Thomas Holtschke

Princess Margaret Cancer Centre

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Ivan D. Horak

Tessa Therapeutic (Singapore)

Anneliese Schimpl

University of Würzburg

Thomas Fehr

University Hospital of Zurich

Martin F. Bachmann

University of Bern

Rolf M. Zinkernagel

University Hospital of Zurich

Tak W. Mak

University Health Network

Bernhard Odermatt

University Hospital of Zurich

Herbert C. Morse

National Institute of Allergy and Infectious Diseases

Klaus‐Peter Knobeloch

University of Freiburg

Nathalia A. Giese

Heidelberg University

Cooperative Institutions

University of Würzburg

University Hospital of Zurich

University of Zurich

National Institutes of Health

National Institute of Allergy and Infectious Diseases

Eunice Kennedy Shriver National Institute of Child Health and Human Development

University Hospital of Basel

Ontario Institute for Cancer Research

University of Freiburg

Roche (Switzerland)

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Immunodeficiency and Chronic Myelogenous Leukemia-like Syndrome in Mice with a Targeted Mutation of the ICSBP Gene

Cell (1996)

Thomas Holtschke Jürgen Löhler Yuka Kanno Thomas Fehr Nathalia A. Giese

Chronic myelogenous leukemia

Immunodeficiency Syndrome

10.1016/s0092-8674(00)81348-3

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Citations (650)

T cell subset distribution and B cell hyperreactivity in mice expressing interleukin‐4 under the control of major histocompatibility complex class I regulatory sequences

European Journal of Immunology (1994)

Klaus J. Erb Thomas Holtschke Kathrin Muth Ivan D. Horak Anneliese Schimpl

Transgenic mice in which interleukin-4 (IL-4) is expressed under the control of the major histocompatibility complex (MHC) class I regulatory sequences show low level expression of IL-4 in all organs investigated. Several weeks after birth the animals develop thymus hypoplasia with a loss of CD4+CD8+ double-positive cells and a relative increase in the mature population, especially, and in contrast to previously published lines, the CD4+ single-positive cells. In the periphery, T lymphocytes eventually decline, CD8+ cells being more strongly affected. Many of the residual T cells exhibit the CD44highMel-14low phenotype of antigenically experienced T cells. B cells also show an activated phenotype with respect to size, MHC class II and CD23 expression, are more readily stimulated by anti-mu F(ab')2 antibodies than are B cells from control littermates, and show a higher spontaneous and antigen-induced production of IgG1 and IgE.

CD23

10.1002/eji.1830240520

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Citations (22)

Development and function of T cells in mice rendered interleukin-2 deficient by gene targeting

Nature (1991)

Hubert Schorle Thomas Holtschke Thomas Hünig Anneliese Schimpl Ivan D. Horak

Interleukin 3

Thymocyte

10.1038/352621a0

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Citations (895)

Crucial Role of Interferon Consensus Sequence Binding Protein, but neither of Interferon Regulatory Factor 1 nor of Nitric Oxide Synthesis for Protection Against Murine Listeriosis

The Journal of Experimental Medicine (1997)

Thomas Fehr Gabriele Schoedon Bernhard Odermatt Thomas Holtschke Markus Schneemann

Listeria monocytogenes is widely used as a model to study immune responses against intracellular bacteria. It has been shown that neutrophils and macrophages play an important role to restrict bacterial replication in the early phase of primary infection in mice, and that the cytokines interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) are essential for protection. However, the involved signaling pathways and effector mechanisms are still poorly understood. This study investigated mouse strains deficient for the IFN-dependent transcription factors interferon consensus sequence binding protein (ICSBP), interferon regulatory factor (IRF)1 or 2 for their capacity to eliminate Listeria in vivo and in vitro and for production of inducible reactive nitrogen intermediates (RNI) or reactive oxygen intermediates (ROI) in macrophages. ICSBP−/− and to a lesser degree also IRF2−/− mice were highly susceptible to Listeria infection. This correlated with impaired elimination of Listeria from infected peritoneal macrophage (PEM) cultures stimulated with IFN-γ in vitro; in addition these cultures showed reduced and delayed oxidative burst upon IFN-γ stimulation, whereas nitric oxide production was normal. In contrast, mice deficient for IRF1 were not able to produce nitric oxide, but they efficiently controlled Listeria in vivo and in vitro. These results indicate that (a) the ICSBP/IRF2 complex is essential for IFN-γ–mediated protection against Listeria and that (b) ROI together with additional still unknown effector mechanisms may be responsible for the anti-Listeria activity of macrophages, whereas IRF1-induced RNI are not limiting.

IRF1

Listeria infection

10.1084/jem.185.5.921

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Citations (165)