CD1d-dependent NKT cells play a protective role in acute and chronic arthritis models by ameliorating antigen-specific Th1 responses.
(2010) In Journal of immunology 185(1). p.345-356- Abstract
- A protective and anti-inflammatory role for CD1d-dependent NKT cells (NKTs) has been reported in experimental and human autoimmune diseases. However, their role in arthritis has been unclear, with conflicting reports of CD1d-dependent NKTs acting both as regulatory and disease-promoting cells in arthritis. These differing modes of action might be due to genetic differences of inbred mice and incomplete backcrossing of gene-modified mice. We therefore put special emphasis on controlling the genetic backgrounds of the mice used. Additionally, we used two different murine arthritis models, Ag-induced arthritis (AIA) and collagen-induced arthritis (CIA), to evaluate acute and chronic arthritis in CD1d knockout mice and mice depleted of... (More)
- A protective and anti-inflammatory role for CD1d-dependent NKT cells (NKTs) has been reported in experimental and human autoimmune diseases. However, their role in arthritis has been unclear, with conflicting reports of CD1d-dependent NKTs acting both as regulatory and disease-promoting cells in arthritis. These differing modes of action might be due to genetic differences of inbred mice and incomplete backcrossing of gene-modified mice. We therefore put special emphasis on controlling the genetic backgrounds of the mice used. Additionally, we used two different murine arthritis models, Ag-induced arthritis (AIA) and collagen-induced arthritis (CIA), to evaluate acute and chronic arthritis in CD1d knockout mice and mice depleted of NK1.1(+) cells. CD1d-deficient mice developed more severe AIA compared with wild-type littermates, with a higher degree of inflammation and proteoglycan depletion. Chronic arthritis in CIA was also worse in the absence of CD1d-dependent NKTs. Elevated levels of Ag-specific IFN-gamma production accompanied these findings rather than changes in IL-17alpha. Depletion of NK1.1(+) cells supported these findings in AIA and CIA. This report provides support for CD1d-dependent NKTs being suppressor cells in acute and chronic arthritis, likely via inhibition of arthritogenic Th1 cells. These results make CD1d-dependent NKTs an attractive target for therapeutic intervention. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1626335
- author
- Teige, Anna ; Bockermann, Robert LU ; Hasan, Maruf ; Berg, Katarina LU ; Liu, Yawei LU and Issazadeh, Shohreh LU
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of immunology
- volume
- 185
- issue
- 1
- pages
- 345 - 356
- publisher
- American Association of Immunologists
- external identifiers
-
- wos:000278933800038
- pmid:20525883
- scopus:77956194304
- pmid:20525883
- ISSN
- 1550-6606
- DOI
- 10.4049/jimmunol.0901693
- language
- English
- LU publication?
- yes
- id
- beab1b51-9050-4b96-ad25-3b4478ab4f85 (old id 1626335)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/20525883?dopt=Abstract
- date added to LUP
- 2016-04-04 09:27:03
- date last changed
- 2022-01-29 17:54:43
@article{beab1b51-9050-4b96-ad25-3b4478ab4f85,
abstract = {{A protective and anti-inflammatory role for CD1d-dependent NKT cells (NKTs) has been reported in experimental and human autoimmune diseases. However, their role in arthritis has been unclear, with conflicting reports of CD1d-dependent NKTs acting both as regulatory and disease-promoting cells in arthritis. These differing modes of action might be due to genetic differences of inbred mice and incomplete backcrossing of gene-modified mice. We therefore put special emphasis on controlling the genetic backgrounds of the mice used. Additionally, we used two different murine arthritis models, Ag-induced arthritis (AIA) and collagen-induced arthritis (CIA), to evaluate acute and chronic arthritis in CD1d knockout mice and mice depleted of NK1.1(+) cells. CD1d-deficient mice developed more severe AIA compared with wild-type littermates, with a higher degree of inflammation and proteoglycan depletion. Chronic arthritis in CIA was also worse in the absence of CD1d-dependent NKTs. Elevated levels of Ag-specific IFN-gamma production accompanied these findings rather than changes in IL-17alpha. Depletion of NK1.1(+) cells supported these findings in AIA and CIA. This report provides support for CD1d-dependent NKTs being suppressor cells in acute and chronic arthritis, likely via inhibition of arthritogenic Th1 cells. These results make CD1d-dependent NKTs an attractive target for therapeutic intervention.}},
author = {{Teige, Anna and Bockermann, Robert and Hasan, Maruf and Berg, Katarina and Liu, Yawei and Issazadeh, Shohreh}},
issn = {{1550-6606}},
language = {{eng}},
number = {{1}},
pages = {{345--356}},
publisher = {{American Association of Immunologists}},
series = {{Journal of immunology}},
title = {{CD1d-dependent NKT cells play a protective role in acute and chronic arthritis models by ameliorating antigen-specific Th1 responses.}},
url = {{http://dx.doi.org/10.4049/jimmunol.0901693}},
doi = {{10.4049/jimmunol.0901693}},
volume = {{185}},
year = {{2010}},
}