About this item:

716 Views | 580 Downloads

Author Notes:

Correspondence: jamlee@uga.edu

JKL designed and performed the studies, participated in the data and statistical analyses, and drafted and revised the manuscript.

GTK participated in experimental design, participated in the experiments, and drafted and revised the manuscript.

JC performed multiplex MSD assay and in vitro proliferation assays and participated in tissue collections and data analysis.

HL performed immunohistochemistry and analyzed the myelination study data.

KLG participated in study design and coordination, provided technical and intellectual advice, performed experiments, participated in data analyses, and drafted and revised the manuscript.

MGT participated in study design and coordination, data interpretation, drafted and revised the manuscript, and supervised personnel involved in the studies.

We thank Bonnie Werner in the Graham lab for technical assistance and members of the Tansey lab for scientific input and many useful discussions. We thank Jianjun Chang for mice colony maintenance and genotyping.

The authors declare that they have no competing interests.


Research Funding:

JKL and MGT were supported by NIH/NINDS 5R01 NS072467-05.

GTK was supported by NIH/NINDS 5F31NS081830-02.

KLG was supported by startup funds from the Department of Physiology at Emory University and Research Scholar Development Award K22 AI81878

JKL was supported by startup funds from the Department of Physiology and Pharmacology at University of Georgia.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Immunology
  • Neurosciences
  • Neurosciences & Neurology
  • Regulator of G-protein signaling (RGS10)
  • Neuroinflammation
  • Monocyte
  • T cell
  • Adoptive transfer
  • Experimental autoimmune encephalomyelitis (EAE)
  • Demyelination

RGS10 deficiency ameliorates the severity of disease in experimental autoimmune encephalomyelitis


Journal Title:

Journal of Neuroinflammation


Volume 13, Number 1


, Pages 24-24

Type of Work:

Article | Final Publisher PDF


Background: Regulator of G-protein signaling (RGS) family proteins, which are GTPase accelerating proteins (GAPs) that negatively regulate G-protein-coupled receptors (GPCRs), are known to be important modulators of immune cell activation and function. Various single-nucleotide polymorphisms in RGS proteins highly correlate with increased risk for multiple sclerosis (MS), an autoimmune, neurodegenerative disorder. An in-depth search of the gene expression omnibus profile database revealed higher levels of RGS10 and RGS1 transcripts in peripheral blood mononuclear cells (PBMCs) in MS patients, suggesting potential functional roles for RGS proteins in MS etiology and/or progression. Methods: To define potential roles for RGS10 in regulating autoimmune responses, we evaluated RGS10-null and wild-type (WT) mice for susceptibility to experimental autoimmune encephalomyelitis (EAE), a widely studied model of MS. Leukocyte distribution and functional responses were assessed using biochemical, immunohistological, and flow cytometry approaches. Results: RGS10-null mice displayed significantly milder clinical symptoms of EAE with reduced disease incidence and severity, as well as delayed onset. We observed fewer CD3+ T lymphocytes and CD11b+ myeloid cells in the central nervous system (CNS) tissues of RGS10-null mice with myelin oligodendrocyte protein (MOG)35-55-induced EAE. Lymph node cells and splenocytes of immunized RGS10-null mice demonstrated decreased proliferative and cytokine responses in response to in vitro MOG memory recall challenge. In adoptive recipients, transferred myelin-reactive RGS10-null Th1 cells (but not Th17 cells) induced EAE that was less severe than their WT counterparts. Conclusions: These data demonstrate a critical role for RGS10 in mediating autoimmune disease through regulation of T lymphocyte function. This is the first study ever conducted to elucidate the function of RGS10 in effector lymphocytes in the context of EAE. The identification of RGS10 as an important regulator of inflammation might open possibilities for the development of more specific therapies for MS.

Copyright information:

© 2016 Lee et al.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/).

Creative Commons License

Export to EndNote