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@ARTICLE{Ravichandran:282601,
      author       = {Ravichandran, Kishore Aravind and Brosseron, Frederic and
                      McManus, Róisín M and Ising, Christina and Görgen, Simon
                      and Schmidt, Susanne V and Santarelli, Fracesco and Lee, Se
                      Young and Jung, Hyuncheol and Chung, Won-Suk and Kim, Chan
                      Hyuk and Ruiz Laza, Agustín and Ruiz de Almodóvar, Carmen
                      and Ramirez, Alfredo and Latz, Eicke and Heneka, Michael T},
      title        = {{E}nhancing {T}yro3 signaling ameliorates {IL}-1β
                      production through {STAT}1 in {A}lzheimer's disease models.},
      journal      = {Journal of leukocyte biology},
      volume       = {117},
      number       = {12},
      issn         = {0741-5400},
      address      = {Tokyo},
      publisher    = {Oxford University Press},
      reportid     = {DZNE-2025-01359},
      pages        = {qiaf157},
      year         = {2025},
      abstract     = {Neuroinflammation plays a vital role in determining the
                      trajectory of Alzheimer's disease (AD) progression. In the
                      AD brain, microglial exposure to pathological amyloid β
                      (Aβ42) and tau peptide aggregates results in an NLRP3
                      inflammasome-activated proinflammatory response that ranges
                      from mild to severe. Recently we have shown that dementia
                      subjects with higher levels of soluble TAM receptors Tyro3
                      and AXL in the cerebrospinal fluid indicated cognitive
                      protection. The molecular mechanism for this protective
                      effect of TAM receptors is unknown. Here, we identified a
                      beneficial role of TAM receptors using Tyro3-overexpressing
                      (Tyro3OE) and Axl-overexpressing THP-1 cells. In the Tyro3OE
                      cells, the levels of the proinflammatory cytokine IL-1β
                      were markedly decreased in the AD microenvironment (tau +
                      Aβ42) and the classical NLRP3 inflammasome model
                      (lipopolysaccharide [LPS] + nigericin) in comparison with
                      the control cells. This was mediated by increased STAT1
                      phosphorylation and reduced IL-1β transcription enhancer
                      C-EBP-β in Tyro3OE cells. The use of the JAK1/2 inhibitor
                      ruxolitinib reduced the phosphorylation of STAT1, leading to
                      a partial restoration of IL-1β in the Tyro3OE cells. Last,
                      we found a significantly reduced IL-1β in the brains of AD
                      mice that has activated TAM signaling through Gas6-α-Aβ
                      lentiviral injection. In summary, TAM receptor Tyro3
                      overexpression decreased AD-associated IL-1β release from
                      macrophages thereby uncovering a potential beneficial role
                      for TAM receptors during neuroinflammation in AD.},
      keywords     = {Alzheimer Disease: metabolism / Alzheimer Disease:
                      pathology / Alzheimer Disease: genetics / Interleukin-1beta:
                      biosynthesis / Interleukin-1beta: metabolism / Animals /
                      Humans / Signal Transduction / Disease Models, Animal /
                      STAT1 Transcription Factor: metabolism / Mice / Receptor
                      Protein-Tyrosine Kinases: metabolism / Receptor
                      Protein-Tyrosine Kinases: genetics / Amyloid beta-Peptides:
                      metabolism / Inflammasomes: metabolism / THP-1 Cells /
                      Proto-Oncogene Proteins: metabolism / Phosphorylation / Axl
                      Receptor Tyrosine Kinase / Male / Mice, Inbred C57BL /
                      Nitriles / Mice, Transgenic / AD (Other) / Alzheimer’s
                      disease (Other) / IL-1β (Other) / NLRP3 (Other) / TAM
                      receptors (Other) / Interleukin-1beta (NLM Chemicals) /
                      STAT1 Transcription Factor (NLM Chemicals) / Receptor
                      Protein-Tyrosine Kinases (NLM Chemicals) / Amyloid
                      beta-Peptides (NLM Chemicals) / Inflammasomes (NLM
                      Chemicals) / Proto-Oncogene Proteins (NLM Chemicals) / Axl
                      Receptor Tyrosine Kinase (NLM Chemicals) / Tyro3 protein,
                      mouse (NLM Chemicals) / TYRO3 protein, human (NLM Chemicals)
                      / Nitriles (NLM Chemicals)},
      cin          = {AG Heneka / AG McManus / AG Latz},
      ddc          = {570},
      cid          = {I:(DE-2719)1011303 / I:(DE-2719)1013042 /
                      I:(DE-2719)1013024},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352) / 351 - Brain Function
                      (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41206011},
      doi          = {10.1093/jleuko/qiaf157},
      url          = {https://pub.dzne.de/record/282601},
}