), which suggests that it is induced in response to trauma and/or inflammation. Indeed, we detected increased Areg expression in microglia at peak EAE, 17 days after disease induction (Fig.…”

Section: Microglia-astrocyte Areg-egfr Signaling Limits Astrocyte Pat...mentioning

confidence: 99%

Droplet-based forward genetic screening of astrocyte–microglia cross-talk

Wheeler

Clark

Lee

et al. 2023

Science

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Cell–cell interactions in the central nervous system play important roles in neurologic diseases. However, little is known about the specific molecular pathways involved, and methods for their systematic identification are limited. Here, we developed a forward genetic screening platform that combines CRISPR-Cas9 perturbations, cell coculture in picoliter droplets, and microfluidic-based fluorescence-activated droplet sorting to identify mechanisms of cell–cell communication. We used SPEAC-seq (systematic perturbation of encapsulated associated cells followed by sequencing), in combination with in vivo genetic perturbations, to identify microglia-produced amphiregulin as a suppressor of disease-promoting astrocyte responses in multiple sclerosis preclinical models and clinical samples. Thus, SPEAC-seq enables the high-throughput systematic identification of cell–cell communication mechanisms.

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“…Since the regulation of ILC2 phenotype in the intestine is different from the lungs ( 57 ), further studies are needed to elucidate the molecular mechanisms of TF regulation in ILCs in different tissues under physiological and pathological conditions. Recently developed mouse model in which ILC2-specific NMUR1 promoter drives the expression of Cre recombinase allows to selectively target ILC2s ( 164 , 165 ). These mice will be helpful to study the specific role of different TFs in ILC2 maintenance and plasticity.…”

Section: Transcriptional Regulation Of Ilc2 Identitymentioning

confidence: 99%

Transcriptional control of ILC identity

Korchagina

Shein²,

Koroleva³

et al. 2023

Front. Immunol.

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Innate lymphoid cells (ILCs) are heterogeneous innate immune cells which participate in host defense, mucosal repair and immunopathology by producing effector cytokines similarly to their adaptive immune cell counterparts. The development of ILC1, 2, and 3 subsets is controlled by core transcription factors: T-bet, GATA3, and RORγt, respectively. ILCs can undergo plasticity and transdifferentiate to other ILC subsets in response to invading pathogens and changes in local tissue environment. Accumulating evidence suggests that the plasticity and the maintenance of ILC identity is controlled by a balance between these and additional transcription factors such as STATs, Batf, Ikaros, Runx3, c-Maf, Bcl11b, and Zbtb46, activated in response to lineage-guiding cytokines. However, how interplay between these transcription factors leads to ILC plasticity and the maintenance of ILC identity remains hypothetical. In this review, we discuss recent advances in understanding transcriptional regulation of ILCs in homeostatic and inflammatory conditions.

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Neuropeptide regulation of non-redundant ILC2 responses at barrier surfaces

Cited by 39 publications

References 59 publications

Diet-mediated constitutive induction of novel IL-4+ ILC2 cells maintains intestinal homeostasis in mice

Diet-mediated constitutive induction of novel IL-4+ ILC2 cells maintains intestinal homeostasis in mice

Droplet-based forward genetic screening of astrocyte–microglia cross-talk

Transcriptional control of ILC identity

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