Inducible nonlymphoid expression of Fas ligand is responsible for superantigen-induced peripheral deletion of T cells

Emanuela Bonfoco; Patrick M. Stuart; Thomas Brunner; Tesu Lin; Thomas S. Griffith; Yakun Gao; Hiroo Nakajima; Pierre A. Henkart; Thomas A. Ferguson; Douglas R. Green

doi:10.1016/S1074-7613(00)80668-8

Inducible nonlymphoid expression of Fas ligand is responsible for superantigen-induced peripheral deletion of T cells

Emanuela Bonfoco, Patrick M. Stuart, Thomas Brunner, Tesu Lin, Thomas S. Griffith, Yakun Gao, Hiroo Nakajima, Pierre A. Henkart, Thomas A. Ferguson, Douglas R. Green

Urology

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

141 Scopus citations

Abstract

Fas (CD95) and Fas ligand (FasL) play major roles in staphylococcal enterotoxin B (SEB)-induced peripheral deletion of Vβ8⁺ T cells. We found that peripheral deletion was defective in radiation chimeras with nonfunctional tissue FasL, regardless of the FasL status of the bone marrow- derived cells. SEB induced a dramatic upregulation of FasL expression and function in nonlymphoid cells of liver and small intestine. This effect was resistant to inhibition by cyclosporin A, which also failed to inhibit peripheral deletion. In SCID animals nonlymphoid tissues did not express FasL in response to SEB unless transplanted lymphocytes were present. Thus, some immune responses induce FasL in nonlymphoid tissues, which in turn kills activated lymphocytes, leading to peripheral T cell deletion.

Original language	English (US)
Pages (from-to)	711-720
Number of pages	10
Journal	Immunity
Volume	9
Issue number	5
DOIs	https://doi.org/10.1016/S1074-7613(00)80668-8
State	Published - Nov 1998

Bibliographical note

Funding Information:
We thank C. Ware, R. Kluck, L. Genestier, H. Beere, and B. Wolf for critically reviewing the manuscript. This work was supported by grants from the United States National Institutes of Health (GM52735 and EY06765). E. B. was supported in part by a fellowship from the Blanceflor and Ludovisi Foundation. This is publication no. 240 of La Jolla Institute for Allergy and Immunology.

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title = "Inducible nonlymphoid expression of Fas ligand is responsible for superantigen-induced peripheral deletion of T cells",

abstract = "Fas (CD95) and Fas ligand (FasL) play major roles in staphylococcal enterotoxin B (SEB)-induced peripheral deletion of Vβ8+ T cells. We found that peripheral deletion was defective in radiation chimeras with nonfunctional tissue FasL, regardless of the FasL status of the bone marrow- derived cells. SEB induced a dramatic upregulation of FasL expression and function in nonlymphoid cells of liver and small intestine. This effect was resistant to inhibition by cyclosporin A, which also failed to inhibit peripheral deletion. In SCID animals nonlymphoid tissues did not express FasL in response to SEB unless transplanted lymphocytes were present. Thus, some immune responses induce FasL in nonlymphoid tissues, which in turn kills activated lymphocytes, leading to peripheral T cell deletion.",

author = "Emanuela Bonfoco and Stuart, {Patrick M.} and Thomas Brunner and Tesu Lin and Griffith, {Thomas S.} and Yakun Gao and Hiroo Nakajima and Henkart, {Pierre A.} and Ferguson, {Thomas A.} and Green, {Douglas R.}",

note = "Funding Information: We thank C. Ware, R. Kluck, L. Genestier, H. Beere, and B. Wolf for critically reviewing the manuscript. This work was supported by grants from the United States National Institutes of Health (GM52735 and EY06765). E. B. was supported in part by a fellowship from the Blanceflor and Ludovisi Foundation. This is publication no. 240 of La Jolla Institute for Allergy and Immunology.",

year = "1998",

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T1 - Inducible nonlymphoid expression of Fas ligand is responsible for superantigen-induced peripheral deletion of T cells

AU - Bonfoco, Emanuela

AU - Stuart, Patrick M.

AU - Brunner, Thomas

AU - Lin, Tesu

AU - Griffith, Thomas S.

AU - Gao, Yakun

AU - Nakajima, Hiroo

AU - Henkart, Pierre A.

AU - Ferguson, Thomas A.

AU - Green, Douglas R.

N1 - Funding Information: We thank C. Ware, R. Kluck, L. Genestier, H. Beere, and B. Wolf for critically reviewing the manuscript. This work was supported by grants from the United States National Institutes of Health (GM52735 and EY06765). E. B. was supported in part by a fellowship from the Blanceflor and Ludovisi Foundation. This is publication no. 240 of La Jolla Institute for Allergy and Immunology.

PY - 1998/11

Y1 - 1998/11

N2 - Fas (CD95) and Fas ligand (FasL) play major roles in staphylococcal enterotoxin B (SEB)-induced peripheral deletion of Vβ8+ T cells. We found that peripheral deletion was defective in radiation chimeras with nonfunctional tissue FasL, regardless of the FasL status of the bone marrow- derived cells. SEB induced a dramatic upregulation of FasL expression and function in nonlymphoid cells of liver and small intestine. This effect was resistant to inhibition by cyclosporin A, which also failed to inhibit peripheral deletion. In SCID animals nonlymphoid tissues did not express FasL in response to SEB unless transplanted lymphocytes were present. Thus, some immune responses induce FasL in nonlymphoid tissues, which in turn kills activated lymphocytes, leading to peripheral T cell deletion.

AB - Fas (CD95) and Fas ligand (FasL) play major roles in staphylococcal enterotoxin B (SEB)-induced peripheral deletion of Vβ8+ T cells. We found that peripheral deletion was defective in radiation chimeras with nonfunctional tissue FasL, regardless of the FasL status of the bone marrow- derived cells. SEB induced a dramatic upregulation of FasL expression and function in nonlymphoid cells of liver and small intestine. This effect was resistant to inhibition by cyclosporin A, which also failed to inhibit peripheral deletion. In SCID animals nonlymphoid tissues did not express FasL in response to SEB unless transplanted lymphocytes were present. Thus, some immune responses induce FasL in nonlymphoid tissues, which in turn kills activated lymphocytes, leading to peripheral T cell deletion.

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Inducible nonlymphoid expression of Fas ligand is responsible for superantigen-induced peripheral deletion of T cells

Abstract

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