scholarly journals The effect of interleukin-10 and transforming growth factor β-1 on HLA-DR expression in colonic epithelial cells

1998 ◽  
Vol 7 (1) ◽  
pp. 7-11 ◽  
Author(s):  
M. J. Zimmerman ◽  
G. R. Radford-Smith ◽  
D. P. Jewell

The aim of this study was to assess whether interleukin-10 (IL-10) and/or transforming growth factor β-1 (TGF β1) downregulate HLA-DR expression using the HT29 cell line as a model of colonic epithelial cells. HLA-DR expression was induced in HT29 cells withγ-interferon. The effects of IL-10 alone, TGF β1alone, and IL-10 and TGF β1in combination were studied. HLA-DR expression was assessed using flow cytometric analysis.γ-Interferon induced HLA-DR expression in a dose-dependent fashion. In the absence ofγ-interferon, neither IL-10 nor TGF β1induced HLA-DR expression. In isolation, neither IL10 nor TGF β1downregulated HLA-DR expression. When IL-10 and TGF β1were added in combination, small (6-30%) statistically significant reductions in HLA-DR expression were seen. The biological significance is unclear.

Respiration ◽  
2007 ◽  
Vol 74 (4) ◽  
pp. 454-459 ◽  
Author(s):  
Naoto Fueki ◽  
Hironori Sagara ◽  
Kazumi Akimoto ◽  
Mayumi Ota ◽  
Takenori Okada ◽  
...  

2004 ◽  
Vol 72 (4) ◽  
pp. 1974-1982 ◽  
Author(s):  
M. S. Khalifeh ◽  
J. R. Stabel

ABSTRACT Gamma interferon (IFN-γ) plays a significant role in the control of mycobacterial infections, including Mycobacterium avium subsp. paratuberculosis. However, the contribution of other immunoregulatory cytokines, such as interleukin-10 (IL-10) and transforming growth factor β (TGF-β), in Johne's disease has not been investigated as yet. In this study, we examined the effects of in vivo and in vitro infection with M. avium subsp. paratuberculosis on the production of IFN-γ, IL-10, and TGF-β by peripheral blood mononuclear cells (PBMC). We also examined the effects of exogenous IFN-γ, IL-10, and TGF-β on M. avium subsp. paratuberculosis survival in the cell cultures. PBMC obtained from naturally infected cows, regardless of their disease status, specifically upregulated IL-10 and TGF-β in culture supernatants in response to stimulation with live M. avium subsp. paratuberculosis. Nonstimulated PBMC recovered from subclinically infected animals secreted the lowest levels of TGF-β, but after stimulation with live M. avium subsp. paratuberculosis, TGF-β levels in the culture supernatants increased to levels similar to that produced by PBMC from healthy animals. The numbers of viable M. avium subsp. paratuberculosis recovered from cultures from naturally infected animals were higher than those from healthy cows after in vitro infection with M. avium subsp. paratuberculosis. The addition of exogenous IL-10 and TGF-β to PBMC isolated from healthy cows inhibited the bactericidal activity of these cells as evidenced by the increased number of viable M. avium subsp. paratuberculosis recovered from these cultures compared to cell cultures containing medium alone. These data suggest important immune regulatory roles for IL-10 and TGF-β during infection with M. avium subsp. paratuberculosis that may be directly related to their effects on macrophage activation and killing of M. avium subsp. paratuberculosis.


2020 ◽  
Vol 217 (3) ◽  
Author(s):  
Nikolaos G. Frangogiannis

TGF-β is extensively implicated in the pathogenesis of fibrosis. In fibrotic lesions, spatially restricted generation of bioactive TGF-β from latent stores requires the cooperation of proteases, integrins, and specialized extracellular matrix molecules. Although fibroblasts are major targets of TGF-β, some fibrogenic actions may reflect activation of other cell types, including macrophages, epithelial cells, and vascular cells. TGF-β–driven fibrosis is mediated through Smad-dependent or non-Smad pathways and is modulated by coreceptors and by interacting networks. This review discusses the role of TGF-β in fibrosis, highlighting mechanisms of TGF-β activation and signaling, the cellular targets of TGF-β actions, and the challenges of therapeutic translation.


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