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Dr. Stefan Wirtz
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Academic Career Length
28Years (1999-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications15 March 2007 in Nature Protocols
Journal Article
SWStefan Wirtz
Stefan WirtzCNClemens Neufert
Clemens Neufert
BWBenno Weigmann
Benno Weigmann
MNMarkus F Neurath
Markus F Neurath
1 May 2000 in Nature Medicine
Journal Article
RAR. Atreya
R. Atreya
JMJ. Mudter
J. Mudter
SFS. Finotto
S. Finotto
JMJ. Müllberg
J. Müllberg
TJT. Jostock
T. Jostock
MNM.F. Neurath
M.F. Neurath
+17
23 February 2014 in Nature
Journal Article
PSPing Shen
Ping Shen
TRToralf Roch
Toralf RochVLVicky Lampropoulou
Vicky Lampropoulou
RORichard A. O’connor
Richard A. O’connor
USUlrik Stervbo
Ulrik StervboSFSimon Fillatreau
Simon Fillatreau +25
29 June 2009 in Journal of Experimental Medicine
Journal Article
GPGeethanjali Pickert
Geethanjali Pickert
CNClemens Neufert
Clemens Neufert
MLMoritz Leppkes
Moritz LeppkesYZYan Zheng
Yan Zheng
NWNadine Wittkopf
Nadine Wittkopf
Christoph Becker +7
Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis, and pathways associated with wound healing in IECs. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22–dependent mucosal wound healing.
1 October 2004 in Immunity
Journal Article
Christoph BeckerMFMassimo C. Fantini
Massimo C. Fantini
CSChristoph Schramm
Christoph SchrammHLHans A. Lehr
Hans A. Lehr
SWStefan Wirtz
Stefan WirtzMNMarkus F. Neurath
Markus F. Neurath
+12
1 August 2013 in Immunity
Journal Article
TMTamar Mchedlidze
Tamar Mchedlidze
MWMaximilian Waldner
Maximilian Waldner
SZSteffen Zopf
Steffen Zopf
JWJennifer Walker
Jennifer Walker
ARAndrew L. Rankin
Andrew L. Rankin
SWStefan Wirtz
Stefan Wirtz +5
About Me
Wirtz S, et al. Caspase-8 in endothelial cells maintains gut homeostasis and prevents small bowel inflammation in mice. EMBO Mol Med. 2022 Jun 8;14(6):e14121. doi: 10.15252/emmm.202114121. Epub 2022 May 2. PMID: 35491615; PMCID: PMC9174885.
Wirtz S, et al. Functional Contribution and Targeted Migration of Group-2 Innate Lymphoid Cells in Inflammatory Lung Diseases: Being at the Right Place at the Right Time. Front Immunol. 2021 Jun 10;12:688879. doi: 10.3389/fimmu.2021.688879. PMID: 34177944; PMCID: PMC8222800.
Wirtz S, et al. Comparative Transcriptomics of IBD Patients Indicates Induction of Type 2 Immunity Irrespective of the Disease Ideotype. Front Med (Lausanne). 2021 May 31;8:664045. doi: 10.3389/fmed.2021.664045. PMID: 34136502; PMCID: PMC8200538.
Wirtz S, et al. The Regulation of Intestinal Inflammation and Cancer Development by Type 2 Immune Responses. Int J Mol Sci. 2020 Dec 21;21(24):9772. doi: 10.3390/ijms21249772. PMID: 33371444; PMCID: PMC7767427.
Wirtz S,et al. Regulation of Human Innate Lymphoid Cells in the Context of Mucosal Inflammation. Front Immunol. 2020 Jun 23;11:1062. doi: 10.3389/fimmu.2020.01062. PMID: 32655549; PMCID: PMC7324478.
Wirtz S. A CCL1/CCR8-dependent feed-forward mechanism drives ILC2 functions in type 2-mediated inflammation. J Exp Med. 2019 Dec 2;216(12):2763-2777. doi: 10.1084/jem.20182111. Epub 2019 Sep 19. PMID: 31537642; PMCID: PMC6888976.