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2. Anti-inflammatory Roles of Glucocorticoids Are Mediated by Foxp3+ Regulatory T Cells via a miR-342-Dependent Mechanism

Author

Kim, Dongkyun, primary, Nguyen, Quang Tam, additional, Lee, Juyeun, additional, Lee, Sung Hwan, additional, Janocha, Allison, additional, Kim, Sohee, additional, Le, Hongnga T., additional, Dvorina, Nina, additional, Weiss, Kelly, additional, Cameron, Mark J., additional, Asosingh, Kewal, additional, Erzurum, Serpil C., additional, Baldwin, William M., additional, Lee, Ju-Seog, additional, and Min, Booki, additional

Published
2020
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8. Anti-inflammatory Roles of Glucocorticoids Are Mediated by Foxp3 + Regulatory T Cells via a miR-342-Dependent Mechanism.

Author

Kim D, Nguyen QT, Lee J, Lee SH, Janocha A, Kim S, Le HT, Dvorina N, Weiss K, Cameron MJ, Asosingh K, Erzurum SC, Baldwin WM 3rd, Lee JS, and Min B

Subjects
Animals, Anti-Inflammatory Agents pharmacology, Forkhead Transcription Factors metabolism, Mechanistic Target of Rapamycin Complex 2 metabolism, Mice, Mice, Inbred C57BL, MicroRNAs biosynthesis, Receptors, Glucocorticoid genetics, T-Lymphocytes, Regulatory metabolism, Dexamethasone pharmacology, Glucocorticoids pharmacology, Inflammation drug therapy, MicroRNAs genetics, Rapamycin-Insensitive Companion of mTOR Protein metabolism, T-Lymphocytes, Regulatory immunology
Abstract

Glucocorticoids (GC) are the mainstay treatment option for inflammatory conditions. Despite the broad usage of GC, the mechanisms by which GC exerts its effects remain elusive. Here, utilizing murine autoimmune and allergic inflammation models, we report that Foxp3 + regulatory T (Treg) cells are irreplaceable GC target cells in vivo. Dexamethasone (Dex) administered in the absence of Treg cells completely lost its ability to control inflammation, and the lack of glucocorticoid receptor in Treg cells alone resulted in the loss of therapeutic ability of Dex. Mechanistically, Dex induced miR-342-3p specifically in Treg cells and miR-342-3p directly targeted the mTORC2 component, Rictor. Altering miRNA-342-3p or Rictor expression in Treg cells dysregulated metabolic programming in Treg cells, controlling their regulatory functions in vivo. Our results uncover a previously unknown contribution of Treg cells during glucocorticoid-mediated treatment of inflammation and the underlying mechanisms operated via the Dex-miR-342-Rictor axis., Competing Interests: Declaration of Interests Authors declare that they have no competing interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Published
2020
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9. Epithelial cell-specific Act1 adaptor mediates interleukin-25-dependent helminth expulsion through expansion of Lin(-)c-Kit(+) innate cell population.

Author

Kang Z, Swaidani S, Yin W, Wang C, Barlow JL, Gulen MF, Bulek K, Do JS, Aronica M, McKenzie AN, Min B, and Li X

Subjects
Adaptor Proteins, Signal Transducing genetics, Adaptor Proteins, Signal Transducing metabolism, Animals, Cell Lineage, Cells, Cultured, Epithelial Cells cytology, Epithelial Cells metabolism, Helminthiasis metabolism, Helminths metabolism, Immunity, Innate immunology, Interleukins metabolism, Intestinal Mucosa cytology, Intestinal Mucosa immunology, Intestinal Mucosa metabolism, Liver cytology, Liver immunology, Liver metabolism, Lung cytology, Lung immunology, Lung metabolism, Lymph Nodes immunology, Lymph Nodes metabolism, Macrophages immunology, Macrophages metabolism, Mice, Mice, Inbred C57BL, Mice, Transgenic, Th2 Cells metabolism, Adaptor Proteins, Signal Transducing immunology, Epithelial Cells immunology, Helminthiasis immunology, Helminths immunology, Interleukins immunology, Th2 Cells immunology
Abstract

Interleukin-25 (IL-25 or IL-17E), a member of the structurally related IL-17 family, functions as an important mediator of T helper 2 cell-type (type 2) responses. We examined the cell type-specific role of IL-25-induced Act1-mediated signaling in protective immunity against helminth infection. Targeted Act1 deficiency in epithelial cells resulted in a marked delay in worm expulsion and abolished the expansion of the Lin(-)c-Kit(+) innate cell population in the mesenteric lymph node, lung, and liver. Th2 cell-inducing cytokine (IL-25 and IL-33) expression were reduced in the intestinal epithelial cells from the infected and IL-25-injected epithelial-specific Act1-deficient mice. Adoptive transfer of Lin(-)c-Kit(+) cells or combined injection of IL-25 and IL-33 restored the type 2 responses in these mice. Taken together, these results suggest that epithelial-specific Act1 mediates the expansion of the Lin(-)c-Kit(+) innate cell population through the positive-feedback loop of IL-25, initiating the type 2 immunity against helminth infection., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Published
2012
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