Abstract
Since 2003, the established paradigm of T cell immunology has defined interleukin (IL)-17 as a dominant Th17 cell derived cytokine driving autoimmune disease. Recent murine studies have challenged this, identifying GM-CSF as a Th17 related cytokine necessary and sufficient for the induction of autoimmunity. The origin of GM-CSF+ T cells and their relationship with IL-17 secreting cells is unclear in human autoimmune disease. Trials of biologic agents targeting the GM-CSF pathway show promise in rheumatoid arthritis, so it is important to establish if GM-CSF contributes to the inflammatory environment of the arthritic joint in Juvenile Idiopathic Arthritis (JIA).
Highlights
Since 2003, the established paradigm of T cell immunology has defined interleukin (IL)-17 as a dominant Th17 cell derived cytokine driving autoimmune disease
synovial fluid mononuclear cells (SFMC) from patients with Juvenile Idiopathic Arthritis (JIA) were enriched for GMCSF-secreting CD4 T cells, compared to matched Peripheral blood mononuclear cells (PBMC) (21% vs 1.7% of CD4 T cells, p = 0.0012)
Following culture in the presence of IL-12, purified Th17 cells preferentially upregulated granulocytemacrophage colony stimulating factor (GM-CSF) compared to IL-17- CD4 T cells (62% vs 35% of CD4 T cells)
Summary
Since 2003, the established paradigm of T cell immunology has defined interleukin (IL)-17 as a dominant Th17 cell derived cytokine driving autoimmune disease. Recent murine studies have challenged this, identifying GM-CSF as a Th17 related cytokine necessary and sufficient for the induction of autoimmunity. The origin of GM-CSF+ T cells and their relationship with IL-17 secreting cells is unclear in human autoimmune disease. Trials of biologic agents targeting the GM-CSF pathway show promise in rheumatoid arthritis, so it is important to establish if GM-CSF contributes to the inflammatory environment of the arthritic joint in Juvenile Idiopathic Arthritis (JIA)
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