The article entitled "Translational Research in IBD" mentions antagonizing Th1 cytokines without really explaining why this is an effective treatment option for IBD...so I looked into it.
First, upon seeing an antigen piece presented to it, helper T cells will differentiate into either Th1 or Th2 cells (just type 1 or type 2 helper T cells). Both these T cells will then produce cytokines and stimulate other functions. In Crohn's Disease (CD), Th1 is of particular interest because of the particular cytokines it produces, namely interferon-gamma. It also encourages macrophages to produce IL-12, which is an pro-inflammatory cytokine, which is obviously bad when you are trying to get rid of an inflammatory disease.
The reason Th1 has been targeted to antagonize instead of Th2 is because Th2 may actually produce IL-10, which the article mentions as an anti-inflammatory cytokine. This may be a limitation to the strategy of blocking T cell activation, which the article mentions as an area of research. Because it is not currently clear how the body decides which helper cell type to produce, this treatment might be very hard to perfect.
On a side note, and for those of you curious to learn more, Digestive Disease Week 2008 is coming up! It goes from May 17-22 in San Diego. Here's a website to it: http://www.ddw.org/wmspage.cfm?parm1=679
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