Publication

Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice

Buonocore, S., Flamand, N. V., Claessen, N., Heeringa, P., Goldman, M. & Florquin, S., Jul-2004, In : Clinical and Experimental Immunology. 137, 1, p. 74-80 7 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Buonocore, S., Flamand, N. V., Claessen, N., Heeringa, P., Goldman, M., & Florquin, S. (2004). Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice. Clinical and Experimental Immunology, 137(1), 74-80. https://doi.org/10.1111/j.1365-2249.2004.02514.x

Author

Buonocore, S ; Flamand, [No Value] ; Claessen, N ; Heeringa, P ; Goldman, M ; Florquin, S. / Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice. In: Clinical and Experimental Immunology. 2004 ; Vol. 137, No. 1. pp. 74-80.

Harvard

Buonocore, S, Flamand, NV, Claessen, N, Heeringa, P, Goldman, M & Florquin, S 2004, 'Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice', Clinical and Experimental Immunology, vol. 137, no. 1, pp. 74-80. https://doi.org/10.1111/j.1365-2249.2004.02514.x

Standard

Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice. / Buonocore, S; Flamand, [No Value]; Claessen, N; Heeringa, P; Goldman, M; Florquin, S.

In: Clinical and Experimental Immunology, Vol. 137, No. 1, 07.2004, p. 74-80.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Buonocore S, Flamand NV, Claessen N, Heeringa P, Goldman M, Florquin S. Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice. Clinical and Experimental Immunology. 2004 Jul;137(1):74-80. https://doi.org/10.1111/j.1365-2249.2004.02514.x


BibTeX

@article{6f66af0f9e9f468cae1e24e0709c12e7,
title = "Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice",
abstract = "Dendritic cells (DC) genetically engineered to express Fas (CD95) ligand (FasL-DC) have been proposed as immunotherapeutic tools to induce tolerance to allografts. However, we and others recently showed that FasL-DC elicit a vigorous inflammatory response involving granulocytes and can promote Th1-type CD4(+) and cytotoxic CD8(+) T lymphocytes. This prompted us to evaluate the pathology induced by intravenous injection of FasL-DC in mice. We observed that FasL-DC obtained after retroviral gene transfer of bone marrow precursors derived from Fas-deficient C57Bl/6 mice induce massive pulmonary inflammation and pleuritis one day after a single intravenous injection in C57Bl/6 mice. Two months later, all mice presented granulomatous vasculitis of small to medium sized vessels, alveolar haemorrhage and pleuritis. In these lesions, apoptotic bodies were found in large number. Anti-neutrophilic cytoplasmic and anti-myeloperoxidase autoantibodies were not detected. This study documents that intravenous injection of FasL-DC causes severe lung granulomatous vasculitis. This new animal model for vasculitis is inducible, highly reproducible and shares many features with human Wegener granulomatosis. This model may be an appropriate tool to further investigate the pathogenesis of vasculitis and test new therapeutic strategies. Moreover, our findings highlight the potential severe complications of FasL-DC-based immunotherapy.",
keywords = "vasculitis, animal model, Fas ligand, apoptosis, dendritic cell, ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES, SMALL-VESSEL VASCULITIS, APOPTOTIC CELLS, IN-VIVO, NECROTIZING VASCULITIS, MERCURIC-CHLORIDE, IMMUNE PRIVILEGE, ANIMAL-MODELS, BONE-MARROW, TGF-BETA",
author = "S Buonocore and Flamand, {[No Value]} and N Claessen and P Heeringa and M Goldman and S Florquin",
year = "2004",
month = "7",
doi = "10.1111/j.1365-2249.2004.02514.x",
language = "English",
volume = "137",
pages = "74--80",
journal = "Clinical and Experimental Immunology",
issn = "0009-9104",
publisher = "Wiley",
number = "1",

}

RIS

TY - JOUR

T1 - Dendritic cells overexpressing Fas-ligand induce pulmonary vasculitis in mice

AU - Buonocore, S

AU - Flamand, [No Value]

AU - Claessen, N

AU - Heeringa, P

AU - Goldman, M

AU - Florquin, S

PY - 2004/7

Y1 - 2004/7

N2 - Dendritic cells (DC) genetically engineered to express Fas (CD95) ligand (FasL-DC) have been proposed as immunotherapeutic tools to induce tolerance to allografts. However, we and others recently showed that FasL-DC elicit a vigorous inflammatory response involving granulocytes and can promote Th1-type CD4(+) and cytotoxic CD8(+) T lymphocytes. This prompted us to evaluate the pathology induced by intravenous injection of FasL-DC in mice. We observed that FasL-DC obtained after retroviral gene transfer of bone marrow precursors derived from Fas-deficient C57Bl/6 mice induce massive pulmonary inflammation and pleuritis one day after a single intravenous injection in C57Bl/6 mice. Two months later, all mice presented granulomatous vasculitis of small to medium sized vessels, alveolar haemorrhage and pleuritis. In these lesions, apoptotic bodies were found in large number. Anti-neutrophilic cytoplasmic and anti-myeloperoxidase autoantibodies were not detected. This study documents that intravenous injection of FasL-DC causes severe lung granulomatous vasculitis. This new animal model for vasculitis is inducible, highly reproducible and shares many features with human Wegener granulomatosis. This model may be an appropriate tool to further investigate the pathogenesis of vasculitis and test new therapeutic strategies. Moreover, our findings highlight the potential severe complications of FasL-DC-based immunotherapy.

AB - Dendritic cells (DC) genetically engineered to express Fas (CD95) ligand (FasL-DC) have been proposed as immunotherapeutic tools to induce tolerance to allografts. However, we and others recently showed that FasL-DC elicit a vigorous inflammatory response involving granulocytes and can promote Th1-type CD4(+) and cytotoxic CD8(+) T lymphocytes. This prompted us to evaluate the pathology induced by intravenous injection of FasL-DC in mice. We observed that FasL-DC obtained after retroviral gene transfer of bone marrow precursors derived from Fas-deficient C57Bl/6 mice induce massive pulmonary inflammation and pleuritis one day after a single intravenous injection in C57Bl/6 mice. Two months later, all mice presented granulomatous vasculitis of small to medium sized vessels, alveolar haemorrhage and pleuritis. In these lesions, apoptotic bodies were found in large number. Anti-neutrophilic cytoplasmic and anti-myeloperoxidase autoantibodies were not detected. This study documents that intravenous injection of FasL-DC causes severe lung granulomatous vasculitis. This new animal model for vasculitis is inducible, highly reproducible and shares many features with human Wegener granulomatosis. This model may be an appropriate tool to further investigate the pathogenesis of vasculitis and test new therapeutic strategies. Moreover, our findings highlight the potential severe complications of FasL-DC-based immunotherapy.

KW - vasculitis

KW - animal model

KW - Fas ligand

KW - apoptosis

KW - dendritic cell

KW - ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES

KW - SMALL-VESSEL VASCULITIS

KW - APOPTOTIC CELLS

KW - IN-VIVO

KW - NECROTIZING VASCULITIS

KW - MERCURIC-CHLORIDE

KW - IMMUNE PRIVILEGE

KW - ANIMAL-MODELS

KW - BONE-MARROW

KW - TGF-BETA

U2 - 10.1111/j.1365-2249.2004.02514.x

DO - 10.1111/j.1365-2249.2004.02514.x

M3 - Article

VL - 137

SP - 74

EP - 80

JO - Clinical and Experimental Immunology

JF - Clinical and Experimental Immunology

SN - 0009-9104

IS - 1

ER -

ID: 13909154