On a study they did at Harvard, when raising transgenic mice (who normally develop arthritis at 4 weeks) were raised in a germ-free environment, the disease progressed a lot slower. Mice grown in germ-free conditions lack T17 cells. T17 is required for the gut bacteria (called segmented filamentous bacteria or SFB) to properly develop. When SFB is properly introduced into these mice, the amount of Th17 cells rises and the IL-17 they produce makes the disease progress quicker. And when an IL-17 blocker is introduced in normally raised mice, progression of the disease slowed down.
Can anyone think of why the absence of IL-17 would slow down the progression of autoimmune arthritis? Or why the bacteria helps Th17 cells to develop?
The Paper:
H.J. Wu et al., "Gut-residing segmented
filamentous bacteria drive
autoimmune arthritis via T helper 17 cells,"
Immunity, 32:815-27, 2010
That is interesting how Th17 cells respond to bacteria like that. I looked into the differentiation process of Th17 cells and found that TGF-beta and IL-6 is thought to be responsible for their differentiation from precursor T helper cells. Also, IL-23 is found to help differentiate more Th17 cells if some already exist (doesn't do anything without some Th17 first present). Also interesting, IFN-gamma and IL-4 (the main stimulators of Th1 and Th2 cells) seem to have an inhibiting effect on Th17 differentiation. It is unknown what other factors stimulate differentiation into Th17 that are not common with other T helper cells.
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