Type II monocytes modulate T cell-mediated central nervous system autoimmune disease

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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 27, 2013

Martin S Weber1, Thomas Prod'homme, Sawsan Youssef

  • 1Department of Neurology and Program in Immunology, University of California, San Francisco, 513 Parnassus Avenue, S-268, San Francisco, California 94143-0435, USA.

Nature Medicine
|August 7, 2007
PubMed

Treatment with glatiramer acetate (GA, copolymer-1, Copaxone), a drug approved for multiple sclerosis (MS), in a mouse model promoted development of anti-inflammatory type II monocytes, characterized by increased secretion of interleukin (IL)-10 and transforming growth factor (TGF)-beta, and decreased production of IL-12 and tumor necrosis factor (TNF). This anti-inflammatory cytokine shift was associated with reduced STAT-1 signaling. Type II monocytes directed differentiation of T(H)2 cells and CD4+CD25+FoxP3+ regulatory T cells (T(reg)) independent of antigen specificity. Type II monocyte-induced regulatory T cells specific for a foreign antigen ameliorated experimental autoimmune encephalomyelitis (EAE), indicating that neither GA specificity nor recognition of self-antigen was required for their therapeutic effect. Adoptive transfer of type II monocytes reversed EAE, suppressed T(H)17 cell development and promoted both T(H)2 differentiation and expansion of T(reg) cells in recipient mice. This demonstration of adoptive immunotherapy by type II monocytes identifies a central role for these cells in T cell immune modulation of autoimmunity.

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