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@ARTICLE{Stockis:291771,
      author       = {J. Stockis and T. Yip and J. Moreno-Vicente and O. Burton
                      and Y. Samarakoon and M. J. Schuijs and S. Raghunathan and
                      C. Garcia and W. Luo and S. K. Whiteside and S. Png and C.
                      Simpson and S. Monk and A. Sawle and K. Yin and J. Barbieri
                      and P. Papadopoulos and H. Wong and H.-R. Rodewald$^*$ and
                      T. Vyse and A. N. J. McKenzie and M. S. Cragg and M. Hoare
                      and D. R. Withers and H. J. Fehling and R. Roychoudhuri and
                      A. Liston and T. Y. F. Halim},
      title        = {{C}ross-talk between {ILC}2 and {G}ata3high {T}regs locally
                      constrains adaptive type 2 immunity.},
      journal      = {Science immunology},
      volume       = {9},
      number       = {97},
      issn         = {2470-9468},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DKFZ-2024-01507},
      pages        = {eadl1903},
      year         = {2024},
      abstract     = {Regulatory T cells (Tregs) control adaptive immunity and
                      restrain type 2 inflammation in allergic disease.
                      Interleukin-33 promotes the expansion of tissue-resident
                      Tregs and group 2 innate lymphoid cells (ILC2s); however,
                      how Tregs locally coordinate their function within the
                      inflammatory niche is not understood. Here, we show that
                      ILC2s are critical orchestrators of Treg function. Using
                      spatial, cellular, and molecular profiling of the type 2
                      inflamed niche, we found that ILC2s and Tregs engage in a
                      direct (OX40L-OX40) and chemotaxis-dependent (CCL1-CCR8)
                      cellular dialogue that enforces the local accumulation of
                      Gata3high Tregs, which are transcriptionally and
                      functionally adapted to the type 2 environment. Genetic
                      interruption of ILC2-Treg communication resulted in
                      uncontrolled type 2 lung inflammation after allergen
                      exposure. Mechanistically, we found that Gata3high Tregs can
                      modulate the local bioavailability of the costimulatory
                      molecule OX40L, which subsequently controlled effector
                      memory T helper 2 cell numbers. Hence, ILC2-Treg
                      interactions represent a critical feedback mechanism to
                      control adaptive type 2 immunity.},
      keywords     = {Animals / T-Lymphocytes, Regulatory: immunology / GATA3
                      Transcription Factor: immunology / GATA3 Transcription
                      Factor: metabolism / Mice / Adaptive Immunity: immunology /
                      Mice, Inbred C57BL / Lymphocytes: immunology / Immunity,
                      Innate: immunology / Mice, Knockout / Th2 Cells: immunology
                      / Female / GATA3 Transcription Factor (NLM Chemicals) /
                      Gata3 protein, mouse (NLM Chemicals)},
      cin          = {D110},
      ddc          = {610},
      cid          = {I:(DE-He78)D110-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39028828},
      doi          = {10.1126/sciimmunol.adl1903},
      url          = {https://inrepo02.dkfz.de/record/291771},
}