The Experts below are selected from a list of 3 Experts worldwide ranked by ideXlab platform
Jens Y Humrich - One of the best experts on this subject based on the ideXlab platform.
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homeostatic imbalance of regulatory and effector t cells due to il 2 deprivation amplifies murine lupus
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Jens Y Humrich, Henner Morbach, R Undeutsch, Philipp Enghard, Stefan Rosenberger, Olivia Weigert, Lutz Kloke, Juliane Heimann, Timo Gaber, Susan BrandenburgAbstract:The origins and consequences of a regulatory T cell (Treg) disorder in systemic lupus erythematosus (SLE) are poorly understood. In the (NZBxNZW) F1 Mouse model of lupus, we found that CD4+Foxp3+ Treg failed to maintain a competitive pool size in the peripheral lymphoid organs resulting in a progressive homeostatic imbalance of CD4+Foxp3+ Treg and CD4+Foxp3− conventional T cells (Tcon). In addition, Treg acquired phenotypic changes that are reminiscent of IL-2 deficiency concomitantly to a progressive decline in IL-2-producing Tcon and an increase in activated, IFN-γ-producing effector Tcon. Nonetheless, Treg from lupus-prone mice were functionally intact and capable to influence the course of disease. Systemic reduction of IL-2 levels early in disease promoted Tcon hyperactivity, induced the imbalance of Treg and effector Tcon, and strongly accelerated disease progression. In contrast, administration of IL-2 partially restored the balance of Treg and effector Tcon by promoting the homeostatic proliferation of endogenous Treg and impeded the progression of established disease. Thus, an acquired and self-amplifying disruption of the Treg-IL-2 axis contributed essentially to Tcon hyperactivity and the development of murine lupus. The reversibility of this homeostatic Treg disorder provides promising approaches for the treatment of SLE.
Henner Morbach - One of the best experts on this subject based on the ideXlab platform.
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homeostatic imbalance of regulatory and effector t cells due to il 2 deprivation amplifies murine lupus
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Jens Y Humrich, Henner Morbach, R Undeutsch, Philipp Enghard, Stefan Rosenberger, Olivia Weigert, Lutz Kloke, Juliane Heimann, Timo Gaber, Susan BrandenburgAbstract:The origins and consequences of a regulatory T cell (Treg) disorder in systemic lupus erythematosus (SLE) are poorly understood. In the (NZBxNZW) F1 Mouse model of lupus, we found that CD4+Foxp3+ Treg failed to maintain a competitive pool size in the peripheral lymphoid organs resulting in a progressive homeostatic imbalance of CD4+Foxp3+ Treg and CD4+Foxp3− conventional T cells (Tcon). In addition, Treg acquired phenotypic changes that are reminiscent of IL-2 deficiency concomitantly to a progressive decline in IL-2-producing Tcon and an increase in activated, IFN-γ-producing effector Tcon. Nonetheless, Treg from lupus-prone mice were functionally intact and capable to influence the course of disease. Systemic reduction of IL-2 levels early in disease promoted Tcon hyperactivity, induced the imbalance of Treg and effector Tcon, and strongly accelerated disease progression. In contrast, administration of IL-2 partially restored the balance of Treg and effector Tcon by promoting the homeostatic proliferation of endogenous Treg and impeded the progression of established disease. Thus, an acquired and self-amplifying disruption of the Treg-IL-2 axis contributed essentially to Tcon hyperactivity and the development of murine lupus. The reversibility of this homeostatic Treg disorder provides promising approaches for the treatment of SLE.
R Undeutsch - One of the best experts on this subject based on the ideXlab platform.
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homeostatic imbalance of regulatory and effector t cells due to il 2 deprivation amplifies murine lupus
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Jens Y Humrich, Henner Morbach, R Undeutsch, Philipp Enghard, Stefan Rosenberger, Olivia Weigert, Lutz Kloke, Juliane Heimann, Timo Gaber, Susan BrandenburgAbstract:The origins and consequences of a regulatory T cell (Treg) disorder in systemic lupus erythematosus (SLE) are poorly understood. In the (NZBxNZW) F1 Mouse model of lupus, we found that CD4+Foxp3+ Treg failed to maintain a competitive pool size in the peripheral lymphoid organs resulting in a progressive homeostatic imbalance of CD4+Foxp3+ Treg and CD4+Foxp3− conventional T cells (Tcon). In addition, Treg acquired phenotypic changes that are reminiscent of IL-2 deficiency concomitantly to a progressive decline in IL-2-producing Tcon and an increase in activated, IFN-γ-producing effector Tcon. Nonetheless, Treg from lupus-prone mice were functionally intact and capable to influence the course of disease. Systemic reduction of IL-2 levels early in disease promoted Tcon hyperactivity, induced the imbalance of Treg and effector Tcon, and strongly accelerated disease progression. In contrast, administration of IL-2 partially restored the balance of Treg and effector Tcon by promoting the homeostatic proliferation of endogenous Treg and impeded the progression of established disease. Thus, an acquired and self-amplifying disruption of the Treg-IL-2 axis contributed essentially to Tcon hyperactivity and the development of murine lupus. The reversibility of this homeostatic Treg disorder provides promising approaches for the treatment of SLE.
Philipp Enghard - One of the best experts on this subject based on the ideXlab platform.
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homeostatic imbalance of regulatory and effector t cells due to il 2 deprivation amplifies murine lupus
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Jens Y Humrich, Henner Morbach, R Undeutsch, Philipp Enghard, Stefan Rosenberger, Olivia Weigert, Lutz Kloke, Juliane Heimann, Timo Gaber, Susan BrandenburgAbstract:The origins and consequences of a regulatory T cell (Treg) disorder in systemic lupus erythematosus (SLE) are poorly understood. In the (NZBxNZW) F1 Mouse model of lupus, we found that CD4+Foxp3+ Treg failed to maintain a competitive pool size in the peripheral lymphoid organs resulting in a progressive homeostatic imbalance of CD4+Foxp3+ Treg and CD4+Foxp3− conventional T cells (Tcon). In addition, Treg acquired phenotypic changes that are reminiscent of IL-2 deficiency concomitantly to a progressive decline in IL-2-producing Tcon and an increase in activated, IFN-γ-producing effector Tcon. Nonetheless, Treg from lupus-prone mice were functionally intact and capable to influence the course of disease. Systemic reduction of IL-2 levels early in disease promoted Tcon hyperactivity, induced the imbalance of Treg and effector Tcon, and strongly accelerated disease progression. In contrast, administration of IL-2 partially restored the balance of Treg and effector Tcon by promoting the homeostatic proliferation of endogenous Treg and impeded the progression of established disease. Thus, an acquired and self-amplifying disruption of the Treg-IL-2 axis contributed essentially to Tcon hyperactivity and the development of murine lupus. The reversibility of this homeostatic Treg disorder provides promising approaches for the treatment of SLE.
Stefan Rosenberger - One of the best experts on this subject based on the ideXlab platform.
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homeostatic imbalance of regulatory and effector t cells due to il 2 deprivation amplifies murine lupus
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Jens Y Humrich, Henner Morbach, R Undeutsch, Philipp Enghard, Stefan Rosenberger, Olivia Weigert, Lutz Kloke, Juliane Heimann, Timo Gaber, Susan BrandenburgAbstract:The origins and consequences of a regulatory T cell (Treg) disorder in systemic lupus erythematosus (SLE) are poorly understood. In the (NZBxNZW) F1 Mouse model of lupus, we found that CD4+Foxp3+ Treg failed to maintain a competitive pool size in the peripheral lymphoid organs resulting in a progressive homeostatic imbalance of CD4+Foxp3+ Treg and CD4+Foxp3− conventional T cells (Tcon). In addition, Treg acquired phenotypic changes that are reminiscent of IL-2 deficiency concomitantly to a progressive decline in IL-2-producing Tcon and an increase in activated, IFN-γ-producing effector Tcon. Nonetheless, Treg from lupus-prone mice were functionally intact and capable to influence the course of disease. Systemic reduction of IL-2 levels early in disease promoted Tcon hyperactivity, induced the imbalance of Treg and effector Tcon, and strongly accelerated disease progression. In contrast, administration of IL-2 partially restored the balance of Treg and effector Tcon by promoting the homeostatic proliferation of endogenous Treg and impeded the progression of established disease. Thus, an acquired and self-amplifying disruption of the Treg-IL-2 axis contributed essentially to Tcon hyperactivity and the development of murine lupus. The reversibility of this homeostatic Treg disorder provides promising approaches for the treatment of SLE.