XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation

Research output: Contribution to journal › Journal article › Research › peer-review

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XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation. / Yabal, Monica; Müller, Nicole; Adler, Heiko; Knies, Nathalie; Groß, Christina J; Damgaard, Rune Busk; Kanegane, Hirokazu; Ringelhan, Marc; Kaufmann, Thomas; Heikenwälder, Mathias; Strasser, Andreas; Groß, Olaf; Ruland, Jürgen; Peschel, Christian; Gyrd-Hansen, Mads; Jost, Philipp J.

In: Cell Reports, Vol. 7, No. 6, 26.06.2014, p. 1796-1808.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Yabal, M, Müller, N, Adler, H, Knies, N, Groß, CJ, Damgaard, RB, Kanegane, H, Ringelhan, M, Kaufmann, T, Heikenwälder, M, Strasser, A, Groß, O, Ruland, J, Peschel, C, Gyrd-Hansen, M & Jost, PJ 2014, 'XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation', Cell Reports, vol. 7, no. 6, pp. 1796-1808. https://doi.org/10.1016/j.celrep.2014.05.008

APA

Yabal, M., Müller, N., Adler, H., Knies, N., Groß, C. J., Damgaard, R. B., Kanegane, H., Ringelhan, M., Kaufmann, T., Heikenwälder, M., Strasser, A., Groß, O., Ruland, J., Peschel, C., Gyrd-Hansen, M., & Jost, P. J. (2014). XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation. Cell Reports, 7(6), 1796-1808. https://doi.org/10.1016/j.celrep.2014.05.008

Vancouver

Yabal M, Müller N, Adler H, Knies N, Groß CJ, Damgaard RB et al. XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation. Cell Reports. 2014 Jun 26;7(6):1796-1808. https://doi.org/10.1016/j.celrep.2014.05.008

Author

Yabal, Monica ; Müller, Nicole ; Adler, Heiko ; Knies, Nathalie ; Groß, Christina J ; Damgaard, Rune Busk ; Kanegane, Hirokazu ; Ringelhan, Marc ; Kaufmann, Thomas ; Heikenwälder, Mathias ; Strasser, Andreas ; Groß, Olaf ; Ruland, Jürgen ; Peschel, Christian ; Gyrd-Hansen, Mads ; Jost, Philipp J. / XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation. In: Cell Reports. 2014 ; Vol. 7, No. 6. pp. 1796-1808.

Bibtex

@article{e6aa15edcf344db587a2e1d94b1b68ba,

title = "XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation",

abstract = "X-linked inhibitor of apoptosis protein (XIAP) has been identified as a potent regulator of innate immune responses, and loss-of-function mutations in XIAP cause the development of the X-linked lymphoproliferative syndrome type 2 (XLP-2) in humans. Using gene-targeted mice, we show that loss of XIAP or deletion of its RING domain lead to excessive cell death and IL-1β secretion from dendritic cells triggered by diverse Toll-like receptor stimuli. Aberrant IL-1β secretion is TNF dependent and requires RIP3 but is independent of cIAP1/cIAP2. The observed cell death also requires TNF and RIP3 but proceeds independently of caspase-1/caspase-11 or caspase-8 function. Loss of XIAP results in aberrantly elevated ubiquitylation of RIP1 outside of TNFR complex I. Virally infected Xiap(-/-) mice present with symptoms reminiscent of XLP-2. Our data show that XIAP controls RIP3-dependent cell death and IL-1β secretion in response to TNF, which might contribute to hyperinflammation in patients with XLP-2.",

author = "Monica Yabal and Nicole M{\"u}ller and Heiko Adler and Nathalie Knies and Gro{\ss}, {Christina J} and Damgaard, {Rune Busk} and Hirokazu Kanegane and Marc Ringelhan and Thomas Kaufmann and Mathias Heikenw{\"a}lder and Andreas Strasser and Olaf Gro{\ss} and J{\"u}rgen Ruland and Christian Peschel and Mads Gyrd-Hansen and Jost, {Philipp J}",

year = "2014",

month = jun,

day = "26",

doi = "10.1016/j.celrep.2014.05.008",

language = "English",

volume = "7",

pages = "1796--1808",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Cell Press",

number = "6",

}

RIS

TY - JOUR

T1 - XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation

AU - Yabal, Monica

AU - Müller, Nicole

AU - Adler, Heiko

AU - Knies, Nathalie

AU - Groß, Christina J

AU - Damgaard, Rune Busk

AU - Kanegane, Hirokazu

AU - Ringelhan, Marc

AU - Kaufmann, Thomas

AU - Heikenwälder, Mathias

AU - Strasser, Andreas

AU - Groß, Olaf

AU - Ruland, Jürgen

AU - Peschel, Christian

AU - Gyrd-Hansen, Mads

AU - Jost, Philipp J

PY - 2014/6/26

Y1 - 2014/6/26

N2 - X-linked inhibitor of apoptosis protein (XIAP) has been identified as a potent regulator of innate immune responses, and loss-of-function mutations in XIAP cause the development of the X-linked lymphoproliferative syndrome type 2 (XLP-2) in humans. Using gene-targeted mice, we show that loss of XIAP or deletion of its RING domain lead to excessive cell death and IL-1β secretion from dendritic cells triggered by diverse Toll-like receptor stimuli. Aberrant IL-1β secretion is TNF dependent and requires RIP3 but is independent of cIAP1/cIAP2. The observed cell death also requires TNF and RIP3 but proceeds independently of caspase-1/caspase-11 or caspase-8 function. Loss of XIAP results in aberrantly elevated ubiquitylation of RIP1 outside of TNFR complex I. Virally infected Xiap(-/-) mice present with symptoms reminiscent of XLP-2. Our data show that XIAP controls RIP3-dependent cell death and IL-1β secretion in response to TNF, which might contribute to hyperinflammation in patients with XLP-2.

AB - X-linked inhibitor of apoptosis protein (XIAP) has been identified as a potent regulator of innate immune responses, and loss-of-function mutations in XIAP cause the development of the X-linked lymphoproliferative syndrome type 2 (XLP-2) in humans. Using gene-targeted mice, we show that loss of XIAP or deletion of its RING domain lead to excessive cell death and IL-1β secretion from dendritic cells triggered by diverse Toll-like receptor stimuli. Aberrant IL-1β secretion is TNF dependent and requires RIP3 but is independent of cIAP1/cIAP2. The observed cell death also requires TNF and RIP3 but proceeds independently of caspase-1/caspase-11 or caspase-8 function. Loss of XIAP results in aberrantly elevated ubiquitylation of RIP1 outside of TNFR complex I. Virally infected Xiap(-/-) mice present with symptoms reminiscent of XLP-2. Our data show that XIAP controls RIP3-dependent cell death and IL-1β secretion in response to TNF, which might contribute to hyperinflammation in patients with XLP-2.

U2 - 10.1016/j.celrep.2014.05.008

DO - 10.1016/j.celrep.2014.05.008

M3 - Journal article

C2 - 24882010

VL - 7

SP - 1796

EP - 1808

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 6

ER -

ID: 117867943

Forskning