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56. TGF-β Regulates Airway Responses Via T Cells

Author

Schramm, Christoph, primary, Herz, Udo, additional, Podlech, Jürgen, additional, Protschka, Martina, additional, Finotto, Susetta, additional, Reddehase, Matthias J., additional, Köhler, Heinz, additional, Galle, Peter R., additional, Lohse, Ansgar W., additional, and Blessing, Manfred, additional

Published
2003
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64. Control of Cytomegalovirus in Bone Marrow Transplantation Chimeras Lacking the Prevailing Antigen-Presenting Molecule in Recipient Tissues Rests Primarily on Recipient-Derived CD8 T Cells

Author

Alterio de Goss, Mariagabriela, primary, Holtappels, Rafaela, additional, Steffens, Hans-Peter, additional, Podlech, Jürgen, additional, Angele, Peter, additional, Dreher, Liane, additional, Thomas, Doris, additional, and Reddehase, Matthias J., additional

Published
1998
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68. Cytomegalovirus Misleads Its Host by Priming of CD8 T Cells Specific for an Epitope Not Presented in Infected Tissues

Author

Holtappels, Rafaela, Podlech, Jürgen, Pahl-Seibert, Marcus-Folker, Jülch, Markus, Thomas, Doris, Simon, Christian O., Wagner, Markus, and Reddehase, Matthias J.

Abstract

Cytomegaloviruses (CMVs) code for several proteins that inhibit the presentation of antigenic peptides to CD8 T cells. Although the molecular mechanisms of CMV interference with the major histocompatibility complex class I pathway are long understood, surprisingly little evidence exists to support a role in vivo. Here we document the first example of the presentation of an antigenic peptide being blocked by a CMV immune evasion protein in organs relevant to CMV disease. Although this Db-restricted peptide, which is derived from the antiapoptotic protein M45 of murine CMV (mCMV), is classified as an immunodominant peptide based on response magnitude and long-term memory, adoptive transfer of M45 epitope-specific CD8 T cells did not protect against infection with wild-type mCMV. Notably, the same cells protected C57BL/6 mice infected with an mCMV mutant in which immune evasion protein m152/gp40 is deleted. These data indicate that direct presentation or cross-presentation of an antigenic peptide by professional antigen-presenting cells can efficiently prime CD8 T cells that fail in protection against CMV organ disease because m152/gp40 prevents presentation of this peptide in pathogenetically relevant tissue cells.

Published
2004
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69. Impairment of TGF-beta signaling in T cells increases susceptibility to experimental autoimmune hepatitis in mice.

Author

Schramm C, Protschka M, Köhler HH, Podlech J, Reddehase MJ, Schirmacher P, Galle PR, Lohse AW, and Blessing M

Subjects
Animals, B-Lymphocytes physiology, Blotting, Northern, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Hepatitis, Autoimmune pathology, Homeostasis physiology, Immunohistochemistry, Mice, Mice, Transgenic, Neutrophil Infiltration physiology, Phenotype, Hepatitis, Autoimmune physiopathology, Signal Transduction physiology, T-Lymphocytes physiology, Transforming Growth Factor beta physiology
Abstract

In autoimmune hepatitis, strong TGF-beta1 expression is found in the inflamed liver. TGF-beta overexpression may be part of a regulatory immune response attempting to suppress autoreactive T cells. To test this hypothesis, we determined whether impairment of TGF-beta signaling in T cells leads to increased susceptibility to experimental autoimmune hepatitis (EAH). Transgenic mice of strain FVB/N were generated expressing a dominant-negative TGF-beta type II receptor in T cells under the control of the human CD2 promoter/locus control region. On induction of EAH, transgenic mice showed markedly increased portal and periportal leukocytic infiltrations with hepatocellular necroses compared with wild-type mice (median histological score = 1.8 +/- 0.26 vs. 0.75 +/- 0.09 in wild-type mice; P < 0.01). Increased IFN-gamma production (118 vs. 45 ng/ml) and less IL-4 production (341 vs. 1,256 pg/ml) by mononuclear cells isolated from transgenic livers was seen. Impairment of TGF-beta signaling in T cells therefore leads to increased susceptibility to EAH in mice. This suggests an important role for TGF-beta in immune homeostasis in the liver and may teleologically explain TGF-beta upregulation in response to T cell-mediated liver injury.

Published
2003
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70. TGF-beta regulates airway responses via T cells.

Author

Schramm C, Herz U, Podlech J, Protschka M, Finotto S, Reddehase MJ, Köhler H, Galle PR, Lohse AW, and Blessing M

Subjects
Administration, Inhalation, Aerosols, Alum Compounds administration & dosage, Animals, Antibody Specificity, Bronchial Hyperreactivity genetics, Bronchial Hyperreactivity immunology, Bronchial Hyperreactivity physiopathology, Bronchoalveolar Lavage Fluid cytology, Bronchoalveolar Lavage Fluid immunology, CD2 Antigens genetics, Cell Movement, Epitopes, T-Lymphocyte administration & dosage, Epitopes, T-Lymphocyte immunology, Humans, Immunoglobulin E blood, Immunohistochemistry, Inflammation genetics, Inflammation immunology, Interferon-gamma blood, Interleukin-13 biosynthesis, Interleukin-13 blood, Lung enzymology, Lung pathology, Lung physiopathology, Mice, Mice, Inbred Strains, Mice, Transgenic, Nitric Oxide Synthase biosynthesis, Nitric Oxide Synthase Type II, Ovalbumin administration & dosage, Ovalbumin immunology, Protein Serine-Threonine Kinases, Receptor, Transforming Growth Factor-beta Type II, Receptors, Transforming Growth Factor beta genetics, Th1 Cells immunology, Lung immunology, T-Lymphocyte Subsets immunology, Transforming Growth Factor beta physiology
Abstract

Allergic asthma is characterized by airway hyperreactivity, inflammation, and a Th2-type cytokine profile favoring IgE production. Beneficial effects of TGF-beta and conflicting results regarding the role of Th1 cytokines have been reported from murine asthma models. In this study, we examined the T cell as a target cell of TGF-beta-mediated immune regulation in a mouse model of asthma. We demonstrate that impairment of TGF-beta signaling in T cells of transgenic mice expressing a dominant-negative TGF-beta type II receptor leads to a decrease in airway reactivity in a non-Ag-dependent model. Increased serum levels of IFN-gamma can be detected in these animals. In contrast, after injection of OVA adsorbed to alum and challenge with OVA aerosol, transgenic animals show an increased airway reactivity and inflammation compared with those of wild-type animals. IL-13 levels in bronchoalveolar lavage fluid and serum as well as the number of inducible NO synthase-expressing cells in lung infiltrates were increased in transgenic animals. These results demonstrate an important role for TGF-beta signaling in T cells in the regulation of airway responses and suggest that the beneficial effects observed for TGF-beta in airway hyperreactivity and inflammation may be due to its regulatory effects on T cells.

Published
2003
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