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IL-17 metabolically reprograms activated fibroblastic reticular cells for proliferation and survival
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IL-17 metabolically reprograms activated fibroblastic reticular cells for proliferation and survival
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Journal Article
IL-17 metabolically reprograms activated fibroblastic reticular cells for proliferation and survival
2019
Overview
Lymph-node (LN) stromal cell populations expand during the inflammation that accompanies T cell activation. Interleukin-17 (IL-17)-producing helper T cells (T
H
17 cells) promote inflammation through the induction of cytokines and chemokines in peripheral tissues. We demonstrate a critical requirement for IL-17 in the proliferation of LN and splenic stromal cells, particularly fibroblastic reticular cells (FRCs), during experimental autoimmune encephalomyelitis and colitis. Without signaling via the IL-17 receptor, activated FRCs underwent cell cycle arrest and apoptosis, accompanied by signs of nutrient stress in vivo. IL-17 signaling in FRCs was not required for the development of T
H
17 cells, but failed FRC proliferation impaired germinal center formation and antigen-specific antibody production. Induction of the transcriptional co-activator IκBζ via IL-17 signaling mediated increased glucose uptake and expression of the gene
Cpt1a
, encoding CPT1A, a rate-limiting enzyme of mitochondrial fatty acid oxidation. Hence, IL-17 produced by locally differentiating T
H
17 cells is an important driver of the activation of inflamed LN stromal cells, through metabolic reprogramming required to support proliferation and survival.
Fibroblastic reticular cells support lymph-node function and adaptive immunity. McGeachy and colleagues show that the cytokine IL-17 is needed to trigger metabolic changes required for the proliferation and survival of these cells in reactive lymph nodes.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Antibody Formation - genetics
/ Antibody Formation - immunology
/ Antigens
/ B cells
/ Biomedical and Life Sciences
/ Cellular signal transduction
/ Colitis
/ Encephalomyelitis, Autoimmune, Experimental - genetics
/ Encephalomyelitis, Autoimmune, Experimental - immunology
/ Encephalomyelitis, Autoimmune, Experimental - metabolism
/ Enzymes
/ Experimental allergic encephalomyelitis
/ Genes
/ Glucose
/ Oxidation-reduction reactions
/ Receptors, Interleukin-17 - genetics
/ Receptors, Interleukin-17 - immunology
/ Receptors, Interleukin-17 - metabolism
/ Spleen
/ T cells
