|Support type:||Scholarships in Brazil - Doctorate|
|Effective date (Start):||November 01, 2011|
|Effective date (End):||August 31, 2014|
|Field of knowledge:||Biological Sciences - Immunology - Applied Immunology|
|Principal Investigator:||Maria Heloisa Souza Lima Blotta|
|Grantee:||Xinaida Taligare Vasconcelos Lima|
|Home Institution:||Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil|
Psoriasis is a chronic inflammatory cutaneous disease that affects about 2% of the world population. Besides skin and joint involvement, psoriasis, one of the immune-mediated inflammatory diseases (IMIDs), is associated with systemic consequences. Patients with psoriasis have higher risk of vascular illnesses, resultant from atherosclerotic disease. Atherosclerosis is also an inflammatory disease, characterized by an intense immunologic activity which leads to lesions in the blood vessels (atheromas) that may rupture, resulting in acute occlusive events with high morbimortality. There are several similar pathological aspects between psoriasis and atherosclerosis. The immune response in both is mediated by T-helper 1 cells, with increased production of interferon gamma, similar activation pattern and elevated concentrations of inflammatory markers, such as C-reactive protein and cytokines. Patients with acute coronary syndrome (ACS) have, characteristically, increased frequency of CD4+CD28null T cells in the peripheral blood. These cells produce inflammatory cytokines and cytotoxic molecules, besides their presence in ruptured atheromas, revealing that they may have considerable role in plaque instability and ACS. CD4+CD28null T are also increased in some IMIDs, such as rheumatoid arthritis, anquilosing spondilitis and psoriatic arthritis and they seem to be related to disease's activity. Based on these data, our study has the objective of evaluate the frequency of CD4+CD28null T cells in the peripheral blood of psoriasis and non-psoriasis (control) patients, in addition to the expression of cytotoxic molecules and inflammatory response.