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By constitutively activating the Ras\/MAPK-pathway via\n                    <jats:italic>\n                      Ras\n                      <jats:sup>V12<\/jats:sup>\n                    <\/jats:italic>\n                    -overexpression in the postmitotic salivary glands (SGs) of\n                    <jats:italic>Drosophila<\/jats:italic>\n                    larvae, we overrode the glands adaptability to growth signals and induced hypertrophy. The accompanied loss of tissue integrity, recognition by cellular immunity, and cell death are all buffered by blocking stress signaling through a genuine tissue-autonomous immune response. This novel, spatio-temporally tightly regulated mechanism relies on the inhibition of a feedback-loop in the JNK-pathway by the immune effector and antimicrobial peptide Drosomycin. While this interaction might allow growing SGs to cope with temporary stress, continuous Drosomycin expression in\n                    <jats:italic>\n                      Ras\n                      <jats:sup>V12<\/jats:sup>\n                    <\/jats:italic>\n                    -glands favors unrestricted hypertrophy. These findings indicate the necessity to refine therapeutic approaches that stimulate immune responses by acknowledging their possible, detrimental effects in damaged or stressed tissues.\n                  <\/jats:p>","DOI":"10.7554\/elife.64919","type":"journal-article","created":{"date-parts":[[2020,12,30]],"date-time":"2020-12-30T12:02:54Z","timestamp":1609329774000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.64919","source":"Crossref","is-referenced-by-count":23,"title":["Tissue-autonomous immune response regulates stress signaling during hypertrophy"],"prefix":"10.7554","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0457-1348","authenticated-orcid":true,"given":"Robert","family":"Krautz","sequence":"first","affiliation":[{"name":"Department of Molecular Biosciences, The Wenner-Gren Institute (MBW), Stockholm University, Stockholm, 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