Nature Search

Structural/functional similarity between proteins involved in complement- and cytotoxic T-lymphocyte-mediated cytolysis

Jürg Tschopp
Danièle Masson
Keith K. Stanley
Research28 Aug 1986
Nature

Volume: 322, P: 831-834
Phosphorylcholine acts as a Ca²⁺-dependent receptor molecule for lymphocyte perforin

Jürg Tschopp
Sylvie Schäfer
Christoph Heusser
Research19 Jan 1989
Nature

Volume: 337, P: 272-274
Formation of transmembrane tubules by spontaneous polymerization of the hydrophilic complement protein C9

Jürg Tschopp
Hans J. Müller-Eberhard
Eckhard R. Podack
Research05 Aug 1982
Nature

Volume: 298, P: 534-538
Cytolytic T-cell cytotoxicity is mediated through perforin and Fas lytic pathways

Bente Lowin
Michael Hahne
Jürg Tschopp
Research25 Aug 1994
Nature

Volume: 370, P: 650-652
Thioredoxin-interacting protein links oxidative stress to inflammasome activation

The signaling intermediates that activate inflammasomes have remained elusive. Tschopp and co-workers now describe that a thioredoxin-binding protein is a reactive oxygen species–regulated component of the NLRP3 inflammasome.

Rongbin Zhou
Aubry Tardivel
Jürg Tschopp
Research20 Dec 2009
Nature Immunology

Volume: 11, P: 136-140
Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor

Kimberly Burns
Jonathan Clatworthy
Filippo Volpe
Research10 May 2000
Nature Cell Biology

Volume: 2, P: 346-351
NALPs: a novel protein family involved in inflammation

Jürg Tschopp
Fabio Martinon
Kimberly Burns
Reviews01 Feb 2003
Nature Reviews Molecular Cell Biology

Volume: 4, P: 95-104
A role for mitochondria in NLRP3 inflammasome activation

Mitochondrial reactive oxygen species are shown to be required for activation of the NLRP3 inflammasome by various stimuli.

Rongbin Zhou
Amir S. Yazdi
Jürg Tschopp
Research01 Dec 2010
Nature

Volume: 469, P: 221-225
RIP1 is an essential mediator of Toll-like receptor 3–induced NF-κB activation

Etienne Meylan
Kim Burns
Jürg Tschopp
Research04 Apr 2004
Nature Immunology

Volume: 5, P: 503-507
Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptors

Margot Thome
Pascal Schneider
Jürg Tschopp
Research03 Apr 1997
Nature

Volume: 386, P: 517-521
Erratum: A role for mitochondria in NLRP3 inflammasome activation

Rongbin Zhou
Amir S. Yazdi
Jürg Tschopp
Amendments and Corrections15 Jun 2011
Nature

Volume: 475, P: 122
TRAIL receptor-2 signals apoptosis through FADD and caspase-8

Jean-Luc Bodmer
Nils Holler
Jürg Tschopp
Research13 Mar 2000
Nature Cell Biology

Volume: 2, P: 241-243
IRAK2 takes its place in TLR signaling

Toll-like receptors trigger an innate immune response by activating signaling pathways that are dependent on IRAK kinases. According to Kawagoe et al., the least understood IRAK member, IRAK2, is required for the perpetuation of these signals.

Etienne Meylan
Jürg Tschopp
News & Views01 Jun 2008
Nature Immunology

Volume: 9, P: 581-582
Regulation of lymphocyte proliferation and death by flip

Margot Thome
Jürg Tschopp
Reviews01 Oct 2001
Nature Reviews Immunology

Volume: 1, P: 50-58
NLRC4 inflammasomes in dendritic cells regulate noncognate effector function by memory CD8⁺ T cells

Noncognate CD8⁺ memory T cells can be rapidly activated by bacteria. Bedoui and colleagues show that this process is specifically dependent on recognition by and activation of the NLRC4 inflammasome.

Andreas Kupz
Greta Guarda
Sammy Bedoui
Research08 Jan 2012
Nature Immunology

Volume: 13, P: 162-169
Syk kinase signalling couples to the Nlrp3 inflammasome for anti-fungal host defence

Interleukin-1β (IL-1β) is a key pro-inflammatory factor in innate antifungal immunity, but the mechanism by which the mammalian immune system regulates IL-1β production after fungal recognition is unclear. Here it is demonstrated that the tyrosine kinase Syk controls both pro-IL-1β synthesis and Nlrp3 inflammasome activation after cell stimulation with Candida albicans.

Olaf Gross
Hendrik Poeck
Jürgen Ruland
Research01 Apr 2009
Nature

Volume: 459, P: 433-436
Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus

Etienne Meylan
Joseph Curran
Jürg Tschopp
Research21 Sept 2005
Nature

Volume: 437, P: 1167-1172
Gout-associated uric acid crystals activate the NALP3 inflammasome

Fabio Martinon
Virginie Pétrilli
Jürg Tschopp
Research11 Jan 2006
Nature

Volume: 440, P: 237-241
T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes

The mechanisms controlling excessive inflammatory responses, which can result in damage to tissues and diseases such as arthritis and type-2 diabetes, are poorly understood. Mouse effector and memory CD4⁺ T cells are now shown to inhibit inflammasome activity, revealing a mechanism by which effector and memory T cells can suppress potentially damaging inflammation while leaving the primary inflammatory response intact.

Greta Guarda
Catherine Dostert
Jürg Tschopp
Research03 Jun 2009
Nature

Volume: 460, P: 269-273
Inhibition of death receptor signals by cellular FLIP

Martin Irmler
Margot Thome
Jürg Tschopp
Research10 Jul 1997
Nature

Volume: 388, P: 190-195
A crucial function of SGT1 and HSP90 in inflammasome activity links mammalian and plant innate immune responses

Annick Mayor
Fabio Martinon
Jürg Tschopp
Research15 Apr 2007
Nature Immunology

Volume: 8, P: 497-503
Fas triggers an alternative, caspase-8–independent cell death pathway using the kinase RIP as effector molecule

Nils Holler
Rossana Zaru
Jürg Tschopp
Research01 Dec 2000
Nature Immunology

Volume: 1, P: 489-495
DEteCTINg fungal pathogens

Fungal infection is 'sensed' by host cell–expressed receptors. Two papers demonstrate that the C-type lectin receptor dectin-1 is required in vivo for cytokine production and killing of different fungal pathogens.

Catherine Dostert
Jürg Tschopp
News & Views01 Jan 2007
Nature Immunology

Volume: 8, P: 17-18
Function of TRADD in tumor necrosis factor receptor 1 signaling and in TRIF-dependent inflammatory responses

The function of the adaptor protein TRADD is uncertain. Teams led by Pasparakis and Liu solidify TRADD's function in TNF receptor signaling and extend its influence to TRIF-dependent Toll-like receptor pathways.

Maria A Ermolaeva
Marie-Cécile Michallet
Manolis Pasparakis
Research20 Jul 2008
Nature Immunology

Volume: 9, P: 1037-1046
CARMA1 is a critical lipid raft–associated regulator of TCR-induced NF-κB activation

Olivier Gaide
Benoît Favier
Margot Thome
Research05 Aug 2002
Nature Immunology

Volume: 3, P: 836-843
Activation of the NLRP3 inflammasome in dendritic cells induces IL-1β–dependent adaptive immunity against tumors

Dying tumor cells release ATP, which activates the NLRP3 inflammasome in dendritic cells, enabling the secretion of interleukin-1β and the subsequent priming of tumor-specific interferon-γ-producing T lymphocytes.

François Ghiringhelli
Lionel Apetoh
Laurence Zitvogel
Research20 Sept 2009
Nature Medicine

Volume: 15, P: 1170-1178
Inhibition of post-ischemic brain injury by clusterin overexpression

Philippe Wehrli
Yves Charnay
Panteleimon Giannakopoulos
Correspondence01 Sept 2001
Nature Medicine

Volume: 7, P: 977-978
Thyroiditis and hepatitis: Fas on the road to disease

Fas-mediated programmed cell death contributes to the pathology of thyroiditis and hepatitis (pages 409–413).

Lars E. French
Jürg Tschopp
News & Views01 Apr 1997
Nature Medicine

Volume: 3, P: 387-388
The TRAIL to selective tumor death

Lars E. French
Jürg Tschopp
News & Views01 Feb 1999
Nature Medicine

Volume: 5, P: 146-147
cFLIP regulation of lymphocyte activation and development

Cellular caspase-8 (FLICE)-like inhibitory protein (cFLIP) was originally identified as an inhibitor of death-receptor signalling. However, this Review discusses new data indicating that cFLIP is also required for the survival and proliferation of T cells following T-cell-receptor stimulation.

Ralph C. Budd
Wen-Chen Yeh
Jürg Tschopp
Reviews01 Mar 2006
Nature Reviews Immunology

Volume: 6, P: 196-204
Caspase-independent cell death in T lymphocytes

Marja Jäättelä
Jürg Tschopp
Reviews01 May 2003
Nature Immunology

Volume: 4, P: 416-423
Intracellular pattern recognition receptors in the host response

Etienne Meylan
Jürg Tschopp
Michael Karin
Reviews06 Jul 2006
Nature

Volume: 442, P: 39-44
Fas-dependent tissue turnover is implicated in tumor cell clearance

Michael Schröter
Janos Peli
Ernst Reichmann
Research06 Apr 2000
Oncogene

Volume: 19, P: 1794-1800
Accelerated degradation of cellular FLIP protein through the ubiquitin-proteasome pathway in p53-mediated apoptosis of human cancer cells

Takuya Fukazawa
Toshiyoshi Fujiwara
Noriaki Tanaka
Research28 Aug 2001
Oncogene

Volume: 20, P: 5225-5231
Ubiquitination of the Epstein–Barr virus-encoded latent membrane protein 1 depends on the integrity of the TRAF binding site

Sylvia Rothenberger
Kimberly Burns
Claude Bron
Research28 Aug 2003
Oncogene

Volume: 22, P: 5614-5618
Inflammation in gout: mechanisms and therapeutic targets

This Review explores the main mechanisms of inflammation and the role of innate immune sensors in gouty arthritis, and discusses potential therapeutic approaches aimed at regulating these processes.

Alexander K. So
Fabio Martinon
Reviews28 Sept 2017
Nature Reviews Rheumatology

Volume: 13, P: 639-647
Protein-based therapeutic approaches targeting death receptors

Lars E French
Jürg Tschopp
Reviews25 Mar 2003
Cell Death & Differentiation

Volume: 10, P: 117-123
Life and death in a medieval atmosphere

Christoph Borner
Laurent Monney
Sébastien Conus
News & Views28 Jan 1999
Cell Death & Differentiation

Volume: 6, P: 201-206
Multifunctional roles for MALT1 in T-cell activation

Recent research on MALT1 (mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1), a protein essential for nuclear factor-κB (NF-κB) activation, has uncovered new mechanisms by which MALT1 can orchestrate intracellular signalling events. Here, Margot Thome highlights recent progress which characterizes how the protease and scaffolding functions of MALT1 modulate T-cell activation.

Margot Thome
Reviews01 Jul 2008
Nature Reviews Immunology

Volume: 8, P: 495-500
The BAFF/APRIL system in SLE pathogenesis

In this article the authors review the 'BAFF/APRIL system', a complex of the cytokines BAFF and APRIL, their receptors and signalling pathways. The efficacy of belimumab, an anti-BAFF biologic agent used in clinical trials for SLE, is used to develop an argument that the BAFF/APRIL system is an important regulator of autoimmunity. Future therapies for SLE could fine-tune these cytokine signalling pathways to regulate autoreactive B cell survival and autoimmunity.

Fabien B. Vincent
Eric F. Morand
Fabienne Mackay
Reviews11 Mar 2014
Nature Reviews Rheumatology

Volume: 10, P: 365-373
CARMA1, BCL-10 and MALT1 in lymphocyte development and activation

Margot Thome
Reviews01 May 2004
Nature Reviews Immunology

Volume: 4, P: 348-359
New players driving inflammation in monogenic autoinflammatory diseases

In this Review, Martinon and Aksentijevich highlight the latest developments in research into the pathogenesis of autoinflammatory diseases. Newly discovered disease-causing mutations and molecular pathways underlying inherited autoinflammatory diseases are discussed.

Fabio Martinon
Ivona Aksentijevich
Reviews23 Sept 2014
Nature Reviews Rheumatology

Volume: 11, P: 11-20

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