Psoriasis is a disease already considered multisystemic, whose most known feature is the joint and skin involvement, with unclear etiology. The affected skin usually presents with erythema and desquamation. At the cellular level, the process involves primarily the activated T cells, macrophages and polymorphonuclear cells. Keratinocytes action and immune-dependent expression of adhesion molecules reveal a complex network of mediators with high biological activity. The presence of these inflammatory cytokines determines changes in Immunoregulatory functions translated by clinical symptoms of the disease. After verification of B hemolytic Streptococcus as a causative agent of guttate psoriasis, several studies has been attempted to relate other etiopathogenic factors capable of exerting a clonal expansion of T cells, as observed in the disease. Among some viruses studied, parvovírus B19 was listed as precipitating agent for arthritis and other autoimmune diseases, and due to be a common virus to produce infection often asymptomatic, spend time in the host, inducing local inflammatory response and mainly reside in the skin have also been researched as an "agent trigger" in the development of psoriasis. In this study, we used the viral DNA by PCR in the skin of psoriatic patients in the skin of eczema patients as controls and did not observe any significant positive results that would differentiate it in the two groups, therefore, no causal relationship or triggering the disease in question. In search of cytokines was observed that expected in psoriatic skin as TNF-a, but also of TH2 cytokines. Eczema in the group, the presence of TH2 cytokines was not altered by the presence of the virus in tissue. Despite the genetic predisposition to disease development, further studies are needed in order to study antigenic stimuli capable of altering immune function and create a profile and a clinical phenotype that can be recognized as psoriasis.
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