Although there are effective treatments for psoriasis, not everyone responds to these therapies and the relief is temporary.
“These therapies don’t reduce disease by 100 percent, and they don’t cure the disease, and if you take patients off those drugs, the disease almost always comes back”, says La Jolla Institute for Immunology (LJI) Professor Michael Croft, Ph.D.
Researchers thought that TWEAK protein might be a potential target for psoriasis to develop a new therapeutic option.
Based on the previous findings that TWEAK can interact with the most common type of skin, researchers investigated TWEAK-deficient mice and found that TWEAK is a driver of inflammation in psoriasis.
The new study also shows that TWEAK does not work alone, it teams up with two other proteins, called tumor necrosis factor (TNF) and interleukin-17 (IL-17), to trigger inflammation. This trio appears to control psoriasis.
The primary implication from these findings is that TWEAK will also be a good drug target.
To test this, the researchers used a mouse model of psoriasis to compare how well a TWEAK-inhibitor measured up to therapies inhibiting IL-17 or TNF.
The results suggest that inhibiting TWEAK will get the same therapeutic effect as inhibiting TNF or IL-17. This finding is especially encouraging because TNF and IL-17 are both FDA-approved drug targets for psoriasis.
Although human clinical trials remain to be done, a future for TWEAK inhibitors as therapies for many types of skin diseases is bright.
Source: Medindia
