| dc.description.abstract | Psoriasis is a chronic inflammatory disease that manifests in the skin affecting both sexes equally and all ages. In Norway, the prevalence reaches 11.43% in adults. Both genetics and environment factors are important in developing the disease. Comorbidities such as cardiovascular disease, psoriatic arthritis and psychiatric disorders are associated with psoriasis. Treatment of the disease depends on comorbidities and disease severity. For moderate to severe disease, the TNF-α inhibitor infliximab is approved. Even though the discovery of biologics revolutionized the treatment of autoimmune diseases, there is still a problem with relapsing disease and non-responders to treatment. Disease specific biomarkers that could help indicate who will respond to treatment and not at earlier stages are therefore required to optimize treatment. Psoriasis is a T cell mediated disease and T cell subsets such as the IL-17 secreting Th17 have been identified as important contributors to disease. However, other cell types and cytokines are also important in the pathophysiology, including dendritic cells and the cytokines TNF-α and IFN-γ. Other cell types are not as investigated in the disease mechanism, and the changes in immunophenotype after treatment are also not fully known. Continued research on these fields is therefore interesting. In this master project, flow cytometry was used to investigate immune cells in 24 psoriasis patients treated with the TNF-α inhibitor infliximab. The cells were immunophenotyped and compared to 33 healthy controls, matched for age, sex and BMI. Whilst we found no changes in frequencies of T cell populations or a trend of activated or inactivated T cells, some of the surface markers were different from the control populations. This change included a decreased expression of CD107a which was also evident on all subtypes of NK cells. NK cells did also not show a trend of increased or decreased activity, but similarly showed a changed expression of some expression markers. Both CD38 and CD27 was significantly increased in patients on CD56dim NK cells. The observations indicated continuous activation of monocytes even after treatment with an increase of frequency of intermediate monocytes, which is implicated in the cardiovascular disease was observed. On these cells, both HLA-DR and CD38 were increased, suggesting increased activity. | |
