Natural killer cell monitoring in cutaneous melanoma - new dynamic biomarker.

Melanoma is responsible for most skin cancer deaths in humans. The immune system plays a major role in regulating tumor cell proliferation by initiating defence responses against tumor aggression. Research on murine cancer models allow for a better understanding of immune response in malignancies, revealing specific changes of the immune status in the presence of tumors. Melanoma resistance to conventional therapies and its high immunogenicity justify the development of new therapies. These features reinforce melanoma as a suitable model for studying antitumor immunity. Recent findings on NK cell activation in cancer patients indicate that several important parameters, such as tumor capacity to modulate the function and phenotype of NK cells, require consideration for the choice of an NK-based therapy. In this study, we investigated T-CD4+ and T-CD8+ lymphocytes, B lymphocytes and NK cells in peripheral blood and spleen cells suspension from melanoma-bearing mice compared to healthy controls in order to assess the potential for tumor growth-promoting immunosuppression. Our results indicate that in a melanoma-bearing mouse model the percentage of NK cells in spleen is reduced and that their phenotype is different compared to control mouse NK cells.

Phenotypic changes of lymphocyte populations in psoriasiform dermatitis animal model.

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.

Immunological investigations in prostatic pathology--a prospective study.

BACKGROUND: BPH with prostatitis represents one of the most common urological pathologies affecting most men. The etiology of both conditions remains at the discretion of the various assumptions. OBJECTIVES: The body's cellular immune response in prostate adenoma is a less studied aspect which we have focused on, in this paper. The correlation with a wide range of information from specific investigations such as prostate-specific antigen (PSA) and total histopathology was the secondary aim of this work. METHODS: The study included 31 patients who underwent surgery for prostate adenoma (TUR-P, simple prostatectomy) between 08.2013 and 03.2014. Patients presenting urinary tract infection were excluded from the study. Preoperative evaluation of the immunological examination consisted of lymphocyte immunophenotyping (T, B, NK cells) from peripheral blood performed by flow cytometry. Total PSA was performed in serum by enzyme immunoassay EIA. RESULTS: In all forms of anatomoclinical BPH we found the presence of two major cellular changes: decrease of suppressor/cytotoxic T-cells and decrease of B cells. These deficits may confer an increased susceptibility to viral infection and tumor transformation. NK cells were grown in BPH associated with inflammation. PSA-prostate specific antigen values were grown at less than 50% of the patients in all clinical forms of BPH.

Regulatory T cells and TH1/TH2 cytokines as immunodiagnosis keys in systemic autoimmune diseases.

We assessed Helper T-cell involvement and possibilities to quantify the cell-based immune response in systemic autoimmune diseases (SAID) in 14 systemic lupus erythematosus (SLE) and 7 rheumatoid arthritis (RA) patients. The goals of investigation were T-CD4+/T-CD8+ ratio, regulatory T cells (Treg) status and TH1/TH2 serum cytokine profiles (IFN-gamma and IL-2, respectively IL-4 and IL-6). SLE group proved significant decreased average Treg value as compared to RA group and controls and showed significant low Treg incidence (86% patients). The distribution of high T-CD4+/T-CD8+ ratio registered no significant distinction among LES and RA groups. SAID patients presented low serum IFN-gamma (86% RA, 60% SLE), high IL-2 (57% RA) and high IL-6 (53% LES), but no significant IL-4 modification. We conclude that Treg percentage remains the only cellular criterion for SAID immune evaluation. In the same time, different secretion mechanisms seem to be involved in SAID, i.e. TH2 in SLE and TH1 in RA.