Cardiac allograft survival in mice treated with IL-2-PE40

H. Lorberboum-Galski; L. V. Barrett; R. L. Kirkman; M. Ogata; M. C. Willingham; D. J. FitzGerald; I. Pastan

doi:10.1073/pnas.86.3.1008

Cardiac allograft survival in mice treated with IL-2-PE40

H. Lorberboum-Galski
, L. V. Barrett
, R. L. Kirkman
, M. Ogata
, M. C. Willingham
, D. J. FitzGerald
, I. Pastan

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

57 Scopus citations

Abstract

IL-2-PE40 is a chimeric protein composed of human interleukin 2 (IL-2) genetically fused to the amino terminus of a modified form of Pseudomonas exotoxin lacking its cell recognition domain. IL-2-PE40, which is extremely cytotoxic to IL-2 receptor-positive cells, was examined for its ability to prevent graft rejection in mice in which activation of T cells is prominent. We demonstrate that intraperitoneally administered IL-2-PE40 specifically and significantly prolongs the survival of vascularized heart allografts in mice. The chimeric toxin, IL-2-PE40, offers an alternative approach to the treatment of autoimmune diseases and transplant rejection in humans.

Original language	English
Pages (from-to)	1008-1012
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	86
Issue number	3
DOIs	https://doi.org/10.1073/pnas.86.3.1008
State	Published - 1989
Externally published	Yes

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title = "Cardiac allograft survival in mice treated with IL-2-PE40",

abstract = "IL-2-PE40 is a chimeric protein composed of human interleukin 2 (IL-2) genetically fused to the amino terminus of a modified form of Pseudomonas exotoxin lacking its cell recognition domain. IL-2-PE40, which is extremely cytotoxic to IL-2 receptor-positive cells, was examined for its ability to prevent graft rejection in mice in which activation of T cells is prominent. We demonstrate that intraperitoneally administered IL-2-PE40 specifically and significantly prolongs the survival of vascularized heart allografts in mice. The chimeric toxin, IL-2-PE40, offers an alternative approach to the treatment of autoimmune diseases and transplant rejection in humans.",

author = "H. Lorberboum-Galski and Barrett, \{L. V.\} and Kirkman, \{R. L.\} and M. Ogata and Willingham, \{M. C.\} and FitzGerald, \{D. J.\} and I. Pastan",

year = "1989",

doi = "10.1073/pnas.86.3.1008",

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T1 - Cardiac allograft survival in mice treated with IL-2-PE40

AU - Lorberboum-Galski, H.

AU - Barrett, L. V.

AU - Kirkman, R. L.

AU - Ogata, M.

AU - Willingham, M. C.

AU - FitzGerald, D. J.

AU - Pastan, I.

PY - 1989

Y1 - 1989

N2 - IL-2-PE40 is a chimeric protein composed of human interleukin 2 (IL-2) genetically fused to the amino terminus of a modified form of Pseudomonas exotoxin lacking its cell recognition domain. IL-2-PE40, which is extremely cytotoxic to IL-2 receptor-positive cells, was examined for its ability to prevent graft rejection in mice in which activation of T cells is prominent. We demonstrate that intraperitoneally administered IL-2-PE40 specifically and significantly prolongs the survival of vascularized heart allografts in mice. The chimeric toxin, IL-2-PE40, offers an alternative approach to the treatment of autoimmune diseases and transplant rejection in humans.

AB - IL-2-PE40 is a chimeric protein composed of human interleukin 2 (IL-2) genetically fused to the amino terminus of a modified form of Pseudomonas exotoxin lacking its cell recognition domain. IL-2-PE40, which is extremely cytotoxic to IL-2 receptor-positive cells, was examined for its ability to prevent graft rejection in mice in which activation of T cells is prominent. We demonstrate that intraperitoneally administered IL-2-PE40 specifically and significantly prolongs the survival of vascularized heart allografts in mice. The chimeric toxin, IL-2-PE40, offers an alternative approach to the treatment of autoimmune diseases and transplant rejection in humans.

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JF - Proceedings of the National Academy of Sciences of the United States of America

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Cardiac allograft survival in mice treated with IL-2-PE40

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