Interferon β1a treatment modulates TH1 expression in γδ + T cells from relapsing-remitting multiple sclerosis patients

Cerise L. Elliott; Samia Y. Ei-Touny; Mary L. Filipi; Kathleen M. Healey; M. Patricia Leuschen

doi:10.1023/A:1011043417159

Interferon β1a treatment modulates T_H1 expression in γδ + T cells from relapsing-remitting multiple sclerosis patients

Cerise L. Elliott, Samia Y. Ei-Touny, Mary L. Filipi, Kathleen M. Healey, M. Patricia Leuschen

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

A paradigm exists that multiple sclerosis is causally related to dysregulation of T_H1 inflammatory cytokines and T_H2 antiinflammatory cytokines. The cytokine source(s) that initiate the imbalances are unknown. In this study, γδ, CD4, and CD8 T cell receptor-positive (TCR+) cells were isolated from the blood of 26 definitive relapsing-remitting multiple sclerosis patients prior to interferon β-1a (IFNβ1a) therapy and following 8-10 weeks of this therapy. The bioactivities of interferon γ (IFNγ), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFNγ, IL10, and IL12 from each cell type did not change significantly with IFNβ1a treatment. The IL10 secreted by γδ TCR+ cells strongly correlated with the IL12 secreted by the same γδ TCR+ cells, supporting the paradigm. Furthermore, IFNβ1a therapy decreased the γδ TCR+ cell secretion of T_H1 cytokines after 8-10 weeks of therapy.

Original language	English (US)
Pages (from-to)	200-209
Number of pages	10
Journal	Journal of Clinical Immunology
Volume	21
Issue number	3
DOIs	https://doi.org/10.1023/A:1011043417159
State	Published - 2001

Keywords

Interferon β1a interleukin 12
Interleukin 10
Multiple sclerosis
γδ T cells

ASJC Scopus subject areas

Immunology and Allergy
Immunology

Access to Document

10.1023/A:1011043417159

Cite this

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title = "Interferon β1a treatment modulates TH1 expression in γδ + T cells from relapsing-remitting multiple sclerosis patients",

abstract = "A paradigm exists that multiple sclerosis is causally related to dysregulation of TH1 inflammatory cytokines and TH2 antiinflammatory cytokines. The cytokine source(s) that initiate the imbalances are unknown. In this study, γδ, CD4, and CD8 T cell receptor-positive (TCR+) cells were isolated from the blood of 26 definitive relapsing-remitting multiple sclerosis patients prior to interferon β-1a (IFNβ1a) therapy and following 8-10 weeks of this therapy. The bioactivities of interferon γ (IFNγ), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFNγ, IL10, and IL12 from each cell type did not change significantly with IFNβ1a treatment. The IL10 secreted by γδ TCR+ cells strongly correlated with the IL12 secreted by the same γδ TCR+ cells, supporting the paradigm. Furthermore, IFNβ1a therapy decreased the γδ TCR+ cell secretion of TH1 cytokines after 8-10 weeks of therapy.",

keywords = "Interferon β1a interleukin 12, Interleukin 10, Multiple sclerosis, γδ T cells",

author = "Elliott, {Cerise L.} and Ei-Touny, {Samia Y.} and Filipi, {Mary L.} and Healey, {Kathleen M.} and Leuschen, {M. Patricia}",

note = "Funding Information: This work was supported in part by a grant from Biogen, Inc.",

year = "2001",

doi = "10.1023/A:1011043417159",

language = "English (US)",

volume = "21",

pages = "200--209",

journal = "Journal of Clinical Immunology",

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T1 - Interferon β1a treatment modulates TH1 expression in γδ + T cells from relapsing-remitting multiple sclerosis patients

AU - Elliott, Cerise L.

AU - Ei-Touny, Samia Y.

AU - Filipi, Mary L.

AU - Healey, Kathleen M.

AU - Leuschen, M. Patricia

N1 - Funding Information: This work was supported in part by a grant from Biogen, Inc.

PY - 2001

Y1 - 2001

N2 - A paradigm exists that multiple sclerosis is causally related to dysregulation of TH1 inflammatory cytokines and TH2 antiinflammatory cytokines. The cytokine source(s) that initiate the imbalances are unknown. In this study, γδ, CD4, and CD8 T cell receptor-positive (TCR+) cells were isolated from the blood of 26 definitive relapsing-remitting multiple sclerosis patients prior to interferon β-1a (IFNβ1a) therapy and following 8-10 weeks of this therapy. The bioactivities of interferon γ (IFNγ), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFNγ, IL10, and IL12 from each cell type did not change significantly with IFNβ1a treatment. The IL10 secreted by γδ TCR+ cells strongly correlated with the IL12 secreted by the same γδ TCR+ cells, supporting the paradigm. Furthermore, IFNβ1a therapy decreased the γδ TCR+ cell secretion of TH1 cytokines after 8-10 weeks of therapy.

AB - A paradigm exists that multiple sclerosis is causally related to dysregulation of TH1 inflammatory cytokines and TH2 antiinflammatory cytokines. The cytokine source(s) that initiate the imbalances are unknown. In this study, γδ, CD4, and CD8 T cell receptor-positive (TCR+) cells were isolated from the blood of 26 definitive relapsing-remitting multiple sclerosis patients prior to interferon β-1a (IFNβ1a) therapy and following 8-10 weeks of this therapy. The bioactivities of interferon γ (IFNγ), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFNγ, IL10, and IL12 from each cell type did not change significantly with IFNβ1a treatment. The IL10 secreted by γδ TCR+ cells strongly correlated with the IL12 secreted by the same γδ TCR+ cells, supporting the paradigm. Furthermore, IFNβ1a therapy decreased the γδ TCR+ cell secretion of TH1 cytokines after 8-10 weeks of therapy.

KW - Interferon β1a interleukin 12

KW - Interleukin 10

KW - Multiple sclerosis

KW - γδ T cells

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