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Invariant natural killer T cells are natural regulators of murine spondylarthritis

Peggy Jacques UGent, Koen Venken UGent, Katrien Van Beneden UGent, Hamida Hammad UGent, Sylvie Seeuws UGent, Michael Drennan UGent, Dieter Deforce UGent, August Verbruggen UGent, Maria Apostolaki, George Kollias, et al. (2010) ARTHRITIS AND RHEUMATISM. 62(4). p.988-999
abstract
Objective. To investigate the role of invariant natural killer T (iNKT) cells in TNF Delta ARE/+ mice, an animal model of spondylarthritis (SpA) with both gut and joint inflammation. Methods. The frequency and activation of iNKT cells were analyzed on mononuclear cells from the lymph nodes and livers of mice, using flow cytometry with alpha-galactosylceramide/CD1d tetramers and quantitative polymerase chain reaction for the invariant V(alpha)14-J(alpha)18 rearrangement. Bone marrow-derived dendritic cells (DCs) were obtained by expansion of primary cells with granulocyte-macrophage colony-stimulating factor followed by coculture with iNKT cell hybridomas, and interleukin-2 release into the cocultures was then measured by enzyme-linked immunosorbent assay (ELISA). Cytokine levels were determined by ELISA or cytometric bead array analyses of freshly isolated DCs and iNKT cells in mixed cocultures. TNF Delta ARE/+ mice were backcrossed onto J(alpha)18(-/-) and CD1d(-/-) mice, and disease onset was evaluated by clinical scoring, positron emission tomography, and histology. CD1d levels were analyzed on mononuclear cells in paired blood and synovial fluid samples from patients with SpA compared with healthy control subjects. Results. In the absence of iNKT cells, symptoms of gut and joint inflammation in TNF Delta ARE/+ mice were aggravated. Invariant NKT cells were activated during the course of the disease. This was linked to an enrichment of inflammatory DCs, characterized by high levels of CD1d, particularly at draining sites of inflammation. A similar increase in CD1d levels was observed on DCs from patients with SpA. Inflammatory DCs from TNF Delta ARE/+ mice stimulated iNKT cells to produce immunomodulatory cytokines, in the absence of exogenous stimulation. Prolonged, continuous exposure, but not short-term exposure, to tumor necrosis factor (TNF) was found to be responsible for the enhanced DC-NKT cell crosstalk. Conclusion. This mode of iNKT cell activation represents a natural counterregulatory mechanism for the dampening of TNF-driven inflammation.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
MOUSE CD1, IN-VIVO, V(ALPHA)14 NKT CELLS, TUMOR-NECROSIS-FACTOR, DENDRITIC CELLS, PSORIATIC-ARTHRITIS, GLYCOLIPID ANTIGENS, FACTOR-ALPHA, CUTTING EDGE, ACTIVATION
journal title
ARTHRITIS AND RHEUMATISM
Arthritis Rheum.
volume
62
issue
4
pages
988 - 999
Web of Science type
Article
Web of Science id
000279432300009
JCR category
RHEUMATOLOGY
JCR impact factor
8.435 (2010)
JCR rank
2/29 (2010)
JCR quartile
1 (2010)
ISSN
0004-3591
DOI
10.1002/art.27324
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1081438
handle
http://hdl.handle.net/1854/LU-1081438
date created
2010-12-01 14:56:44
date last changed
2016-12-19 15:46:28
@article{1081438,
  abstract     = {Objective. To investigate the role of invariant natural killer T (iNKT) cells in TNF Delta ARE/+ mice, an animal model of spondylarthritis (SpA) with both gut and joint inflammation. 
Methods. The frequency and activation of iNKT cells were analyzed on mononuclear cells from the lymph nodes and livers of mice, using flow cytometry with alpha-galactosylceramide/CD1d tetramers and quantitative polymerase chain reaction for the invariant V(alpha)14-J(alpha)18 rearrangement. Bone marrow-derived dendritic cells (DCs) were obtained by expansion of primary cells with granulocyte-macrophage colony-stimulating factor followed by coculture with iNKT cell hybridomas, and interleukin-2 release into the cocultures was then measured by enzyme-linked immunosorbent assay (ELISA). Cytokine levels were determined by ELISA or cytometric bead array analyses of freshly isolated DCs and iNKT cells in mixed cocultures. TNF Delta ARE/+ mice were backcrossed onto J(alpha)18(-/-) and CD1d(-/-) mice, and disease onset was evaluated by clinical scoring, positron emission tomography, and histology. CD1d levels were analyzed on mononuclear cells in paired blood and synovial fluid samples from patients with SpA compared with healthy control subjects.
Results. In the absence of iNKT cells, symptoms of gut and joint inflammation in TNF Delta ARE/+ mice were aggravated. Invariant NKT cells were activated during the course of the disease. This was linked to an enrichment of inflammatory DCs, characterized by high levels of CD1d, particularly at draining sites of inflammation. A similar increase in CD1d levels was observed on DCs from patients with SpA. Inflammatory DCs from TNF Delta ARE/+ mice stimulated iNKT cells to produce immunomodulatory cytokines, in the absence of exogenous stimulation. Prolonged, continuous exposure, but not short-term exposure, to tumor necrosis factor (TNF) was found to be responsible for the enhanced DC-NKT cell crosstalk.
Conclusion. This mode of iNKT cell activation represents a natural counterregulatory mechanism for the dampening of TNF-driven inflammation.},
  author       = {Jacques, Peggy and Venken, Koen and Van Beneden, Katrien and Hammad, Hamida and Seeuws, Sylvie and Drennan, Michael and Deforce, Dieter and Verbruggen, August and Apostolaki, Maria and Kollias, George and Lambrecht, Bart and De Vos, Martine and Elewaut, Dirk},
  issn         = {0004-3591},
  journal      = {ARTHRITIS AND RHEUMATISM},
  keyword      = {MOUSE CD1,IN-VIVO,V(ALPHA)14 NKT CELLS,TUMOR-NECROSIS-FACTOR,DENDRITIC CELLS,PSORIATIC-ARTHRITIS,GLYCOLIPID ANTIGENS,FACTOR-ALPHA,CUTTING EDGE,ACTIVATION},
  language     = {eng},
  number       = {4},
  pages        = {988--999},
  title        = {Invariant natural killer T cells are natural regulators of murine spondylarthritis},
  url          = {http://dx.doi.org/10.1002/art.27324},
  volume       = {62},
  year         = {2010},
}

Chicago
Jacques, Peggy, Koen Venken, Katrien Van Beneden, Hamida Hammad, Sylvie Seeuws, Michael Drennan, Dieter Deforce, et al. 2010. “Invariant Natural Killer T Cells Are Natural Regulators of Murine Spondylarthritis.” Arthritis and Rheumatism 62 (4): 988–999.
APA
Jacques, Peggy, Venken, K., Van Beneden, K., Hammad, H., Seeuws, S., Drennan, M., Deforce, D., et al. (2010). Invariant natural killer T cells are natural regulators of murine spondylarthritis. ARTHRITIS AND RHEUMATISM, 62(4), 988–999.
Vancouver
1.
Jacques P, Venken K, Van Beneden K, Hammad H, Seeuws S, Drennan M, et al. Invariant natural killer T cells are natural regulators of murine spondylarthritis. ARTHRITIS AND RHEUMATISM. 2010;62(4):988–99.
MLA
Jacques, Peggy, Koen Venken, Katrien Van Beneden, et al. “Invariant Natural Killer T Cells Are Natural Regulators of Murine Spondylarthritis.” ARTHRITIS AND RHEUMATISM 62.4 (2010): 988–999. Print.