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6 results on '"Irmler, Martin"'

1. Gut HIF2α signaling is increased after VSG, and gut activation of HIF2α decreases weight, improves glucose, and increases GLP-1 secretion

Author

Evers, Simon S., primary, Shao, Yikai, additional, Ramakrishnan, Sadeesh K., additional, Shin, Jae Hoon, additional, Bozadjieva-Kramer, Nadejda, additional, Irmler, Martin, additional, Stemmer, Kerstin, additional, Sandoval, Darleen A., additional, Shah, Yatrik M., additional, and Seeley, Randy J., additional

Published
2022
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2. Dynamic adoption of anergy by antigen-exhausted CD4+ T cells

Author

Trefzer, Anne, primary, Kadam, Pallavi, additional, Wang, Shu-Hung, additional, Pennavaria, Stefanie, additional, Lober, Benedikt, additional, Akçabozan, Batuhan, additional, Kranich, Jan, additional, Brocker, Thomas, additional, Nakano, Naoko, additional, Irmler, Martin, additional, Beckers, Johannes, additional, Straub, Tobias, additional, and Obst, Reinhard, additional

Published
2021
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3. The Aryl Hydrocarbon Receptor Pathway Defines the Time Frame for Restorative Neurogenesis

Author

Di Giaimo, Rossella, primary, Durovic, Tamara, additional, Barquin, Pablo, additional, Kociaj, Anita, additional, Lepko, Tjasa, additional, Aschenbroich, Sven, additional, Breunig, Christopher T., additional, Irmler, Martin, additional, Cernilogar, Filippo M., additional, Schotta, Gunnar, additional, Barbosa, Joana S., additional, Trümbach, Dietrich, additional, Baumgart, Emily Violette, additional, Neuner, Andrea M., additional, Beckers, Johannes, additional, Wurst, Wolfgang, additional, Stricker, Stefan H., additional, and Ninkovic, Jovica, additional

Published
2018
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4. Stem-Cell-like Properties and Epithelial Plasticity Arise as Stable Traits after Transient Twist1 Activation

Author

Schmidt, Johanna M., primary, Panzilius, Elena, additional, Bartsch, Harald S., additional, Irmler, Martin, additional, Beckers, Johannes, additional, Kari, Vijayalakshmi, additional, Linnemann, Jelena R., additional, Dragoi, Diana, additional, Hirschi, Benjamin, additional, Kloos, Uwe J., additional, Sass, Steffen, additional, Theis, Fabian, additional, Kahlert, Steffen, additional, Johnsen, Steven A., additional, Sotlar, Karl, additional, and Scheel, Christina H., additional

Published
2015
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5. Dynamic adoption of anergy by antigen-exhausted CD4+T cells

Author

Trefzer, Anne, Kadam, Pallavi, Wang, Shu-Hung, Pennavaria, Stefanie, Lober, Benedikt, Akçabozan, Batuhan, Kranich, Jan, Brocker, Thomas, Nakano, Naoko, Irmler, Martin, Beckers, Johannes, Straub, Tobias, and Obst, Reinhard

Abstract

Exhausted immune responses to chronic diseases represent a major challenge to global health. We study CD4+T cells in a mouse model with regulatable antigen presentation. When the cells are driven through the effector phase and are then exposed to different levels of persistent antigen, they lose their T helper 1 (Th1) functions, upregulate exhaustion markers, resemble naturally anergic cells, and modulate their MAPK, mTORC1, and Ca2+/calcineurin signaling pathways with increasing dose and time. They also become unable to help B cells and, at the highest dose, undergo apoptosis. Transcriptomic analyses show the dynamic adjustment of gene expression and the accumulation of T cell receptor (TCR) signals over a period of weeks. Upon antigen removal, the cells recover their functionality while losing exhaustion and anergy markers. Our data suggest an adjustable response of CD4+T cells to different levels of persisting antigen and contribute to a better understanding of chronic disease.

Published
2021
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6. Dynamic adoption of anergy by antigen-exhausted CD4 + T cells.

Author

Trefzer A, Kadam P, Wang SH, Pennavaria S, Lober B, Akçabozan B, Kranich J, Brocker T, Nakano N, Irmler M, Beckers J, Straub T, and Obst R

Subjects
Animals, Antigens genetics, B-Lymphocytes immunology, Calcium Signaling genetics, Female, Gene Expression Profiling, MAP Kinase Signaling System genetics, Mechanistic Target of Rapamycin Complex 1 genetics, Mechanistic Target of Rapamycin Complex 1 immunology, Mice, Mice, Transgenic, Receptors, Antigen, T-Cell genetics, Receptors, Antigen, T-Cell immunology, Antigens immunology, Calcium Signaling immunology, Clonal Anergy, Gene Expression Regulation immunology, MAP Kinase Signaling System immunology, Th1 Cells immunology
Abstract

Exhausted immune responses to chronic diseases represent a major challenge to global health. We study CD4 + T cells in a mouse model with regulatable antigen presentation. When the cells are driven through the effector phase and are then exposed to different levels of persistent antigen, they lose their T helper 1 (Th1) functions, upregulate exhaustion markers, resemble naturally anergic cells, and modulate their MAPK, mTORC1, and Ca 2+ /calcineurin signaling pathways with increasing dose and time. They also become unable to help B cells and, at the highest dose, undergo apoptosis. Transcriptomic analyses show the dynamic adjustment of gene expression and the accumulation of T cell receptor (TCR) signals over a period of weeks. Upon antigen removal, the cells recover their functionality while losing exhaustion and anergy markers. Our data suggest an adjustable response of CD4 + T cells to different levels of persisting antigen and contribute to a better understanding of chronic disease., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2021
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