Heat shock protein 60 elicits abnormal response in macrophages of diabetes-prone non-obese diabetic mice

Thure Adler; Hidehiko Akiyama; Christian Herder; Hubert Kolb; Volker Burkart

doi:10.1016/S0006-291X(02)00522-3

Heat shock protein 60 elicits abnormal response in macrophages of diabetes-prone non-obese diabetic mice

Thure Adler, Hidehiko Akiyama, Christian Herder, Hubert Kolb, Volker Burkart

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

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Abstract

Heat shock protein 60 (hsp60) is a target antigen in autoimmune diabetes and injections of human hsp60 for tolerance induction were found to protect non-obese diabetic (NOD) mice an animal model of human type 1 diabetes from disease development. We tested whether innate immune cells of NOD mice exhibit an abnormal response to extracellular hsp60. Bone marrow derived macrophages (BMM) were grown from NOD C57BL/6J non-obese non-diabetic (NON) mice and NOD-related congenic variants differing in the Idd-3 Idd-10/18 or major histocompatibility complex (MHC) region. Hsp60-stimulated BMM of NOD mice were found to produce high levels of interleukin (IL)-12(p70). The addition of IL-10 downregulated whereas cyclooxygenase inhibitors elevated IL-12(p70) production of activated BMM. BMM of NON NON-NOD-H-2^g7 as well as of NOD-NON-H-2^nbl mice produced significantly less IL-12(p70) than BMM of NOD mice indicating that an interaction between the MHC haplotype and non-MHC genes of the NOD mouse is required for hyperresponsiveness to hsp60.

Original language	English
Pages (from-to)	592-596
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	294
Issue number	3
DOIs	https://doi.org/10.1016/S0006-291X(02)00522-3
Publication status	Published - 2002
Externally published	Yes

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0006-291X(02)00522-3

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title = "Heat shock protein 60 elicits abnormal response in macrophages of diabetes-prone non-obese diabetic mice",

abstract = "Heat shock protein 60 (hsp60) is a target antigen in autoimmune diabetes and injections of human hsp60 for tolerance induction were found to protect non-obese diabetic (NOD) mice an animal model of human type 1 diabetes from disease development. We tested whether innate immune cells of NOD mice exhibit an abnormal response to extracellular hsp60. Bone marrow derived macrophages (BMM) were grown from NOD C57BL/6J non-obese non-diabetic (NON) mice and NOD-related congenic variants differing in the Idd-3 Idd-10/18 or major histocompatibility complex (MHC) region. Hsp60-stimulated BMM of NOD mice were found to produce high levels of interleukin (IL)-12(p70). The addition of IL-10 downregulated whereas cyclooxygenase inhibitors elevated IL-12(p70) production of activated BMM. BMM of NON NON-NOD-H-2g7 as well as of NOD-NON-H-2nbl mice produced significantly less IL-12(p70) than BMM of NOD mice indicating that an interaction between the MHC haplotype and non-MHC genes of the NOD mouse is required for hyperresponsiveness to hsp60.",

author = "Thure Adler and Hidehiko Akiyama and Christian Herder and Hubert Kolb and Volker Burkart",

note = "Funding Information: This work was supported by grants from the Deutsche Forschungsgemeinschaft, the Bundesministerium f{\"u}r Gesundheit, the Ministerium f{\"u}r Wissenschaft und Forschung des Landes Nordrhein-Westfalen, and Peptor GmbH, Erkrath, Germany. Furthermore, we thank Peptor GmbH for providing recombinant human hsp60.",

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doi = "10.1016/S0006-291X(02)00522-3",

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pages = "592--596",

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AU - Adler, Thure

AU - Akiyama, Hidehiko

AU - Herder, Christian

AU - Kolb, Hubert

AU - Burkart, Volker

N1 - Funding Information: This work was supported by grants from the Deutsche Forschungsgemeinschaft, the Bundesministerium für Gesundheit, the Ministerium für Wissenschaft und Forschung des Landes Nordrhein-Westfalen, and Peptor GmbH, Erkrath, Germany. Furthermore, we thank Peptor GmbH for providing recombinant human hsp60.

PY - 2002

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N2 - Heat shock protein 60 (hsp60) is a target antigen in autoimmune diabetes and injections of human hsp60 for tolerance induction were found to protect non-obese diabetic (NOD) mice an animal model of human type 1 diabetes from disease development. We tested whether innate immune cells of NOD mice exhibit an abnormal response to extracellular hsp60. Bone marrow derived macrophages (BMM) were grown from NOD C57BL/6J non-obese non-diabetic (NON) mice and NOD-related congenic variants differing in the Idd-3 Idd-10/18 or major histocompatibility complex (MHC) region. Hsp60-stimulated BMM of NOD mice were found to produce high levels of interleukin (IL)-12(p70). The addition of IL-10 downregulated whereas cyclooxygenase inhibitors elevated IL-12(p70) production of activated BMM. BMM of NON NON-NOD-H-2g7 as well as of NOD-NON-H-2nbl mice produced significantly less IL-12(p70) than BMM of NOD mice indicating that an interaction between the MHC haplotype and non-MHC genes of the NOD mouse is required for hyperresponsiveness to hsp60.

AB - Heat shock protein 60 (hsp60) is a target antigen in autoimmune diabetes and injections of human hsp60 for tolerance induction were found to protect non-obese diabetic (NOD) mice an animal model of human type 1 diabetes from disease development. We tested whether innate immune cells of NOD mice exhibit an abnormal response to extracellular hsp60. Bone marrow derived macrophages (BMM) were grown from NOD C57BL/6J non-obese non-diabetic (NON) mice and NOD-related congenic variants differing in the Idd-3 Idd-10/18 or major histocompatibility complex (MHC) region. Hsp60-stimulated BMM of NOD mice were found to produce high levels of interleukin (IL)-12(p70). The addition of IL-10 downregulated whereas cyclooxygenase inhibitors elevated IL-12(p70) production of activated BMM. BMM of NON NON-NOD-H-2g7 as well as of NOD-NON-H-2nbl mice produced significantly less IL-12(p70) than BMM of NOD mice indicating that an interaction between the MHC haplotype and non-MHC genes of the NOD mouse is required for hyperresponsiveness to hsp60.

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Heat shock protein 60 elicits abnormal response in macrophages of diabetes-prone non-obese diabetic mice

Abstract

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