Soluble Fas ligand-susceptible "memory" cells in mice but not in human: Potential role of soluble Fas ligand in deletion of auto-reactive cells

Sunshin Kim; Ja Young Kim; Tae H. Lee; Kyungho Suk; Hoon Suk Cha; Eun Mi Koh; Hideo Yagita; Myung Shik Lee

doi:10.1080/08916930290005882

Soluble Fas ligand-susceptible "memory" cells in mice but not in human: Potential role of soluble Fas ligand in deletion of auto-reactive cells

Sunshin Kim, Ja Young Kim, Tae H. Lee, Kyungho Suk, Hoon Suk Cha, Eun Mi Koh, Hideo Yagita, Myung Shik Lee

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

Human soluble Fas ligand (sFasL) has an apoptotic activity in contrast to murine sFasL. The physiological function of human sFasL is not known, while the pathological consequence of sFasL overproduction has been reported. To understand the physiological function of (human) sFasL, murine and human lymphocytes were treated with sFasL. sFasL treatment significantly decreased CD45RB^lo "memory" CD4+ lymphocyte fraction and increased propidium iodide (PI)+ apoptotic CD45RB^loCD4+ lymphocytes among murine peripheral lymphocytes. However, sFasL treatment neither decreased CD45RO+ "memory" CD4+ lymphocyte fraction nor increased PI+ CD45RO+CD+ lymphocytes among human peripheral lymphocytes, suggesting that the deletion of memory cells by sFasL had already occurred in vivo. Patients with systemic lupus erythematosus had sFasL-susceptible "memory" cell fraction suggesting an incomplete deletion of such "memory" cells. These results suggest that the physiological function of human sFasL is to delete the potentially auto-reactive "memory" lymphocytes, which complements membrane FasL (mFasL)-mediated deletion of auto-reactive cells in human beings but not in mice.

Original language	English
Pages (from-to)	15-20
Number of pages	6
Journal	Autoimmunity
Volume	35
Issue number	1
DOIs	https://doi.org/10.1080/08916930290005882
Publication status	Published - 2002

Bibliographical note

Funding Information:
This work was supported by the National Research Laboratory Grants from the Korea Institute of Science and Technology Evaluation and Planning (2000-N-NL-01-C-232), and Science Research Center Grants from Korea Science and Engineering Foundation. Lee M-S is an awardee of the Juvenile Diabetes Foundation International Research Grant (1-1999-760).

All Science Journal Classification (ASJC) codes

Immunology and Allergy
Immunology

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10.1080/08916930290005882

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title = "Soluble Fas ligand-susceptible {"}memory{"} cells in mice but not in human: Potential role of soluble Fas ligand in deletion of auto-reactive cells",

abstract = "Human soluble Fas ligand (sFasL) has an apoptotic activity in contrast to murine sFasL. The physiological function of human sFasL is not known, while the pathological consequence of sFasL overproduction has been reported. To understand the physiological function of (human) sFasL, murine and human lymphocytes were treated with sFasL. sFasL treatment significantly decreased CD45RBlo {"}memory{"} CD4+ lymphocyte fraction and increased propidium iodide (PI)+ apoptotic CD45RBloCD4+ lymphocytes among murine peripheral lymphocytes. However, sFasL treatment neither decreased CD45RO+ {"}memory{"} CD4+ lymphocyte fraction nor increased PI+ CD45RO+CD+ lymphocytes among human peripheral lymphocytes, suggesting that the deletion of memory cells by sFasL had already occurred in vivo. Patients with systemic lupus erythematosus had sFasL-susceptible {"}memory{"} cell fraction suggesting an incomplete deletion of such {"}memory{"} cells. These results suggest that the physiological function of human sFasL is to delete the potentially auto-reactive {"}memory{"} lymphocytes, which complements membrane FasL (mFasL)-mediated deletion of auto-reactive cells in human beings but not in mice.",

author = "Sunshin Kim and Kim, {Ja Young} and Lee, {Tae H.} and Kyungho Suk and Cha, {Hoon Suk} and Koh, {Eun Mi} and Hideo Yagita and Lee, {Myung Shik}",

note = "Funding Information: This work was supported by the National Research Laboratory Grants from the Korea Institute of Science and Technology Evaluation and Planning (2000-N-NL-01-C-232), and Science Research Center Grants from Korea Science and Engineering Foundation. Lee M-S is an awardee of the Juvenile Diabetes Foundation International Research Grant (1-1999-760).",

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T2 - Potential role of soluble Fas ligand in deletion of auto-reactive cells

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AU - Kim, Ja Young

AU - Lee, Tae H.

AU - Suk, Kyungho

AU - Cha, Hoon Suk

AU - Koh, Eun Mi

AU - Yagita, Hideo

AU - Lee, Myung Shik

N1 - Funding Information: This work was supported by the National Research Laboratory Grants from the Korea Institute of Science and Technology Evaluation and Planning (2000-N-NL-01-C-232), and Science Research Center Grants from Korea Science and Engineering Foundation. Lee M-S is an awardee of the Juvenile Diabetes Foundation International Research Grant (1-1999-760).

PY - 2002

Y1 - 2002

N2 - Human soluble Fas ligand (sFasL) has an apoptotic activity in contrast to murine sFasL. The physiological function of human sFasL is not known, while the pathological consequence of sFasL overproduction has been reported. To understand the physiological function of (human) sFasL, murine and human lymphocytes were treated with sFasL. sFasL treatment significantly decreased CD45RBlo "memory" CD4+ lymphocyte fraction and increased propidium iodide (PI)+ apoptotic CD45RBloCD4+ lymphocytes among murine peripheral lymphocytes. However, sFasL treatment neither decreased CD45RO+ "memory" CD4+ lymphocyte fraction nor increased PI+ CD45RO+CD+ lymphocytes among human peripheral lymphocytes, suggesting that the deletion of memory cells by sFasL had already occurred in vivo. Patients with systemic lupus erythematosus had sFasL-susceptible "memory" cell fraction suggesting an incomplete deletion of such "memory" cells. These results suggest that the physiological function of human sFasL is to delete the potentially auto-reactive "memory" lymphocytes, which complements membrane FasL (mFasL)-mediated deletion of auto-reactive cells in human beings but not in mice.

AB - Human soluble Fas ligand (sFasL) has an apoptotic activity in contrast to murine sFasL. The physiological function of human sFasL is not known, while the pathological consequence of sFasL overproduction has been reported. To understand the physiological function of (human) sFasL, murine and human lymphocytes were treated with sFasL. sFasL treatment significantly decreased CD45RBlo "memory" CD4+ lymphocyte fraction and increased propidium iodide (PI)+ apoptotic CD45RBloCD4+ lymphocytes among murine peripheral lymphocytes. However, sFasL treatment neither decreased CD45RO+ "memory" CD4+ lymphocyte fraction nor increased PI+ CD45RO+CD+ lymphocytes among human peripheral lymphocytes, suggesting that the deletion of memory cells by sFasL had already occurred in vivo. Patients with systemic lupus erythematosus had sFasL-susceptible "memory" cell fraction suggesting an incomplete deletion of such "memory" cells. These results suggest that the physiological function of human sFasL is to delete the potentially auto-reactive "memory" lymphocytes, which complements membrane FasL (mFasL)-mediated deletion of auto-reactive cells in human beings but not in mice.

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Soluble Fas ligand-susceptible "memory" cells in mice but not in human: Potential role of soluble Fas ligand in deletion of auto-reactive cells

Abstract

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