Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation

Yingyu Ma; Hongtao Liu; Hoang Tu-Rapp; Hans Juergen Thiesen; Saleh M. Ibrahim; Shawn M. Cole; Richard M. Pope

doi:10.1038/ni1054

Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation

Yingyu Ma, Hongtao Liu, Hoang Tu-Rapp, Hans Juergen Thiesen, Saleh M. Ibrahim, Shawn M. Cole, Richard M. Pope^*

^*Korrespondierende/r Autor/-in für diese Arbeit

Klinik für Dermatologie, Allergologie und Venerologie

129 Zitate (Scopus)

Abstract

The nonapoptotic functions of Fas ligation are incompletely characterized. In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice. Despite having milder arthritis, Fas-deficient mice had more of the critical pro-inflammatory mediator interleukin-1β (IL-1β) in their joints, suggesting inefficient activation through IL-1 receptor 1 (IL-1R1) when Fas signaling is deficient. In primary human macrophages and macrophages from Fas- or Fas ligand (FasL -deficient mice, interruption of Fas-FasL signaling suppressed nuclear factor-κB activation and cytokine expression induced by IL-1β and lipopolysaccharide. This cross-talk was mediated by the Fas-associated death domain through interaction with myeloid differentiation factor 88. These observations document a unique mechanism whereby Fas-FasL interactions enhance activation through the IL-1R1 or Toll-like receptor 4 pathway, which may contribute to the pathogenesis of chronic arthritis.

Originalsprache	Englisch
Zeitschrift	Nature Immunology
Jahrgang	5
Ausgabenummer	4
Seiten (von - bis)	380-387
Seitenumfang	8
ISSN	1529-2908
DOIs	https://doi.org/10.1038/ni1054
Publikationsstatus	Veröffentlicht - 04.2004

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also thank H. Perlman, P.H. Stern, N.A. Clipstone and A. Lin for critical review of the manuscript; M.E. Peter for advice on the immunoprecipitation experiments; C.J. Zander for technical assistance; and H.-J. Kreutzer for help evaluating joint histopathology. Supported by the National Institutes of Health (R01-AR049217) and The Veterans Administration Research Service (Merit Review), the National and Greater Chicagoland Chapters of the Arthritis Foundation and Deutsche Forschungsgemeinschaft (IB 24/3-1 to S.M.I.).

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Forschungsschwerpunkt: Infektion und Entzündung - Zentrum für Infektions- und Entzündungsforschung Lübeck (ZIEL)

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title = "Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation",

abstract = "The nonapoptotic functions of Fas ligation are incompletely characterized. In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice. Despite having milder arthritis, Fas-deficient mice had more of the critical pro-inflammatory mediator interleukin-1β (IL-1β) in their joints, suggesting inefficient activation through IL-1 receptor 1 (IL-1R1) when Fas signaling is deficient. In primary human macrophages and macrophages from Fas- or Fas ligand (FasL -deficient mice, interruption of Fas-FasL signaling suppressed nuclear factor-κB activation and cytokine expression induced by IL-1β and lipopolysaccharide. This cross-talk was mediated by the Fas-associated death domain through interaction with myeloid differentiation factor 88. These observations document a unique mechanism whereby Fas-FasL interactions enhance activation through the IL-1R1 or Toll-like receptor 4 pathway, which may contribute to the pathogenesis of chronic arthritis.",

author = "Yingyu Ma and Hongtao Liu and Hoang Tu-Rapp and Thiesen, \{Hans Juergen\} and Ibrahim, \{Saleh M.\} and Cole, \{Shawn M.\} and Pope, \{Richard M.\}",

note = "Funding Information: also thank H. Perlman, P.H. Stern, N.A. Clipstone and A. Lin for critical review of the manuscript; M.E. Peter for advice on the immunoprecipitation experiments; C.J. Zander for technical assistance; and H.-J. Kreutzer for help evaluating joint histopathology. Supported by the National Institutes of Health (R01-AR049217) and The Veterans Administration Research Service (Merit Review), the National and Greater Chicagoland Chapters of the Arthritis Foundation and Deutsche Forschungsgemeinschaft (IB 24/3-1 to S.M.I.).",

year = "2004",

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doi = "10.1038/ni1054",

language = "English",

volume = "5",

pages = "380--387",

journal = "Nature Immunology",

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T1 - Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation

AU - Ma, Yingyu

AU - Liu, Hongtao

AU - Tu-Rapp, Hoang

AU - Thiesen, Hans Juergen

AU - Ibrahim, Saleh M.

AU - Cole, Shawn M.

AU - Pope, Richard M.

N1 - Funding Information: also thank H. Perlman, P.H. Stern, N.A. Clipstone and A. Lin for critical review of the manuscript; M.E. Peter for advice on the immunoprecipitation experiments; C.J. Zander for technical assistance; and H.-J. Kreutzer for help evaluating joint histopathology. Supported by the National Institutes of Health (R01-AR049217) and The Veterans Administration Research Service (Merit Review), the National and Greater Chicagoland Chapters of the Arthritis Foundation and Deutsche Forschungsgemeinschaft (IB 24/3-1 to S.M.I.).

PY - 2004/4

Y1 - 2004/4

N2 - The nonapoptotic functions of Fas ligation are incompletely characterized. In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice. Despite having milder arthritis, Fas-deficient mice had more of the critical pro-inflammatory mediator interleukin-1β (IL-1β) in their joints, suggesting inefficient activation through IL-1 receptor 1 (IL-1R1) when Fas signaling is deficient. In primary human macrophages and macrophages from Fas- or Fas ligand (FasL -deficient mice, interruption of Fas-FasL signaling suppressed nuclear factor-κB activation and cytokine expression induced by IL-1β and lipopolysaccharide. This cross-talk was mediated by the Fas-associated death domain through interaction with myeloid differentiation factor 88. These observations document a unique mechanism whereby Fas-FasL interactions enhance activation through the IL-1R1 or Toll-like receptor 4 pathway, which may contribute to the pathogenesis of chronic arthritis.

AB - The nonapoptotic functions of Fas ligation are incompletely characterized. In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice. Despite having milder arthritis, Fas-deficient mice had more of the critical pro-inflammatory mediator interleukin-1β (IL-1β) in their joints, suggesting inefficient activation through IL-1 receptor 1 (IL-1R1) when Fas signaling is deficient. In primary human macrophages and macrophages from Fas- or Fas ligand (FasL -deficient mice, interruption of Fas-FasL signaling suppressed nuclear factor-κB activation and cytokine expression induced by IL-1β and lipopolysaccharide. This cross-talk was mediated by the Fas-associated death domain through interaction with myeloid differentiation factor 88. These observations document a unique mechanism whereby Fas-FasL interactions enhance activation through the IL-1R1 or Toll-like receptor 4 pathway, which may contribute to the pathogenesis of chronic arthritis.

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U2 - 10.1038/ni1054

DO - 10.1038/ni1054

M3 - Journal articles

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AN - SCOPUS:5044228305

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EP - 387

JO - Nature Immunology

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ER -

Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation

Abstract

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