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Cutting edge

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Cutting edge : FAS (CD95) mediates noncanonical IL-1β and IL-18 maturation via caspase-8 in an RIP3-independent manner. / Bossaller, Lukas; Chiang, Ping-I; Schmidt-Lauber, Christian; Ganesan, Sandhya; Kaiser, William J; Rathinam, Vijay A K; Mocarski, Edward S; Subramanian, Deepa; Green, Douglas R; Silverman, Neal; Fitzgerald, Katherine A; Marshak-Rothstein, Ann; Latz, Eicke.

in: J IMMUNOL, Jahrgang 189, Nr. 12, 15.12.2012, S. 5508-12.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Bossaller, L, Chiang, P-I, Schmidt-Lauber, C, Ganesan, S, Kaiser, WJ, Rathinam, VAK, Mocarski, ES, Subramanian, D, Green, DR, Silverman, N, Fitzgerald, KA, Marshak-Rothstein, A & Latz, E 2012, 'Cutting edge: FAS (CD95) mediates noncanonical IL-1β and IL-18 maturation via caspase-8 in an RIP3-independent manner', J IMMUNOL, Jg. 189, Nr. 12, S. 5508-12. https://doi.org/10.4049/jimmunol.1202121

APA

Bossaller, L., Chiang, P-I., Schmidt-Lauber, C., Ganesan, S., Kaiser, W. J., Rathinam, V. A. K., Mocarski, E. S., Subramanian, D., Green, D. R., Silverman, N., Fitzgerald, K. A., Marshak-Rothstein, A., & Latz, E. (2012). Cutting edge: FAS (CD95) mediates noncanonical IL-1β and IL-18 maturation via caspase-8 in an RIP3-independent manner. J IMMUNOL, 189(12), 5508-12. https://doi.org/10.4049/jimmunol.1202121

Vancouver

Bossaller L, Chiang P-I, Schmidt-Lauber C, Ganesan S, Kaiser WJ, Rathinam VAK et al. Cutting edge: FAS (CD95) mediates noncanonical IL-1β and IL-18 maturation via caspase-8 in an RIP3-independent manner. J IMMUNOL. 2012 Dez 15;189(12):5508-12. https://doi.org/10.4049/jimmunol.1202121

Bibtex

@article{265d3e3cbd3f467cb17c8902ccedb3da,
title = "Cutting edge: FAS (CD95) mediates noncanonical IL-1β and IL-18 maturation via caspase-8 in an RIP3-independent manner",
abstract = "Fas, a TNF family receptor, is activated by the membrane protein Fas ligand expressed on various immune cells. Fas signaling triggers apoptosis and induces inflammatory cytokine production. Among the Fas-induced cytokines, the IL-1β family cytokines require proteolysis to gain biological activity. Inflammasomes, which respond to pathogens and danger signals, cleave IL-1β cytokines via caspase-1. However, the mechanisms by which Fas regulates IL-1β activation remain unresolved. In this article, we demonstrate that macrophages exposed to TLR ligands upregulate Fas, which renders them responsive to receptor engagement by Fas ligand. Fas signaling activates caspase-8 in macrophages and dendritic cells, leading to the maturation of IL-1β and IL-18 independently of inflammasomes or RIP3. Hence, Fas controls a novel noncanonical IL-1β activation pathway in myeloid cells, which could play an essential role in inflammatory processes, tumor surveillance, and control of infectious diseases.",
keywords = "Animals, Caspase 8/genetics, Dendritic Cells/enzymology, Enzyme Activation/immunology, Fas-Associated Death Domain Protein/deficiency, Inflammasomes/metabolism, Interleukin-18/biosynthesis, Interleukin-1beta/biosynthesis, Macrophages, Peritoneal/enzymology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Receptor-Interacting Protein Serine-Threonine Kinases/deficiency, Signal Transduction/genetics, fas Receptor/physiology",
author = "Lukas Bossaller and Ping-I Chiang and Christian Schmidt-Lauber and Sandhya Ganesan and Kaiser, {William J} and Rathinam, {Vijay A K} and Mocarski, {Edward S} and Deepa Subramanian and Green, {Douglas R} and Neal Silverman and Fitzgerald, {Katherine A} and Ann Marshak-Rothstein and Eicke Latz",
year = "2012",
month = dec,
day = "15",
doi = "10.4049/jimmunol.1202121",
language = "English",
volume = "189",
pages = "5508--12",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "12",

}

RIS

TY - JOUR

T1 - Cutting edge

T2 - FAS (CD95) mediates noncanonical IL-1β and IL-18 maturation via caspase-8 in an RIP3-independent manner

AU - Bossaller, Lukas

AU - Chiang, Ping-I

AU - Schmidt-Lauber, Christian

AU - Ganesan, Sandhya

AU - Kaiser, William J

AU - Rathinam, Vijay A K

AU - Mocarski, Edward S

AU - Subramanian, Deepa

AU - Green, Douglas R

AU - Silverman, Neal

AU - Fitzgerald, Katherine A

AU - Marshak-Rothstein, Ann

AU - Latz, Eicke

PY - 2012/12/15

Y1 - 2012/12/15

N2 - Fas, a TNF family receptor, is activated by the membrane protein Fas ligand expressed on various immune cells. Fas signaling triggers apoptosis and induces inflammatory cytokine production. Among the Fas-induced cytokines, the IL-1β family cytokines require proteolysis to gain biological activity. Inflammasomes, which respond to pathogens and danger signals, cleave IL-1β cytokines via caspase-1. However, the mechanisms by which Fas regulates IL-1β activation remain unresolved. In this article, we demonstrate that macrophages exposed to TLR ligands upregulate Fas, which renders them responsive to receptor engagement by Fas ligand. Fas signaling activates caspase-8 in macrophages and dendritic cells, leading to the maturation of IL-1β and IL-18 independently of inflammasomes or RIP3. Hence, Fas controls a novel noncanonical IL-1β activation pathway in myeloid cells, which could play an essential role in inflammatory processes, tumor surveillance, and control of infectious diseases.

AB - Fas, a TNF family receptor, is activated by the membrane protein Fas ligand expressed on various immune cells. Fas signaling triggers apoptosis and induces inflammatory cytokine production. Among the Fas-induced cytokines, the IL-1β family cytokines require proteolysis to gain biological activity. Inflammasomes, which respond to pathogens and danger signals, cleave IL-1β cytokines via caspase-1. However, the mechanisms by which Fas regulates IL-1β activation remain unresolved. In this article, we demonstrate that macrophages exposed to TLR ligands upregulate Fas, which renders them responsive to receptor engagement by Fas ligand. Fas signaling activates caspase-8 in macrophages and dendritic cells, leading to the maturation of IL-1β and IL-18 independently of inflammasomes or RIP3. Hence, Fas controls a novel noncanonical IL-1β activation pathway in myeloid cells, which could play an essential role in inflammatory processes, tumor surveillance, and control of infectious diseases.

KW - Animals

KW - Caspase 8/genetics

KW - Dendritic Cells/enzymology

KW - Enzyme Activation/immunology

KW - Fas-Associated Death Domain Protein/deficiency

KW - Inflammasomes/metabolism

KW - Interleukin-18/biosynthesis

KW - Interleukin-1beta/biosynthesis

KW - Macrophages, Peritoneal/enzymology

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Receptor-Interacting Protein Serine-Threonine Kinases/deficiency

KW - Signal Transduction/genetics

KW - fas Receptor/physiology

U2 - 10.4049/jimmunol.1202121

DO - 10.4049/jimmunol.1202121

M3 - SCORING: Journal article

C2 - 23144495

VL - 189

SP - 5508

EP - 5512

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 12

ER -