@Article{dbt_mods_00053641,
  author = 	{Peters, Isabel
		and M{\"u}ller, Sylvia
		and K{\"u}chler, Claudia
		and J{\"a}ger, Ute
		and Drube, Sebastian},
  editor = 	{Traina, Giovanna},
  title = 	{The Heat Shock Protein 90 (HSP90) Is Required for the IL-33-Induced Cytokine Production in Mast Cells (MCs)},
  journal = 	{International journal of molecular sciences},
  year = 	{2022},
  month = 	{Sep},
  day = 	{17},
  publisher = 	{Molecular Diversity Preservation International},
  address = 	{Basel},
  volume = 	{23},
  number = 	{18},
  pages = 	{1--11},
  keywords = 	{mast cells; IL-33; HSP90; 17AAG; Molek{\"u}l},
  abstract = 	{The alarmin interleukin-33 (IL-33) is released upon cell stress and damage in peripheral tissues. The receptor for IL-33 is the Toll/Interleukin-1 receptor (TIR)-family member T1/ST2 (the IL-33R), which is highly and constitutively expressed on MCs. The sensing of IL-33 by MCs induces the MyD88−TAK1−IKK2-dependent activation of p65/RelA and MAP-kinases, which mediate the production of pro-inflammatory cytokines and amplify Fc$\epsilon$RI-mediated MC-effector functions and the resulting allergic reactions. Therefore, the investigation of IL-33-induced signaling is of interest for developing therapeutic interventions effective against allergic reactions. Importantly, beside the release of IL-33, heat shock proteins (HSPs) are upregulated during allergic reactions. This maintains the biological functions of signaling molecules and/or cytokines but unfortunately also strengthens the severity of inflammatory reactions. Here, we demonstrate that HSP90 does not support the IL-33-induced and MyD88−TAK1−IKK2-dependent activation of p65/RelA and of mitogen-activated protein (MAP)-kinases. We found that HSP90 acts downstream of these signaling pathways, mediates the stability of produced cytokine mRNAs, and therefore facilitates the resulting cytokine production. These data show that IL-33 enables MCs to perform an effective cytokine production by the upregulation of HSP90. Consequently, HSP90 might be an attractive therapeutic target for blocking IL-33-mediated inflammatory reactions.},
  note = 	{Zweitver{\"o}ffentlichung},
  note = 	{1.2000 -},
  issn = 	{1422-0067},
  doi = 	{10.3390/ijms231810855},
  url = 	{https://www.db-thueringen.de/receive/dbt_mods_00053641},
  url = 	{http://uri.gbv.de/document/gvk:ppn:316340715},
  url = 	{https://doi.org/10.3390/ijms231810855},
  file = 	{:https://www.db-thueringen.de/servlets/MCRFileNodeServlet/dbt_derivate_00057447/ijms-23-10855.pdf:PDF},
  language = 	{en}
}