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Expression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-β Therapy

Javad Rasouli, Bogoljub Ciric, Jaime Imitola, Patricia Gonnella, Daniel Hwang, Kedar Mahajan, Elisabeth R. Mari, Farinaz Safavi, Thomas P. Leist, Guang-Xian Zhang and Abdolmohamad Rostami
J Immunol June 1, 2015, 194 (11) 5085-5093; DOI: https://doi.org/10.4049/jimmunol.1403243
Javad Rasouli
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Bogoljub Ciric
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Jaime Imitola
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Patricia Gonnella
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Daniel Hwang
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Kedar Mahajan
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Elisabeth R. Mari
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Farinaz Safavi
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Thomas P. Leist
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Guang-Xian Zhang
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Abdolmohamad Rostami
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107
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Abstract

Multiple sclerosis (MS) is an autoimmune disease of the CNS. Studies in animal models of MS have shown that GM-CSF produced by T cells is necessary for the development of autoimmune CNS inflammation. This suggests that GM-CSF may have a pathogenic role in MS as well, and a clinical trial testing its blockade is ongoing. However, there have been few reports on GM-CSF production by T cells in MS. The objective of this study was to characterize GM-CSF production by T cells of MS patients and to determine the effect of IFN-β therapy on its production. GM-CSF production by peripheral blood (PB) T cells and the effects of IFN-β were characterized in samples of untreated and IFN-β–treated MS patients versus healthy subjects. GM-CSF production by T cells in MS brain lesions was analyzed by immunofluorescence. Untreated MS patients had significantly greater numbers of GM-CSF+CD4+ and CD8+ T cells in PB compared with healthy controls and IFN-β–treated MS patients. IFN-β significantly suppressed GM-CSF production by T cells in vitro. A number of CD4+ and CD8+ T cells in MS brain lesions expressed GM-CSF. Elevated GM-CSF production by PB T cells in MS is indicative of aberrant hyperactivation of the immune system. Given its essential role in animal models, abundant GM-CSF production at the sites of CNS inflammation suggests that GM-CSF contributes to MS pathogenesis. Our findings also reveal a potential mechanism of IFN-β therapy, namely suppression of GM-CSF production.

Footnotes

  • This work was supported by National Institutes of Health Grants 5U19AI082726 and 1R01NS088729-01.

  • The online version of this article contains supplemental material.

  • Abbreviations used in this article:

    EAE
    experimental autoimmune encephalomyelitis
    MS
    multiple sclerosis
    PB
    peripheral blood.

  • Received December 30, 2014.
  • Accepted March 21, 2015.
  • Copyright © 2015 by The American Association of Immunologists, Inc.
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The Journal of Immunology: 194 (11)
The Journal of Immunology
Vol. 194, Issue 11
1 Jun 2015
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Expression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-β Therapy
Javad Rasouli, Bogoljub Ciric, Jaime Imitola, Patricia Gonnella, Daniel Hwang, Kedar Mahajan, Elisabeth R. Mari, Farinaz Safavi, Thomas P. Leist, Guang-Xian Zhang, Abdolmohamad Rostami
The Journal of Immunology June 1, 2015, 194 (11) 5085-5093; DOI: 10.4049/jimmunol.1403243

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Expression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-β Therapy
Javad Rasouli, Bogoljub Ciric, Jaime Imitola, Patricia Gonnella, Daniel Hwang, Kedar Mahajan, Elisabeth R. Mari, Farinaz Safavi, Thomas P. Leist, Guang-Xian Zhang, Abdolmohamad Rostami
The Journal of Immunology June 1, 2015, 194 (11) 5085-5093; DOI: 10.4049/jimmunol.1403243
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