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Biomedical subjects

F Spinozzi

Publications and source records attributed to F Spinozzi.

108 records · Page 6Linked to original sources
PubMed1984

Lymphocyte surface antigens: a longitudinal study during the first month of human life.

A longitudinal study on human T lymphoid surface antigens was performed on blood samples from 6 infants during their first month of life. Although the results indicate a sudden increase in the percentage of OKT3+ and E-RF+ cell types a few hours after birth and a less rapid decrease of OKT6+ and OKT9+ circulating cells, high levels of OKT10+ cells persisted. This finding suggests that infant blood contains immature phenotypic T lymphocytes after birth.

Age Factors↗
PubMed1983

The in vivo effect of thymic factor (thymostimulin) administration on circulating immune complexes and serum lysozyme levels in untreated Hodgkin's disease patients.

The in vivo effect of a calf thymus extract, thymostimulin, on the levels of circulating immune complexes (CIC) and serum lysozyme was evaluated in 32 patients with untreated Hodgkin's disease. Using the platelet aggregation test for detecting CICs, 12 patients (37%) had positive titers before thymostimulin treatment; 3 patients (10%) remained positive following therapy. Serum levels of Clq-binding immune complexes were evaluated (greater than 24.5 micrograms/ml) in 8 patients prior to thymostimulin therapy (mean value: 42.3 micrograms/ml); 3 patients continued to have elevated levels after treatment. Serum lysozyme levels for Hodgkin's patients was similar to control values (10.6 vs. 8.3 micrograms/ml); however, the Hodgkin's patients with initially elevated CICs had a lower serum lysozyme level than patients with initially normal CICs (12.9 vs. 7.3, p less than 0.02). Thymostimulin increased serum lysozyme levels in the Hodgkin's patients in whom the CICs were initially elevated (7.3 vs. 10.4 micrograms/ml, p less than 0.05). These data suggest that thymostimulin exerts an effect on the nonspecific immune system of Hodgkin's disease patients.

Animals↗
PubMed1983

The in vivo effect of thymic factor (thymostimulin) administration in Hodgkin's disease patients. Correlation of skin reactivity and leukocyte migration-inhibition factor in the sera of anergic subjects.

The correlation between leukocyte migration-inhibition and delayed skin hypersensitivity was studied in the sera of 15 anergic untreated Hodgkin's disease patients before and after administration of thymostimulin. Skin tests, negative in all patients before treatment, turned positive in 9 after thymostimulin. Prior to treatment, 10 patients had normal and 5 enhanced migration; none was leukocyte migration-inhibition factor (LIF) positive (mean 1.14 +/- 0.30). Seven of the 9 patients (77.9%) whose skin tests became positive, 3 of whom had an initially enhanced migration, were LIF positive after thymostimulin. LIF closely paralleled skin hypersensitivity both before and after thymostimulin. It is suggested that thymostimulin evokes the differentiation of a lymphocyte subpopulation(s) responsible for both factors investigated.

Cell Migration Inhibition↗
PubMed1983

Circulating immune complexes and serum lysozyme levels in untreated Hodgkin's disease. Their relationship to immune function.

Complement-fixing and non-complement-fixing circulating immune complexes were determined in 42 previously untreated Hodgkin's disease patients by Pl.A.T., C1qB-ELISA and KgB tests. The functional status of the monocyte-macrophage system was evaluated by measuring the serum lysozyme levels. These parameters were then correlated with the patient's immunocompetence, as assessed by the percentage of E-rosette forming cells and the PHA response. The Pl.A.T. was positive in 35.7% patients, the KgB-test in 34.3% and the C1qB-ELISA in 19%. There was overlapping of positive results in 37.5% patients. No correlation was found between CIC levels and stage, unfavourable histology or B symptoms. The PHA response was significantly depressed in CIC + patients, as detected by the C1qB-ELISA technique (p less than 0.0025). The data on serum lysozyme offer an insight into the possible mechanism regulating serum levels of CICs in Hodgkin's disease. Two distinct situations seem to exist: in the first, high CIC levels are associated with normal or low serum lysozyme values (p versus normal controls: n.s.); in the second, serum lysozyme levels are high and CIC absent (p less than 0.005 versus control values). The lowest lysozyme levels are also associated with a depressed lymphocyte PHA response. It could, therefore, be concluded that, in Hodgkin's disease, the presence, or absence, of CICs is directly correlated to the degree of monocyte-macrophage clearance activity and that the host's immunocompetence plays an important role in the induction and/or maintenance of this functional defect.

Antigen-Antibody Complex↗
PubMed1982

The in vivo effect of a thymic factor (thymostimulin) on immunologic parameters of patients with untreated Hodgkin's disease.

The in vivo effect of a calf thymus extract (thymostimulin, TS) on the E-rosetting capacity, PHA blastogenic response, serum migration inhibitory activity (LIF) and skin reactivity to recall antigens was evaluated in 19 untreated patients with Hodgkin's disease. In patients the mean percentage of peripheral blood lymphocytes forming E-rosettes increased from 47 to 55.7% (P less than or equal to 0.001; normal: 58.9). The mean PHA stimulation index rose with all three concentrations tested but did not reach normal values. Serum LIF was positive in only one patient prior to treatment with a mean LIF for all patients of 0.75 (P less than or equal to 0.005). Skin tests were positive in ten patients (52.6%) prior to therapy and 18 patients following therapy (94.7%; P less than or equal to 0.05). Thymostimulin, in vivo, appears to return immunologic competency to a population of untreated patients with Hodgkin's disease.

Adult↗
PubMed1982

The in vitro effect of a calf thymus extract (thymostimulin) on T cell phenotypes in cord blood lymphocytes.

An investigation was carried out on the in vitro effect of a calf thymus extract, thymostimulin, on the distribution of T cell phenotypes as defined by OKT3, OKT4, and OKT8 murine monoclonal antibodies and on E-rosetting cells in human cord blood lymphocytes from healthy newborns. The percentages of E-rosette-forming lymphocytes and OKT3+ total T population were lower in newborns than in adults (E-rosettes: 43.8% +/- 13% vs 57.9% +/- 7.9%, p less than 0.01; OKT3+ cells: 53.3% +/- 15.5% vs 79.9% +/- 4.7%, p less than 0.01), while the OKT4+/OKT8+ (helper/suppressor) cell ratio was normal in both (newborns: 3.40; adults: 2.44-NS). Thymostimulin increased the number of E-rosette-forming cells from 43.8% +/- 13% to 49.9% +/- 12.7% (p less than 0.01), as well as the percentage of phenotypic T lymphocytes. The highest increases were observed in the OKT4+ cells (37.7% +/- 14% to 49.1% +/- 13.8%, p less than 0.001), while smaller changes were observed in the OKT3+ cells (53.3% +/- 15.5% to 58.1% +/- 13.3%, p less than 0.02) and OKT8+ cells (12.8% +/- 6.4% to 16.6% +/- 6.5%, p less than 0.02). The results of the present study suggest that thymostimulin mainly provokes an increase in the helper T cell phenotype in cord blood lymphocytes.

Antigens, Surface↗
PubMed1981

Cell surface marker analysis in diagnosis of the early phase of chronic lymphocytic leukaemia.

Cell surface marker analysis was carried out in 50 CLL patients; 15 were preclinical or low count, that is with a total peripheral lymphocyte count well below 15,000/cmm and little or no infiltrative syndrome. Data of the cell surface marker in these 15 patients were compared with those of 15 patients with non-neoplastic benign lymphocytosis. Monoclonal B-cell compartment proliferation was found in low count cases, with analogous immnofunctional characteristics to typical CLL. On the other hand, there was a symmetrical increase in both T and B cell compartments in non-neoplastic lymphocytosis. This suggests that cell marker analysis is a very useful diagnostic tool during the preclinical phase of CLL, as it permits it to be readily differentiated from non-neoplastic lymphocytosis.

Aged↗
PubMed1979

[Cellular immunity in patients with Hodgkin's disease: modification induced by incubating lymphocytes with fetal calf serum and Hodgkin's serum].

The capacity of peripheral blood lymphocytes from fifteen patients with untreated Hodgkin's disease to form E-rosettes with sheep erytrocytes and to respond to PHA stimulation was found to be impaired in 47% of patients. When peripheral blood lymphocytes were incubated overnight in culture medium containing 20% fetal calf serum, E-RFC levels and the capacity to respond to PHA returned to normal. These functions were resuppressed by additional incubation with Hodgkin's disease serum but not from normal serum. The Hodgkin's disease serum inhibited normal peripheral blood lymphocytes to form E-rosettes and to respond to PHA.

Animals↗
PubMed1978

[Rosette formation test with mouse erythrocytes in chronic lymphatic leukosis: correlation with other membrane receptors].

The lymphocyte subpopulations of CLL patients have been studied. IgM and IgD membrane-associated immunoglobulins alone or in combination have been found, IgG being present in only one case. A marked increase in mouse-complement receptors (as shown by the EACt rosettes) as compared with human complement receptors (as shown by the EACa rosettes) was observed. The population of SIg-bearing lymphocytes was significantly greater than that of complement bearing lymphocytes. Moreover a mean percentage of 60.7 +/- 17 of the leukaemic lymphocytes formed rosettes with mouse red blood cells. In a significant number of patients the E-rosettes forming cells were also increased.

Erythrocytes↗
PubMedDate not supplied

Anti-CD3 and anti-CD2-induced T-cell activation in primary Sjögren's syndrome.

Because T-cell dysfunctions have been reported in patients with primary Sjögren's syndrome (SS), peripheral blood mononuclear cell (PBMC) proliferation obtained with anti-CD3 and anti-CD2 monoclonal antibodies was evaluated in these patients. Anti-CD3-induced mitogenesis, which varied widely among the patients, was lower in subjects with evidence of anti-SSA and anti-SSB antibodies than in controls. Moreover, the anti-CD2-induced response was depressed in about half the patients and the nonresponders were mainly those with anti-SSA and anti-SSB antibodies. Phorbol myristate acetate, a protein kinase C activator, used alone or added to anti-CD3, induced greater proliferation in patients than in control PBMC. In contrast, exogenous recombinant interleukin 2 (rIL-2) did not significantly enhance the anti-CD2-induced response of patients' PBMC, as it did in normal PBMC. Peripheral blood and parotid T cells from a patient with well-defined primary SS and parotid enlargement also responded poorly to anti-CD2 stimulation. Exogenous rIL-2 restored T-cell proliferation only in the salivary gland cultures of this patient. The present findings suggest that there is a T-cell activation defect in subjects with primary SS, particularly in those with circulating anti-SSA and anti-SSB antibodies. In addition, the difference in the response to IL-2 of peripheral blood and parotid-infiltrating T cells would seem to indicate that T-cell subsets are differently distributed in the blood and inflammation site.

Adult↗
PubMedDate not supplied

Systemic lupus erythematosus following total body irradiation for malignant lymphoma.

A case of a 63-year old man, who developed systemic lupus erythematosus three years after an initial diagnosis of small-cleaved centrofollicular lymphoma is described. The diagnosis of SLE was made on the basis of the accepted "1982 revised criteria for the classification of SLE". The autoimmune disease arose after a cycle of total body irradiation, despite the treatment with combination chemotherapeutic doses such a CVP or COAP or Cyclophosphamide, Vincristine, VM-26 and Prednisone. Genetic, immunological and exogenous environmental factors may co-exist and might equally be implicated in the pathogenesis of SLE and malignant lymphoma. However, the onset of SLE after total body irradiation could have been caused by the inactivation of suppressor T lymphocytes, which are known to be sensitive to radiations in vitro.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

Protein tyrosine kinase inhibition and cell proliferation: is the [3H]-thymidine uptake assay representative of the T-lymphocyte proliferation rate?

T-cell growth is controlled to a large degree by extracellular signals that bind to specific receptors on the surface of cells. A number of these receptors have intrinsic protein tyrosine kinase (PTK) activity. Their action on second messenger generation, and thus on cell proliferation, has been indirectly demonstrated by the decrease in [3H]-thymidine (TdR) uptake that follows co-stimulation of T-cells with mitogens and PTK inhibitors such as genistein (GEN). In this paper we report that the [3H]-TdR uptake assay is not a valid and reliable tool for investigating the proliferative activity of certain T-cell lines. In fact, a concomitant assessment of both [3H]-TdR uptake and cell cycle progression demonstrated that GEN is able to block G2/M progression of Jurkat T-lymphocytes even at doses (5 micrograms/ml) that do not influence [3H]-TdR uptake. Pretreatment with sodium o-vanadate (100 nM) could not reverse the GEN-related cell cycle perturbation, but was able to restore optimal [3H]-TdR uptake. Finally, GEN treatment was able to induce concentration-dependent apoptotic cell death of Jurkat T-cells. The control of cell activation, proliferation and programmed cell death is undoubtedly influenced by receptor-associated PTKs. The final effect on cell survival is almost entirely dependent on the activation state of the cell. The [3H]-TdR uptake assay seems to be inadequate for a correct interpretation of the expected results.

Cell Cycle↗
PubMedDate not supplied

Functional characterization of T cells bearing the gamma/delta T-cell receptor in patients with primary Sjögren's syndrome.

High percentages of gamma/delta+ T cells in the peripheral blood of a subgroup of patients with primary Sjögren's syndrome (SS) were found. This allowed us to purify and analyze them without their being previously expanded in vitro, and to investigate, therefore, the role of these cells in the pathological immune response which characterizes such systemic autoimmune disorders. The results showed poor proliferation of patient gamma/delta+ T cells in response to anti-CD3, due not to macrophage-dependent suppression but to defective interleukin 2 (IL-2) synthesis. Despite the defective proliferation patient gamma/delta+ cells, unlike those of the normal controls, provided a helper effect in inducing B cells to secrete immunoglobulins (Ig), particularly when they were preincubated with IL-2. The relative increase in a gamma/delta+ T cell subset which, although it secretes low levels of IL-2, is able to provide help for B-cell Ig synthesis, suggests that this T-cell subpopulation may be functional in vivo and may be involved in the pathological immune response encountered in pSS.

Adolescent↗