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Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior

Barron, Jerika J. ; Mroz, Nicholas M. ; Taloma, Sunrae E. ; Dahlgren, Madelene W. LU orcid ; Ortiz-Carpena, Jorge F. ; Keefe, Matthew G. ; Escoubas, Caroline C. ; Dorman, Leah C. ; Vainchtein, Ilia D. and Chiaranunt, Pailin , et al. (2024) In Science 386(6721).
Abstract

The innate immune system shapes brain development and is implicated in neurodevelopmental diseases. It is critical to define the relevant immune cells and signals and their impact on brain circuits. In this work, we found that group 2 innate lymphoid cells (ILC2s) and their cytokine interleukin-13 (IL-13) signaled directly to inhibitory interneurons to increase inhibitory synapse density in the developing mouse brain. ILC2s expanded and produced IL-13 in the developing brain meninges. Loss of ILC2s or IL-13 signaling to interneurons decreased inhibitory, but not excitatory, cortical synapses. Conversely, ILC2s and IL-13 were sufficient to increase inhibitory synapses. Loss of this signaling pathway led to selective impairments in social... (More)

The innate immune system shapes brain development and is implicated in neurodevelopmental diseases. It is critical to define the relevant immune cells and signals and their impact on brain circuits. In this work, we found that group 2 innate lymphoid cells (ILC2s) and their cytokine interleukin-13 (IL-13) signaled directly to inhibitory interneurons to increase inhibitory synapse density in the developing mouse brain. ILC2s expanded and produced IL-13 in the developing brain meninges. Loss of ILC2s or IL-13 signaling to interneurons decreased inhibitory, but not excitatory, cortical synapses. Conversely, ILC2s and IL-13 were sufficient to increase inhibitory synapses. Loss of this signaling pathway led to selective impairments in social interaction. These data define a type 2 neuroimmune circuit in early life that shapes inhibitory synapse development and behavior.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Science
volume
386
issue
6721
article number
eadi1025
publisher
American Association for the Advancement of Science (AAAS)
external identifiers
  • pmid:39480923
  • scopus:85208291368
ISSN
1095-9203
DOI
10.1126/science.adi1025
language
English
LU publication?
yes
id
136cf6f8-fbe5-4654-927c-73871635d888
date added to LUP
2025-01-09 11:12:20
date last changed
2025-07-11 15:55:15
@article{136cf6f8-fbe5-4654-927c-73871635d888,
  abstract     = {{<p>The innate immune system shapes brain development and is implicated in neurodevelopmental diseases. It is critical to define the relevant immune cells and signals and their impact on brain circuits. In this work, we found that group 2 innate lymphoid cells (ILC2s) and their cytokine interleukin-13 (IL-13) signaled directly to inhibitory interneurons to increase inhibitory synapse density in the developing mouse brain. ILC2s expanded and produced IL-13 in the developing brain meninges. Loss of ILC2s or IL-13 signaling to interneurons decreased inhibitory, but not excitatory, cortical synapses. Conversely, ILC2s and IL-13 were sufficient to increase inhibitory synapses. Loss of this signaling pathway led to selective impairments in social interaction. These data define a type 2 neuroimmune circuit in early life that shapes inhibitory synapse development and behavior.</p>}},
  author       = {{Barron, Jerika J. and Mroz, Nicholas M. and Taloma, Sunrae E. and Dahlgren, Madelene W. and Ortiz-Carpena, Jorge F. and Keefe, Matthew G. and Escoubas, Caroline C. and Dorman, Leah C. and Vainchtein, Ilia D. and Chiaranunt, Pailin and Kotas, Maya E. and Nowakowski, Tomasz J. and Bender, Kevin J. and Molofsky, Ari B. and Molofsky, Anna V.}},
  issn         = {{1095-9203}},
  language     = {{eng}},
  number       = {{6721}},
  publisher    = {{American Association for the Advancement of Science (AAAS)}},
  series       = {{Science}},
  title        = {{Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior}},
  url          = {{http://dx.doi.org/10.1126/science.adi1025}},
  doi          = {{10.1126/science.adi1025}},
  volume       = {{386}},
  year         = {{2024}},
}