| dc.description.abstract | Atopic Dermatitis (AD) is a chronic T-cell mediated inflammatory disease. Unlike most allergic diseases, Th2 polarization is only associated to acute AD lesions, while a Th1 environment is present in chronic lesions, including very high IFN-γ levels. CD4+ T-cells have always been regarded pivotal in the pathogenesis of AD, but interest in the role of CD8+ T-cells has sparked as several papers have found evidence for their involvement in the disease. Expression of CD30 and CD69 on CD8+ T-cells in AD lesions has been stated to correlate with disease severity. Furthermore, correlations between disease severity and the amount of IL-22 producing CD8+ T-cells in AD lesions and TREC levels in CD8+ T-cells from the peripheral blood of AD patients have been described. Additionally, CD8+ T-cells were shown to be essential for AD lesions formation in a mouse model of AD. CD8+ T-cells could also have an anti-inflammatory role in AD pathogenesis, as they can kill invading pathogens, preventing further inflammation and tissue damage. They are also able to restore the barrier function of the skin by inducing upregulation of components of the stratum corneum. The role of CD8+ T-cells in AD pathogenesis has been underestimated for many years and increasing amounts of evidence for their role will be published. The net effect that CD8+ T-cells have on AD pathogenesis remains difficult to assess, as there are so many different processes they can influence. But, judging from the evidence that is available at this time, they appear to attribute to the disease rather than decrease it. | |
