More effective treatments for managing psoriasis are possible with the identification of the genetic mutation that causes the inflammation, a new report has suggested.
Researchers from the Vlaams Institute for Biotechnology (VIB) said preventing the activation of MALT1, which triggers immune response to the inflammation, can become the basis of treatment formulation for psoriasis.
Genetic mutation in CARD14 makes the skin cells become more susceptible to developing psoriasis. CARD14 is a known epidermal regulator of the NF-kB protein, but recent findings suggest that CARD14 also regulates another signaling pathway that accelerates inflammation and causes psoriasis. CARD14 also regulates p38 and JNK MAP kinase pathways, which are both dependent on the MALT1 paracaspase.
It does not mean the psoriasis can be cured, however. Its symptoms can only be managed by blocking the immunologic response that causes the skin cells to grow at a rapid rate.
Researchers were able to identify physical and functional activation of MALT1 by CARD14 in isolated keratinocytes or skin cells that produce keratin. By blocking the MALT1 activation, significant reductions in the proteins responsible for inflammation and cell growth were seen, making MALT1 a valuable target for psoriasis treatment. However, the current finding suggests that MALT1 inhibition would only be beneficial for those with CARD14 mutation type of psoriasis.
"Whether MALT1 inhibitors may also be useful for the treatment of more common forms of psoriasis is currently under investigation," said VIB and Ghent University professor Rudi Beyaert.
Psoriasis is a type of auto immune disease that affects 2 to 4 percent of the population in the west. Patients commonly complain of red scaly patches of skin on their knees, elbows, or scalp. Individuals with severe psoriasis have been found to have other serious illnesses such as heart diseases, diabetes, and uncontrolled hypertension.
The findings of the study were published in EMBO Reports on April 25.
