3183) now find that switching off one type of T helper (Th) cell is enough to break the circuit and heal the lesions.
Th1 cells that secrete interferon (IFN)-γ were initially thought to be the main villains within psoriatic plaques—build-ups of overproliferating skin cells. In animal models of psoriasis, IFN-γ thickens plaques by further increasing the proliferation of skin cells and enhancing their production of chemokines that recruit inflammatory cells.
But cytokines other than IFN-γ may be more to blame. Inhibitors of tumor necrosis factor (TNF)—originally given to patients to treat Crohn's disease and other inflammatory illnesses—have been shown to alleviate psoriasis- like lesions. How they work, however, was unclear.
Zaba et al. now find that blocking TNF prevents psoriasis by inactivating Th17 cells. Th17 cells are normally activated by TNF-stimulated dendritic cells (DCs) and induce epithelial cell proliferation by secreting IL-22. But fewer DCs and lower levels of IL-22 were found in treated plaques, which disappeared after two weeks of treatment with the TNF blocker.
Immediate relief from psoriasis might thus be made possible by getting rid of Th17 cells. Future studies might therefore benefit from focusing on Th17 cells rather than on Th1 cells, which survive in the plaques weeks longer than Th17 cells but fail to perpetuate disease.