Psoriasis Disease

Psoriasis is a chronic skin disease that affects approximately 2–3% of individuals in the Western world.  New data, generated by Karin Scharffetter-Kochanek and colleagues, at the University of Ulm, Germany, have indicated that a subset of immune cells known as Tregs (which act to prevent other immune cells from responding inappropriately) are dysfunctional in a mouse model of psoriasis and that this dysfunction contributes substantially to the development of disease.

Mice that express a reduced amount of the protein CD18 (Cd18hypo mice) develop a skin disease that resembles the symptoms of individuals with psoriasis.  In the study, Tregs isolated from Cd18hypo mice failed to suppress the proliferation of disease-causing immune cells because they secreted lower levels of the soluble factor TGF-beta than normal Tregs.  This was also important for their inability to control disease in vivo, as transplantation of normal Tregs into Cd18hypo mice resulted in a substantial improvement in the psoriasis-like disease, whereas if these cells were transplanted in the presence of antibodies that neutralized TGF-beta there was no improvement in disease.  The authors therefore conclude that psoriasis-like disease in Cd18hypo mice is caused mainly by a defect in Treg function and suggest that maintaining CD18 levels is important for ensuring that Tregs function optimally.

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