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24 April 2014 11:45 am ,
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Major climate data sets have underestimated the rate of global warming in the last 15 years owing largely to poor data...
The tsetse fly is best known as the vector for the trypanosome parasites that cause sleeping sickness and a disease in...
The National Institutes of Health is revising its "two strikes" rule, which allowed researchers only one chance to...
By stabilizing the components of retromers, molecular complexes that act like recycling bins in cells, a recently...
Fossil fuels power modern society by generating heat, but much of that heat is wasted. Semiconductor devices called...
Researchers are gaining insights into what made Supertyphoon Haiyan so powerful and devastating through post-storm...
Millions around the world got a first-hand look at what it was like to be in Tacloban while it was pummeled by...
- 24 April 2014 11:45 am , Vol. 344 , #6182
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Probing the Cause of Psoriasis
14 September 2005 (All day)
Is psoriasis a skin disease or an immune system disorder? The answer--key to developing an effective therapy--has remained elusive. Now genetic evidence indicates that psoriasis begins as a skin disorder that can also trigger an immune system response.
Psoriasis, a noncontagious, lifelong disease characterized by skin lesions, red patches, white blisters, and sometimes arthritic inflammation, afflicts about 4.5 million adults in the United States. Researchers have been of two minds about the cause. One theory argues that it progresses from a haywire immune system response, signaled by elevated T-cells found in psoriatic lesions. But the disease may also be a genetic skin disorder, a theory supported by observed mutations in skin cell DNA. That skin disorder may then trigger an immune system response.
To gain better insight, researchers led by molecular pathologist Erwin Wagner of the Research Institute of Molecular Pathology in Vienna, Austria, set out to induce human psoriasislike symptoms in mice. They found they could do this by inhibiting two genes: JunB and c-Jun, both known to regulate cell proliferation and mutations. This pointed strongly to a genetic trigger for the disease.
Then, to examine what role the immune system plays in psoriasis, the researchers inhibited T-cell response in the genetically deficient mice. They found that although the animals' arthritic inflammations and associated bone destruction largely disappeared, the skin lesions were still present, though milder. The researchers saw a similar response when they blocked another immune system trigger thought to be associated with the disease, TNF-alpha.
Overall, the findings suggest that psoriasis is fundamentally a skin disorder, though the immune system's T cells and TNF-alpha exacerbate the disease's inflammatory symptoms, the team reports 15 September in Nature. Though the study reinforces the idea that skin cells are more than passive "brick-and-mortar" walls shielding against disease, there is likely to be a complicated interplay of triggers between the immune system and mutated skin cells, notes immunologist Brian Nickoloff of Loyola University of Chicago Medical Center. However, he adds, the study makes an important clinical contribution by helping to identify new therapeutic targets.