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γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis

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γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis. / Blink, Sarah E; Caldis, Matthew W; Goings, Gwendolyn E; Harp, Christopher T; Malissen, Bernard; Prinz, Immo; Xu, Dan; Miller, Stephen D.

in: CELL IMMUNOL, Jahrgang 290, Nr. 1, 07.2014, S. 39-51.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Blink, SE, Caldis, MW, Goings, GE, Harp, CT, Malissen, B, Prinz, I, Xu, D & Miller, SD 2014, 'γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis', CELL IMMUNOL, Jg. 290, Nr. 1, S. 39-51. https://doi.org/10.1016/j.cellimm.2014.04.013

APA

Blink, S. E., Caldis, M. W., Goings, G. E., Harp, C. T., Malissen, B., Prinz, I., Xu, D., & Miller, S. D. (2014). γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis. CELL IMMUNOL, 290(1), 39-51. https://doi.org/10.1016/j.cellimm.2014.04.013

Vancouver

Blink SE, Caldis MW, Goings GE, Harp CT, Malissen B, Prinz I et al. γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis. CELL IMMUNOL. 2014 Jul;290(1):39-51. https://doi.org/10.1016/j.cellimm.2014.04.013

Bibtex

@article{d733a49d57e3489697ec872c887a94ef,
title = "γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis",
abstract = "γδ T cells are resident in cerebrospinal fluid and central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but as multifaceted cells exhibiting innate and adaptive characteristics, their function remains unknown. Previous studies in experimental autoimmune encephalomyelitis (EAE) are contradictory and identified these cells as either promoting or suppressing disease pathogenesis. This study examines distinct γδ T cell subsets during EAE and indicates they mediate differential functions in CNS inflammation and demyelination resulting in pathogenesis or protection. We identified two γδ subsets in the CNS, Vγ1(+) and Vγ4(+), with distinct cytokine profiles and tissue specificity. Anti-γδ T cell receptor (TCR) monoclonal antibody (mAb) administration results in activation and downregulation of surface TCR, rendering the cells undetectable, but with opposing effects: anti-Vγ4 treatment exacerbates disease whereas anti-Vγ1 treatment is protective. The Vγ4(+) subset produces multiple pro-inflammatory cytokines including high levels of IL-17, and accounts for 15-20% of the interleukin-17 (IL-17) producing cells in the CNS, but utilize a variant transcriptional program than CD4(+) Th17 cells. In contrast, the Vγ1 subset produces CCR5 ligands, which may promote regulatory T cell differentiation. γδ T cell subsets thus play distinct and opposing roles during EAE, providing an explanation for previous reports and suggesting selective targeting to optimize regulation as a potential therapy for MS.",
keywords = "Animals, Antibodies, Monoclonal/administration & dosage, Cell Differentiation/immunology, Central Nervous System/cytology, Down-Regulation, Encephalomyelitis, Autoimmune, Experimental/immunology, Female, Interleukin-17/biosynthesis, Lymphocyte Activation/immunology, Mice, Mice, Inbred C57BL, Mice, Knockout, Multiple Sclerosis/immunology, Oligodendroglia/immunology, Receptors, Antigen, T-Cell, gamma-delta/immunology, Receptors, CCR5/biosynthesis, Th17 Cells/immunology",
author = "Blink, {Sarah E} and Caldis, {Matthew W} and Goings, {Gwendolyn E} and Harp, {Christopher T} and Bernard Malissen and Immo Prinz and Dan Xu and Miller, {Stephen D}",
note = "Copyright {\textcopyright} 2014 Elsevier Inc. All rights reserved.",
year = "2014",
month = jul,
doi = "10.1016/j.cellimm.2014.04.013",
language = "English",
volume = "290",
pages = "39--51",
journal = "CELL IMMUNOL",
issn = "0008-8749",
publisher = "Academic Press Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis

AU - Blink, Sarah E

AU - Caldis, Matthew W

AU - Goings, Gwendolyn E

AU - Harp, Christopher T

AU - Malissen, Bernard

AU - Prinz, Immo

AU - Xu, Dan

AU - Miller, Stephen D

N1 - Copyright © 2014 Elsevier Inc. All rights reserved.

PY - 2014/7

Y1 - 2014/7

N2 - γδ T cells are resident in cerebrospinal fluid and central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but as multifaceted cells exhibiting innate and adaptive characteristics, their function remains unknown. Previous studies in experimental autoimmune encephalomyelitis (EAE) are contradictory and identified these cells as either promoting or suppressing disease pathogenesis. This study examines distinct γδ T cell subsets during EAE and indicates they mediate differential functions in CNS inflammation and demyelination resulting in pathogenesis or protection. We identified two γδ subsets in the CNS, Vγ1(+) and Vγ4(+), with distinct cytokine profiles and tissue specificity. Anti-γδ T cell receptor (TCR) monoclonal antibody (mAb) administration results in activation and downregulation of surface TCR, rendering the cells undetectable, but with opposing effects: anti-Vγ4 treatment exacerbates disease whereas anti-Vγ1 treatment is protective. The Vγ4(+) subset produces multiple pro-inflammatory cytokines including high levels of IL-17, and accounts for 15-20% of the interleukin-17 (IL-17) producing cells in the CNS, but utilize a variant transcriptional program than CD4(+) Th17 cells. In contrast, the Vγ1 subset produces CCR5 ligands, which may promote regulatory T cell differentiation. γδ T cell subsets thus play distinct and opposing roles during EAE, providing an explanation for previous reports and suggesting selective targeting to optimize regulation as a potential therapy for MS.

AB - γδ T cells are resident in cerebrospinal fluid and central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but as multifaceted cells exhibiting innate and adaptive characteristics, their function remains unknown. Previous studies in experimental autoimmune encephalomyelitis (EAE) are contradictory and identified these cells as either promoting or suppressing disease pathogenesis. This study examines distinct γδ T cell subsets during EAE and indicates they mediate differential functions in CNS inflammation and demyelination resulting in pathogenesis or protection. We identified two γδ subsets in the CNS, Vγ1(+) and Vγ4(+), with distinct cytokine profiles and tissue specificity. Anti-γδ T cell receptor (TCR) monoclonal antibody (mAb) administration results in activation and downregulation of surface TCR, rendering the cells undetectable, but with opposing effects: anti-Vγ4 treatment exacerbates disease whereas anti-Vγ1 treatment is protective. The Vγ4(+) subset produces multiple pro-inflammatory cytokines including high levels of IL-17, and accounts for 15-20% of the interleukin-17 (IL-17) producing cells in the CNS, but utilize a variant transcriptional program than CD4(+) Th17 cells. In contrast, the Vγ1 subset produces CCR5 ligands, which may promote regulatory T cell differentiation. γδ T cell subsets thus play distinct and opposing roles during EAE, providing an explanation for previous reports and suggesting selective targeting to optimize regulation as a potential therapy for MS.

KW - Animals

KW - Antibodies, Monoclonal/administration & dosage

KW - Cell Differentiation/immunology

KW - Central Nervous System/cytology

KW - Down-Regulation

KW - Encephalomyelitis, Autoimmune, Experimental/immunology

KW - Female

KW - Interleukin-17/biosynthesis

KW - Lymphocyte Activation/immunology

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Multiple Sclerosis/immunology

KW - Oligodendroglia/immunology

KW - Receptors, Antigen, T-Cell, gamma-delta/immunology

KW - Receptors, CCR5/biosynthesis

KW - Th17 Cells/immunology

U2 - 10.1016/j.cellimm.2014.04.013

DO - 10.1016/j.cellimm.2014.04.013

M3 - SCORING: Journal article

C2 - 24860937

VL - 290

SP - 39

EP - 51

JO - CELL IMMUNOL

JF - CELL IMMUNOL

SN - 0008-8749

IS - 1

ER -