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Inhibition of the transcription factors AP-1 and NF-kappaB in CD4 T cells by peroxisome proliferator-activated receptor gamma ligands

Wang, P ; Anderson, P O LU ; Chen, Shangwu ; Paulsson, K M LU orcid ; Sjögren, H O LU and Li, S LU (2001) In International Immunopharmacology 1(4). p.12-803
Abstract

The peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear hormone receptor superfamily, is essential for adipocyte differentiation and glucose homeostasis. PPARgamma has been found recently to regulate macrophage activation in response to mitogens and inflammation. Our study shows PPARgamma to be preferentially expressed in the nuclei of resting T cells and to increase upon activation of T cells by either anti-CD3 and anti-CD28 or phorbol myristyl acetate (PMA). We also found the PPARgamma ligand ciglitizone to attenuate the activation of T cells by inhibiting cytokine gene expression and anti-CD3 and anti-CD28 or PMA-induced proliferative responses. Inhibition of both the proliferative response and... (More)

The peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear hormone receptor superfamily, is essential for adipocyte differentiation and glucose homeostasis. PPARgamma has been found recently to regulate macrophage activation in response to mitogens and inflammation. Our study shows PPARgamma to be preferentially expressed in the nuclei of resting T cells and to increase upon activation of T cells by either anti-CD3 and anti-CD28 or phorbol myristyl acetate (PMA). We also found the PPARgamma ligand ciglitizone to attenuate the activation of T cells by inhibiting cytokine gene expression and anti-CD3 and anti-CD28 or PMA-induced proliferative responses. Inhibition of both the proliferative response and inflammatory cytokine expression in CD4 T cells was correlated with suppression of the activated transcription factors AP1 and NF-kappaB. PPARgamma ligands also strongly inhibited SEA-induced Vbeta3 T cell activation in vivo. These results, together with previous findings of the inhibitory effect of PPARgamma ligands on activated macrophages, provide clear evidence for PPARgamma as a negative regulator of the inflammatory activation of both macrophage and T cells. PPARgamma may thus be a potential therapeutic target for the treatment of autoimmunity.

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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Animals, CD4-Positive T-Lymphocytes, Cytokines, Female, Ligands, Lymphocyte Activation, Mice, Mice, Inbred C57BL, NF-kappa B, Receptors, Antigen, T-Cell, Receptors, Cytoplasmic and Nuclear, Transcription Factor AP-1, Transcription Factors, Journal Article, Research Support, Non-U.S. Gov't
in
International Immunopharmacology
volume
1
issue
4
pages
10 pages
publisher
Elsevier
external identifiers
  • scopus:0035105403
  • pmid:11357893
ISSN
1567-5769
DOI
10.1016/S1567-5769(01)00015-7
language
English
LU publication?
yes
id
41fa4cb3-8061-4c28-b789-88eac8ad6f1a
date added to LUP
2016-10-28 09:05:04
date last changed
2025-04-04 14:53:35
@article{41fa4cb3-8061-4c28-b789-88eac8ad6f1a,
  abstract     = {{<p>The peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear hormone receptor superfamily, is essential for adipocyte differentiation and glucose homeostasis. PPARgamma has been found recently to regulate macrophage activation in response to mitogens and inflammation. Our study shows PPARgamma to be preferentially expressed in the nuclei of resting T cells and to increase upon activation of T cells by either anti-CD3 and anti-CD28 or phorbol myristyl acetate (PMA). We also found the PPARgamma ligand ciglitizone to attenuate the activation of T cells by inhibiting cytokine gene expression and anti-CD3 and anti-CD28 or PMA-induced proliferative responses. Inhibition of both the proliferative response and inflammatory cytokine expression in CD4 T cells was correlated with suppression of the activated transcription factors AP1 and NF-kappaB. PPARgamma ligands also strongly inhibited SEA-induced Vbeta3 T cell activation in vivo. These results, together with previous findings of the inhibitory effect of PPARgamma ligands on activated macrophages, provide clear evidence for PPARgamma as a negative regulator of the inflammatory activation of both macrophage and T cells. PPARgamma may thus be a potential therapeutic target for the treatment of autoimmunity.</p>}},
  author       = {{Wang, P and Anderson, P O and Chen, Shangwu and Paulsson, K M and Sjögren, H O and Li, S}},
  issn         = {{1567-5769}},
  keywords     = {{Animals; CD4-Positive T-Lymphocytes; Cytokines; Female; Ligands; Lymphocyte Activation; Mice; Mice, Inbred C57BL; NF-kappa B; Receptors, Antigen, T-Cell; Receptors, Cytoplasmic and Nuclear; Transcription Factor AP-1; Transcription Factors; Journal Article; Research Support, Non-U.S. Gov't}},
  language     = {{eng}},
  number       = {{4}},
  pages        = {{12--803}},
  publisher    = {{Elsevier}},
  series       = {{International Immunopharmacology}},
  title        = {{Inhibition of the transcription factors AP-1 and NF-kappaB in CD4 T cells by peroxisome proliferator-activated receptor gamma ligands}},
  url          = {{http://dx.doi.org/10.1016/S1567-5769(01)00015-7}},
  doi          = {{10.1016/S1567-5769(01)00015-7}},
  volume       = {{1}},
  year         = {{2001}},
}