TNF-α suppresses dendritic cell death and the production of reactive oxygen intermediates induced by plasma withdrawal

Hong Duck Um, Young Hun Cho, Do Kyun Kim, Jong Ran Shin, Yung Jae Lee, Kwang Sung Choi, Jin Moon Kang, Mingeol Lee

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Mature dendritic cells (DCs) were generated by culturing human peripheral blood monocytes for 7 days and, then, treating them with a cytokine cocktail for 2 days. The viability of the mature DCs (Day 9) obtained was approximately 60-70%, and this gradually declined when they were recultured in X-VIVO 15 media containing 2% human plasma (40% viability after 3 days of reculture). DC death accelerated on withdrawing plasma from the culture (20% viability after 3 days). However, the addition of tumor necrosis factor-α (TNF-α) to the medium completely restored DC viability in the absence of plasma. Such a protective effect was not afforded by other cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1α (IL-1α), IL-4, IL-6 and prostaglandin E2 which are used for the maturation of DCs. These results indicate that TNF-α is specifically required to maintain the viability of mature DCs. The withdrawal of plasma rapidly (within 15 min elevated cellular levels of reactive oxygen intermediates (ROIs), which have been proposed to regulate the ability of DCs to control inflammatory reactions. The possibility that ROIs act as mediators of DC death was eliminated by the observation that scavengers of ROIs, such as catalase, N-acetylcysteine, glutathione, failed to prolong DC life span in the absence of plasma. Interestingly, TNF-α was found to almost completely abolish the production of ROIs induced by plasma withdrawal. To summarize, our results suggest that TNF-α controls not only the inflammatory functions of DCs but also their survival.

Original languageEnglish
Pages (from-to)282-288
Number of pages7
JournalExperimental dermatology
Volume13
Issue number5
DOIs
Publication statusPublished - 2004 May 1

Fingerprint

Cell death
Dendritic Cells
Cell Death
Tumor Necrosis Factor-alpha
Oxygen
Plasmas
Cytokines
Plasma (human)
Macrophage Colony-Stimulating Factor
Acetylcysteine
Granulocyte-Macrophage Colony-Stimulating Factor
Interleukin-1
Cell culture
Dinoprostone
Interleukin-4
Catalase
Glutathione
Monocytes
Interleukin-6
Cell Survival

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Dermatology

Cite this

Um, Hong Duck ; Cho, Young Hun ; Kim, Do Kyun ; Shin, Jong Ran ; Lee, Yung Jae ; Choi, Kwang Sung ; Kang, Jin Moon ; Lee, Mingeol. / TNF-α suppresses dendritic cell death and the production of reactive oxygen intermediates induced by plasma withdrawal. In: Experimental dermatology. 2004 ; Vol. 13, No. 5. pp. 282-288.
@article{4ba5f9b349bd49438e33afba27a364d4,
title = "TNF-α suppresses dendritic cell death and the production of reactive oxygen intermediates induced by plasma withdrawal",
abstract = "Mature dendritic cells (DCs) were generated by culturing human peripheral blood monocytes for 7 days and, then, treating them with a cytokine cocktail for 2 days. The viability of the mature DCs (Day 9) obtained was approximately 60-70{\%}, and this gradually declined when they were recultured in X-VIVO 15 media containing 2{\%} human plasma (40{\%} viability after 3 days of reculture). DC death accelerated on withdrawing plasma from the culture (20{\%} viability after 3 days). However, the addition of tumor necrosis factor-α (TNF-α) to the medium completely restored DC viability in the absence of plasma. Such a protective effect was not afforded by other cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1α (IL-1α), IL-4, IL-6 and prostaglandin E2 which are used for the maturation of DCs. These results indicate that TNF-α is specifically required to maintain the viability of mature DCs. The withdrawal of plasma rapidly (within 15 min elevated cellular levels of reactive oxygen intermediates (ROIs), which have been proposed to regulate the ability of DCs to control inflammatory reactions. The possibility that ROIs act as mediators of DC death was eliminated by the observation that scavengers of ROIs, such as catalase, N-acetylcysteine, glutathione, failed to prolong DC life span in the absence of plasma. Interestingly, TNF-α was found to almost completely abolish the production of ROIs induced by plasma withdrawal. To summarize, our results suggest that TNF-α controls not only the inflammatory functions of DCs but also their survival.",
author = "Um, {Hong Duck} and Cho, {Young Hun} and Kim, {Do Kyun} and Shin, {Jong Ran} and Lee, {Yung Jae} and Choi, {Kwang Sung} and Kang, {Jin Moon} and Mingeol Lee",
year = "2004",
month = "5",
day = "1",
doi = "10.1111/j.0906-6705.2004.00146.x",
language = "English",
volume = "13",
pages = "282--288",
journal = "Experimental Dermatology",
issn = "0906-6705",
publisher = "Wiley-Blackwell",
number = "5",

}

TNF-α suppresses dendritic cell death and the production of reactive oxygen intermediates induced by plasma withdrawal. / Um, Hong Duck; Cho, Young Hun; Kim, Do Kyun; Shin, Jong Ran; Lee, Yung Jae; Choi, Kwang Sung; Kang, Jin Moon; Lee, Mingeol.

In: Experimental dermatology, Vol. 13, No. 5, 01.05.2004, p. 282-288.

Research output: Contribution to journalArticle

TY - JOUR

T1 - TNF-α suppresses dendritic cell death and the production of reactive oxygen intermediates induced by plasma withdrawal

AU - Um, Hong Duck

AU - Cho, Young Hun

AU - Kim, Do Kyun

AU - Shin, Jong Ran

AU - Lee, Yung Jae

AU - Choi, Kwang Sung

AU - Kang, Jin Moon

AU - Lee, Mingeol

PY - 2004/5/1

Y1 - 2004/5/1

N2 - Mature dendritic cells (DCs) were generated by culturing human peripheral blood monocytes for 7 days and, then, treating them with a cytokine cocktail for 2 days. The viability of the mature DCs (Day 9) obtained was approximately 60-70%, and this gradually declined when they were recultured in X-VIVO 15 media containing 2% human plasma (40% viability after 3 days of reculture). DC death accelerated on withdrawing plasma from the culture (20% viability after 3 days). However, the addition of tumor necrosis factor-α (TNF-α) to the medium completely restored DC viability in the absence of plasma. Such a protective effect was not afforded by other cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1α (IL-1α), IL-4, IL-6 and prostaglandin E2 which are used for the maturation of DCs. These results indicate that TNF-α is specifically required to maintain the viability of mature DCs. The withdrawal of plasma rapidly (within 15 min elevated cellular levels of reactive oxygen intermediates (ROIs), which have been proposed to regulate the ability of DCs to control inflammatory reactions. The possibility that ROIs act as mediators of DC death was eliminated by the observation that scavengers of ROIs, such as catalase, N-acetylcysteine, glutathione, failed to prolong DC life span in the absence of plasma. Interestingly, TNF-α was found to almost completely abolish the production of ROIs induced by plasma withdrawal. To summarize, our results suggest that TNF-α controls not only the inflammatory functions of DCs but also their survival.

AB - Mature dendritic cells (DCs) were generated by culturing human peripheral blood monocytes for 7 days and, then, treating them with a cytokine cocktail for 2 days. The viability of the mature DCs (Day 9) obtained was approximately 60-70%, and this gradually declined when they were recultured in X-VIVO 15 media containing 2% human plasma (40% viability after 3 days of reculture). DC death accelerated on withdrawing plasma from the culture (20% viability after 3 days). However, the addition of tumor necrosis factor-α (TNF-α) to the medium completely restored DC viability in the absence of plasma. Such a protective effect was not afforded by other cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1α (IL-1α), IL-4, IL-6 and prostaglandin E2 which are used for the maturation of DCs. These results indicate that TNF-α is specifically required to maintain the viability of mature DCs. The withdrawal of plasma rapidly (within 15 min elevated cellular levels of reactive oxygen intermediates (ROIs), which have been proposed to regulate the ability of DCs to control inflammatory reactions. The possibility that ROIs act as mediators of DC death was eliminated by the observation that scavengers of ROIs, such as catalase, N-acetylcysteine, glutathione, failed to prolong DC life span in the absence of plasma. Interestingly, TNF-α was found to almost completely abolish the production of ROIs induced by plasma withdrawal. To summarize, our results suggest that TNF-α controls not only the inflammatory functions of DCs but also their survival.

UR - http://www.scopus.com/inward/record.url?scp=2642526842&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2642526842&partnerID=8YFLogxK

U2 - 10.1111/j.0906-6705.2004.00146.x

DO - 10.1111/j.0906-6705.2004.00146.x

M3 - Article

VL - 13

SP - 282

EP - 288

JO - Experimental Dermatology

JF - Experimental Dermatology

SN - 0906-6705

IS - 5

ER -