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Marina Saresella

Publications and source records attributed to Marina Saresella.

10 recordsLinked to original sources
PubMed2004

Human alpha defensin in HIV-exposed but uninfected individuals.

Human alpha defensins 1, 2, and 3 are produced by CD8 T cells of HIV-infected long-term nonprogressors and have an antiviral activity. alpha Defensins were examined in peripheral blood mononuclear cells (PBMCs), cervical-vaginal mononuclear cells (CVMCs), and cervical biopsies of 9 HIV-1-exposed but uninfected women (ESNs), 10 HIV-infected patients (HIV), and 13 low-risk healthy controls (HCs). Results showed that, whereas alpha defensin production and alpha defensin-expressing CD8 lymphocytes were comparable in ESNs and HIV patients, constitutive alpha defensin production by peripheral CD8 and CVMCs was augmented in ESNs compared with HCs (P = 0.001 and P = 0.058, respectively); alpha defensin mRNA was increased in PBMCs of ESNs; unstimulated, alpha defensin-expressing peripheral and mucosal CD8 lymphocytes were 10-fold higher in ESNs compared with HCs (P = 0.003 and P = 0.01, respectively); and alpha defensin mRNA and alpha defensin-expressing cells were augmented in cervical biopsies of ESN compared with HCs (mRNA:P = 0.03). The differences were reduced upon in vitro mitogen stimulation. A robust constitutive production of alpha defensin is seen in HIV-exposed uninfected individuals; these peptides could have a role in the potentially protective immune response that characterizes ESNs.

Biopsy↗
PubMed2004

Growth hormone in T-lymphocyte thymic and postthymic development: a study in HIV-infected children.

OBJECTIVES: Growth hormone (GH) plays a role in thymic function, and recombinant GH may stimulate thymopoiesis in HIV-infected individuals. We performed immunologic analyses in 26 antiretroviral-treated children matched for age, pubertal status, clinical parameters, and antiretroviral exposure who did or did not show an impaired response to GH-release stimulation tests with arginine + GH-releasing hormone. RESULTS: The following abnormalities were found in GH-deficient compared with GH-nondeficient children after >4 years of therapy: CD4 count ( P = .02) and percentage ( P = .03), CD4 as percentage of normal cells for age ( P = .003), serum interleukin-7 concentration ( P = .02), and thymic volume ( P = .01). Naive CD4 (4+62+RA+ and 4+CCR7+RA+) and CD8 (8+CCR7+RA+) lymphocytes were lower in GH-deficient children ( P = .003; P = .007; and P = .02, respectively). Postthymic pathways were also impaired in GH-deficient children. Thus, central memory (4+CCR7+RA-) CD4+ cells were reduced ( P = .006), whereas effector memory (4+CCR7-RA-) CD4+ cells ( P = .002) and late effector CD8+ lymphocytes (8+CCR7-RA+ and 8+27-28-) ( P = .009 and P = .002, respectively) were increased in these children. CONCLUSIONS: Growth hormone plays a role in thymic and postthymic pathways, and defective GH production may be associated with incomplete immunoreconstitution. Immunomodulant agents (including GH) could be useful in patients with defective GH production.

Adolescent↗
PubMed2004

Immunomodulation induced by tucaresol in HIV infection: results of a 16 week pilot Phase I/II trial.

OBJECTIVE: Immune reconstitution in highly active antiretroviral therapy (HAART)-treated individuals is incomplete and immunomodulatory compounds are needed to improve the outcome of HIV therapy. In a Phase I/II clinical trial performed on HIV-positive patients we analysed the safety and immunomodulating effects of tucaresol, a novel compound that has previously been described tn enhance cell-mediated immune responses. PATIENTS AND METHODS: Sixteen weeks pulse dose escalation protocol. Four groups of HIV-positive patients were enrolled: group A (n=6): HAART, CD4+ 300-500 cells/microl, HIV RNA <80 copies/ml; group B (n=6): HAART-naive, CD4+ <500 cells/microl, HIV RNA >10 000 copies/ml; group C (n=3): HAART-naive, CD4+ >500 cells/microl, HIV RNA <10000 copies/ml; and group D (n=6): HAART, CD4+ <200cells/microl, HIV RNA <80 copies/ml. Tucaresol was added to HAART in group A and D patients; group B patients started tucaresol with HAART, group C patients received tucaresol alone. Clinical and immunological analyses were performed at different time points. RESULTS: Tucaresol-related serious adverse events were observed in the first week of therapy in 2/21 patients who were viraemic when commencing treatment, but did not occur in patients on stable HAART. Tucaresol did not affect HIV viraemia whereas increases in CD4+ percentages, mainly supported by naive CD4+ cells, were observed. CD8+/28-/45RA+ cells and HIV-specific CD8+ IFNgamma- and perforin-producing cells improved whereas IL-10 mRNA diminished in tucaresol-treated patients. The effects were greater with 25 mg given every other day for 1 week. CONCLUSION: In HAART-receiving patients with proper virus suppression, tucaresol was not associated with serious adverse events and resulted in qualitative and quantitative stimulation of HIV-specific cytotoxic T lymphocyte activity and generation of naive T cells. These data may support further exploration of tucaresol use in reconstitution of immune system parameters in HIV patients with proper virus suppression while on HAART.

Adult↗
PubMed2003

1-40 Beta-amyloid protein fragment modulates the expression of CD44 and CD71 on the astrocytoma cell line in the presence of IL1beta and TNFalpha.

The modulation of CD44, VCAM-1 and CD71 expression was analysed by flow cytometry in the 1321N1 astrocytoma cell line in the presence of interleukin-1beta (IL1beta), tumour necrosis factor-alpha (TNFalpha) and 1-40 or 25-35 beta-amyloid (Abeta) fragments. The percentage of 1321N1 astrocytoma cell line expressing these markers increased significantly after treatment with TNFalpha or IL1beta. The presence of Abeta 1-40 fragment, alone or in combination with IL1beta, induced an increase in the percentage of cells expressing CD44, but not VCAM-1. However, the concomitant presence of Abeta 1-40 fragment and of IL1beta or TNFalpha caused an increase in the percentage of CD71 positive cells. In contrast, the shorter Abeta 25-35 fragment was always inactive. These results indicates that Abeta 1-40 fragment, in association with cytokines, can activate this astrocyte-derived cell line and add further elements in favour of the hypothesis that beta-amyloid can act as immunological mediator.

Amyloid beta-Peptides↗
PubMed2003

Significant association of HLA A2-DR11 with CD4 naive decrease in autistic children.

Nine autistic children and 37 ethnically homogenous controls were enrolled in the study to assess their human leukocyte antigen (HLA) pattern, and eight healthy children were studied to define their peripheral blood cell subsets. We observed a significant decrease in CD4+ naive and an increase in CD4+ memory T cells in autistic children. These differences were significantly more pronounced in the autistic children bearing the HLA A2 and DR11 alleles. These data support the hypothesis that autism could be due to an immune imbalance occurring in genetically predisposed children.

Autistic Disorder↗
PubMed2003

Distinct immune profiles characterize patients with diffuse or limited systemic sclerosis.

Mitogen-stimulated IL-2, IFN-gamma, TNF-alpha (type 1 cytokines), and IL-10 (type 2 cytokine) production by peripheral blood mononuclear cells, as well as expression of surface markers on immune cells, was evaluated in systemic sclerosis (SSc) patients. Fifty-four SSc patients with either diffuse (dSSc) or limited (lSSc) disease and 20 age- and sex-matched healthy controls (HCs) were examined. Fourteen patients were treated with prednisone and 9 patients with prednisone and cyclophosphamide pulses. Results showed that (1) IL-2 production is significantly decreased, whereas IL-10 is higher in untreated patients compared to HCs; IL-10, IFN-gamma, and TNF-alpha production is higher in lSSc compared to dSSc patients; (2) CD4+25+ (IL-2R), CD8+, and CD8+45RA-28+57- (memory) lymphocytes are reduced in patients compared to HCs; (3) CD95-expressing CD4+ and CD8+ cells are significantly higher in dSSc patients; and (4) steroids are more effective alone than in combination with cyclophosphamide in reducing IL-10 and IFN-gamma production in these patients. These results confirm that a complex imbalance in cytokine production is present in SSc patients and suggest that peculiar phenotypic populations are underrepresented in these patients. Overexpression of Fas in dSSc could results from the attempt of the immune system to induce apoptosis of autoreactive T-cell clones.

Aged↗
PubMed2003

Research on psychoimmunology.

Several lines of evidence suggest a role for the immune system in the multifactorial pathogenesis of schizophrenia and other psychiatric and neurodegenerative disease. Later, the role of immune mediators like cytokines became a source of main interest related to the process on inflammation in the CSM. In this article we report the results of our research on cytokines in a different groups of psychiatric patients following their clinical symptomatology and the course of diseases. In particular, we observed a prevalent type 1 cytokine profile in acute multiple sclerosis patients, while IL-10 production predominated in stable multiple sclerosis individuals. The modifications of cytokine profiles observed in schizophrenic patients suggests that clinical improvement is associated with a reduction in the inflammatory-like situation present in those not currently under treatment. Our data on Alzheimer's disease (AD) support the role of the inflammatory process in the pathogenesis of AD and reinforce the hypothesis that the neurodegenerative processes in the AD patients are associated with an abnormal antigen-specific immune response. The activation of immune system mechanisms observed in obsessive compulsive disorders could be due to the combination of endogenous (hormonal alterations associated to the modifications in the hypothalamic-pituitary-adrenal axis) and exogenous (viral or bacterial infections) factors.

Alzheimer Disease↗
PubMed2002

B7-H1 is up-regulated in HIV infection and is a novel surrogate marker of disease progression.

The ligation of programmed death-ligand 1 (B7-H1) to T cells results in the preferential production of interleukin 10 (IL-10). We investigated if B7-H1 would be up-regulated in HIV infection, a disease characterized by increased IL-10 production, by measuring B7-H1, B7-1 (CD80), and B7-2 (CD86) expression and mRNA in 36 HIV-infected patients and in 22 healthy controls (HCs). Results showed that (1) B7-H1 expression and mRNA are augmented in cells of HIV patients; (2) increased IL-10 production in these patients is largely induced by B7-H1-expressing CD14(+) cells; (3) an inverse correlation is detected between B7-H1 expression and CD4 counts, whereas the up-regulation of B7-H1 is directly associated with HIV plasma viremia; (4) antiviral therapy results in the parallel down modulation of IL-10 production and B7-H1 expression/synthesis; and (5) B7-H1/CD80 and B7-H1/CD86 mRNA ratios are increased in peripheral blood mononuclear cells (PBMCs) of HIV patients compared with HCs. B7-H1 synthesis and expression are up-regulated in HIV infection, and the degree of dysregulation correlates with the severity of disease. Aberrant antigen presentation by antigen-presenting cells (APCs) that exhibit increased B7-H1 expression and IL-10 production in HIV infection could be responsible for T-lymphocyte unresponsiveness and loss of protective immunity. B7-H1 is a surrogate marker potentially involved in AIDS disease progression.

Antigens, CD↗