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Among skin pathologies, psoriasis is one of the most challenging disorders in terms of therapy and clinical monitoring of the patient.Psoriasis is a chronic inflammatory skin condition that has an autoimmune mechanism mediated by T cells, with involvement of innate immune cells.An important role is played by different subsets ofT-helper lymphocytes, as well as a number of proinflammatory cytokines that maintain the chronic inflammatory state. Although some evidence suggests that NK cells play animportant role in psoriasis, their contribution to disease's development and progression remains incompletely understood. Experimental models are an indispensable tool in psoriasis research for both pathogenesis evaluation and for possible therapeutic targets identification. Due to its advantages, experimental models such as the Imiquimod-based mice model is one of the most popular animalmodel to study psoriasiform dermatitis in mice. In order to highlight the role of NK cells in the development of psoriasis, we performed the Imiquimod-based mice model and analysed NK cells distribution and phenotype by flow cytometry. Skin inflammation induced by Imiquimodwas assessed based on in vivo parameters (erythema, desquamation, thickening), PASI score, evaluation of splenomegaly and pathological examination. NK cells distribution was evaluated on three immune levels: peripheral blood spleen and skin There were quantified NK cells subsets based on the expression of CD27 and CDUb, and NK1.1+CD11c+CD45R+subset. The expression of CD43, KLRG1 and CD69, markers with an important role in NK cells maturation and activation, was analysed.Our data show that, although a somewhat neglected cell in psoriasis, NKs correlate with the gravity of the auto-immune disease. [ABSTRACT FROM AUTHOR]

Psoriasis is a T cell mediated, chronic inflammatory autoimmune skin disease that affects up to 2–3% of the global population and leads to a decrease in quality of life. Experimental data accumulated in recent years highlighted the important role played by the immune system in the pathogenesis of this disease. Non-human psoriasis models are an important research tool that attempts to reproduce the clinical features of the disease in order to explain the pathogenesis of psoriasis and to identify possible therapeutic targets. Imiquimod-based murine model of psoriatic dermatitis is an alternative to traditional models of experimental psoriasis in mice and the induced dermatitis closely mimics the pathologic changes in human psoriasis. In order to emphasize changes in immune cell populations involved in lesion pathogenesis, we performed a murine model of psoriasiform dermatitis model by topical IMQ application. The progress and the severity of IMQ-induced skin inflammation were clinically (PASI score) and histopathologically evaluated. The immunological changes induced by IMQ treatment in lymphocyte populations from peripheral blood and spleen were evaluated by flow cytometry. The main changes observed in peripheral blood were the significantly increased T-CD8a+ lymphocyte and NK1.1+ cell percentages and the decreased T-CD4+ and B lymphocyte percentages in IMQ-treated mice. In spleen samples, lymphocytes showed the same tendency of variation as in peripheral blood, but without statistical significance. A significant decrease of B cells percentages was observed in spleen suspensions. Data obtained in skin samples may suggest the involvement of CD3ε+, CD4+ and CD8a+ cells in the lesional process. This murine model was analyzed by performing a basic cellular profile at three levels: peripheral blood, spleen and skin. The evaluation aimed to establish the immune framework of this experimental model that could further be used for etipathogenic mechanism identification and/or for studies regarding targeted therapies. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a systemic inflammatory disorder that manifests predominantly in the synovial joint, where it causes a chronic inflammatory process, leading to early osteoarticular destructions. These destructions are progressive and irreversible, generating a significant functional deficiency. During the last years, the diagnostic approach of RA has focused on early arthritis. Early arthritis can develop into established RA or another established arthropathy, like systemic lupus erythematosus or psoriatic arthritis. It can have a spontaneous resolution or may remain undifferentiated for indefinite periods of time. The management of early arthritis has changed considerably in the past few years, under the influence of new concepts of diagnosis and new effective therapies. The treatment goal of early arthritis should now be the clinical remission and prevention of joint destruction. Methotrexate is the first line of therapy, used to treat early arthralgia and to reverse or limit impending exacerbation to RA. Biological treatment is used as a second line therapy in patients with severe disease who do not respond or have a contraindication to disease-modifying antirheumatic drugs (DMARDs). Patients with early arthritis should usually be identified and directed to rheumatologists to confirm the presence of arthritis, and to establish the correct diagnosis plus to initiate the proper treatment strategies. [ABSTRACT FROM AUTHOR]