Lise Wogensen

Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma

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Standard

Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma. / Wogensen, L; Molony, L; Gu, D; Krahl, T; Zhu, S; Sarvetnick, N.

I: Journal of interferon research, Bind 14, Nr. 3, 06.1994, s. 111-6.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Wogensen, L, Molony, L, Gu, D, Krahl, T, Zhu, S & Sarvetnick, N 1994, 'Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma', Journal of interferon research, bind 14, nr. 3, s. 111-6.

APA

Wogensen, L., Molony, L., Gu, D., Krahl, T., Zhu, S., & Sarvetnick, N. (1994). Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma. Journal of interferon research, 14(3), 111-6.

CBE

Wogensen L, Molony L, Gu D, Krahl T, Zhu S, Sarvetnick N. 1994. Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma. Journal of interferon research. 14(3):111-6.

MLA

Vancouver

Wogensen L, Molony L, Gu D, Krahl T, Zhu S, Sarvetnick N. Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma. Journal of interferon research. 1994 jun;14(3):111-6.

Author

Wogensen, L ; Molony, L ; Gu, D ; Krahl, T ; Zhu, S ; Sarvetnick, N. / Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma. I: Journal of interferon research. 1994 ; Bind 14, Nr. 3. s. 111-6.

Bibtex

@article{1536e48b0895402d8a88d60bd5cd406f,
title = "Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma",
abstract = "beta-Cell-targeted expression of interferon-gamma (IFN-gamma) leads to pancreatitis and immune sensitization to beta-cells. This transgenic model is used to explore the possible role of locally produced IFN-gamma in loss of tolerance to beta-cell-specific antigens in insulin-dependent diabetes mellitus (IDDM). The aim of the present study was to test if postnatal treatment with antibodies against IFN-gamma could inhibit morphological changes in the IFN-gamma transgenic pancreas, even though the transgene is expressed during embryogenesis. Treatment with a monoclonal rat anti-mouse IFN-gamma antibody for 6 weeks, starting from 5 to 7 days of age, completely inhibited IFN-gamma-induced morphological changes in the pancreas, and only a modest inflammatory reaction emerged after prolonged treatment for 12 weeks. The lack of morphological changes may reflect the ability of nonterminally differentiated neonatal pancreatic cells to compensate for transgene-induced pathological alterations occurring in utero prior to the antibody treatment. We conclude that inflammation and altered pancreas morphology in the transgenic mice is the result of the biological actions of IFN-gamma and not by disrupted islet development due to transgene overexpression in the pancreatic beta-cells. Furthermore, our treatment schedule can serve as a model for future intervention studies in the transgenic mice, elaborating the role of IFN-gamma in localized inflammatory reactions, IDDM in particular.",
keywords = "Animals, Antibodies, Monoclonal, Disease Models, Animal, Interferon-gamma, Islets of Langerhans, Mice, Mice, Transgenic, Pancreatitis, Solubility",
author = "L Wogensen and L Molony and D Gu and T Krahl and S Zhu and N Sarvetnick",
year = "1994",
month = jun,
language = "English",
volume = "14",
pages = "111--6",
journal = "Journal of interferon research",
issn = "0197-8357",
publisher = "Mary Ann Liebert Inc.",
number = "3",

}

RIS

TY - JOUR

T1 - Postnatal anti-interferon-gamma treatment prevents pancreatic inflammation in transgenic mice with beta-cell expression of interferon-gamma

AU - Wogensen, L

AU - Molony, L

AU - Gu, D

AU - Krahl, T

AU - Zhu, S

AU - Sarvetnick, N

PY - 1994/6

Y1 - 1994/6

N2 - beta-Cell-targeted expression of interferon-gamma (IFN-gamma) leads to pancreatitis and immune sensitization to beta-cells. This transgenic model is used to explore the possible role of locally produced IFN-gamma in loss of tolerance to beta-cell-specific antigens in insulin-dependent diabetes mellitus (IDDM). The aim of the present study was to test if postnatal treatment with antibodies against IFN-gamma could inhibit morphological changes in the IFN-gamma transgenic pancreas, even though the transgene is expressed during embryogenesis. Treatment with a monoclonal rat anti-mouse IFN-gamma antibody for 6 weeks, starting from 5 to 7 days of age, completely inhibited IFN-gamma-induced morphological changes in the pancreas, and only a modest inflammatory reaction emerged after prolonged treatment for 12 weeks. The lack of morphological changes may reflect the ability of nonterminally differentiated neonatal pancreatic cells to compensate for transgene-induced pathological alterations occurring in utero prior to the antibody treatment. We conclude that inflammation and altered pancreas morphology in the transgenic mice is the result of the biological actions of IFN-gamma and not by disrupted islet development due to transgene overexpression in the pancreatic beta-cells. Furthermore, our treatment schedule can serve as a model for future intervention studies in the transgenic mice, elaborating the role of IFN-gamma in localized inflammatory reactions, IDDM in particular.

AB - beta-Cell-targeted expression of interferon-gamma (IFN-gamma) leads to pancreatitis and immune sensitization to beta-cells. This transgenic model is used to explore the possible role of locally produced IFN-gamma in loss of tolerance to beta-cell-specific antigens in insulin-dependent diabetes mellitus (IDDM). The aim of the present study was to test if postnatal treatment with antibodies against IFN-gamma could inhibit morphological changes in the IFN-gamma transgenic pancreas, even though the transgene is expressed during embryogenesis. Treatment with a monoclonal rat anti-mouse IFN-gamma antibody for 6 weeks, starting from 5 to 7 days of age, completely inhibited IFN-gamma-induced morphological changes in the pancreas, and only a modest inflammatory reaction emerged after prolonged treatment for 12 weeks. The lack of morphological changes may reflect the ability of nonterminally differentiated neonatal pancreatic cells to compensate for transgene-induced pathological alterations occurring in utero prior to the antibody treatment. We conclude that inflammation and altered pancreas morphology in the transgenic mice is the result of the biological actions of IFN-gamma and not by disrupted islet development due to transgene overexpression in the pancreatic beta-cells. Furthermore, our treatment schedule can serve as a model for future intervention studies in the transgenic mice, elaborating the role of IFN-gamma in localized inflammatory reactions, IDDM in particular.

KW - Animals

KW - Antibodies, Monoclonal

KW - Disease Models, Animal

KW - Interferon-gamma

KW - Islets of Langerhans

KW - Mice

KW - Mice, Transgenic

KW - Pancreatitis

KW - Solubility

M3 - Journal article

C2 - 7930757

VL - 14

SP - 111

EP - 116

JO - Journal of interferon research

JF - Journal of interferon research

SN - 0197-8357

IS - 3

ER -