NDLI: IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis.

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IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Duhen, Rebekka Eberl, Gerard Arbelaez, Carlos A. Bettelli, Estelle Oukka, Mohamed Glatigny, Simon
Description	Author Affiliation: Arbelaez CA ( Department of Immunology, University of Washington, Seattle, WA 98101); Glatigny S ( Department of Immunology, University of Washington, Seattle, WA 98101); Duhen R ( Department of Immunology, University of Washington, Seattle, WA 98101); Eberl G ( Lymphoid Tissue Development Unit, Pasteur Institute, Paris 75724, France); Oukka M ( Department of Immunology, University of Washington, Seattle, WA 98101); Bettelli E ( Department of Immunology, University of Washington, Seattle, WA 98101)
Abstract	IL-17-producing CD4(+) T (Th17) cells, along with IFN-Î³-expressing Th1 cells, represent two major pathogenic T cell subsets in experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). The cytokines and transcription factors involved in the development and effector functions of Th1 and Th17 cells have been largely characterized. Among them, IL-23 is essential for the generation of stable and encephalitogenic Th17 cells and for the development of EAE. The IL-7/IL-7R signaling axis participates in cell survival, and perturbation of this pathway has been associated with enhanced susceptibility to MS. A link between IL-23-driven pathogenic T cells and IL-7/IL-7R signaling has previously been proposed, but has not been formally addressed. In the current study, we showed that Th17 cells from mice with EAE express high levels of IL-7R compared with Th1 cells. Using mice that constitutively express IL-7R on T cells, we determined that sustained IL-7R expression in IL-23R-deficient mice could not drive pathogenic T cells and the development of EAE. IL-7 inhibited the differentiation of Th17 cells, but promoted IFN-Î³ and GM-CSF secretion in vitro. In vivo IL-7/anti-IL-7 mAb complexes selectively expanded and enhanced the proliferation of CXCR3-expressing Th1 cells, but did not impact Th17 cells and EAE development in wild-type and IL-23R-deficient mice. Importantly, high IL-7 expression was detected in the CNS during EAE and could drive the plasticity of Th17 cells to IFN-Î³-producing T cells. Together, these data address the contribution of IL-23/IL-23R and IL-7/IL-7R signaling in Th17 and Th1 cell dynamics during CNS autoimmunity.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1403135
Journal	The Journal of Immunology
Issue Number	5
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd4-positive T-lymphocytes Immunology Encephalomyelitis, Autoimmune, Experimental Interleukin-7 Receptors, Interleukin-7 Signal Transduction Animals Metabolism Cell Differentiation Genetics Cells, Cultured Disease Models, Animal Flow Cytometry Interferon-gamma Interleukin-23 Mice, Inbred C57bl Mice, Knockout Mice, Transgenic Multiple Sclerosis Receptors, Interleukin T-lymphocyte Subsets Th1 Cells Th17 Cells Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Th17 cells induce Th1-polarizing monocyte-derived dendritic cells.

Interleukin-7 is required for CD4(+) T cell activation and autoimmune neuroinflammation.

Invariant NKT cells producing IL-4 or IL-10, but not IFN-gamma, inhibit the Th1 response in experimental autoimmune encephalomyelitis, whereas none of these cells inhibits the Th17 response.

SLAM-SAP signaling promotes differentiation of IL-17-producing T cells and progression of experimental autoimmune encephalomyelitis.

Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.

Cutting edge: Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis.

Cutting Edge: MicroRNA-223 Regulates Myeloid Dendritic Cell-Driven Th17 Responses in Experimental Autoimmune Encephalomyelitis.

Current Views on the Roles of Th1 and Th17 Cells in Experimental Autoimmune Encephalomyelitis

Mesenchymal stem cells differentially modulate effector CD8+ T cell subsets and exacerbate experimental autoimmune encephalomyelitis.

IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis.

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Invariant NKT cells producing IL-4 or IL-10, but not IFN-gamma, inhibit the Th1 response in experimental autoimmune encephalomyelitis, whereas none of these cells inhibits the Th17 response.

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