Search

Lymphoid cells infiltrating metastatic melanomas were grown directly from cell suspensions of tumour tissue by the addition of T cell growth factor. Lymphoid cells grew' out at the expense of tumour cells in six of seven freshly excised tumours. and cells from two cultures were expanded for in vitro testing of cytolytic function against different target cells. Early in culture the tumour derived lymphocytes killed fresh autologous melanoma cells and, particularly later in culture, were highly arid non-specifically cytolytic For cultured melanoma and non-melanoma cells, Cultured peripheral blood lymphocytes from patients with melanoma, and from normal subjects. were cytolytic to the same degree as tumour derived lymphocytes, and also resembled cells grown from tumour tissue in possessing acid phosphatase activity which was resistant to tartrate. Cultured lymphoblasts from both tumour and peripheral blood had a T cell phenotype when analysed with monoclonal antibodies. An in vitro co-culture system was employed to study the kinetics and the precursors of these non-specific killer cells among blood mononuclear cells. Blood mononuclear cells cultured with irradiated B lymphoblasts led to the generation of non-specific cytolytic cells, referred to as activated lymphocyte killer (ALK) cells, after 7 10 days of culture and the progenitors of these ALK cells were demonstrated to be distinct from those ol specific cytolytic T cells. [ABSTRACT FROM AUTHOR]

A number of different immunological properties have been attributed to iron (Fe3+ and Fe2+) and Iron-binding proteins. However, in many previous studies, high concentrations of iron were used and cell-cell interactions were not excluded as a possible cause of the observed immunomodulatory effects. In this study, clonal techniques have been used to examine the effect of non-transferrin-bound iron (Fe3+) on the T lymphocyte subsets required for the generation of cytotoxic T lymphocytes (CTL). Concentrations of nontransferrin-bound Fe3+ of 10 μM or greater were shown to inhibit the generation of C57, BALB/c and CBA allo-speeific CTL in bulk culture. Limit-dilution analysis revealed that: (i) Fe3+ reduced the cloning efficiency of CTL-precursors (CTL-P) by up to 96% without affecting the rate of clone growth; (ii) Fe3+ did not affect the cloning efficiency of allo-stimulated Ly-2-ve T cell precursors but reduced the rate of clone growth of these cells; (iii) Fe3+ enhanced, by more than 13-fold, the function of clones of Concanavalin A (Con A)- induced suppressor T lymphocytes (STL) which suppressed in vitro the development of CTL from their precursor cells. The data provide further evidence that low concentrations of non-transferrin-bound Fe3+, of the same order as those reported to be present in the scrum of patients with iron-overload, have significant immunoregulatory properties. [ABSTRACT FROM AUTHOR]

The effect of iron (Fe3+) and normal human liver ferritin on the proliferative response of normal human lymphocytes to tetanus toxoid was examined. This proliferative response involved memory T4+ lymphocytes as shown by a selective depletion study. Limit dilution analysis revealed that iron, present as ferric citrate, affected the initiation of clone development, and that concentrations of ferric citrate from 30 μM to 1 mM were able to reduce significantly the cloning efficiency of precursor T cells (up to 90% reduction). The reduced cloning frequency was not due to immunological suppression. Clone size was also reduced when iron was present during culture. In contrast, the presence of normal human liver ferritin during culture (concentration range: 300μg/l-10,000 /μg/1) had no effect on lymphocyte proliferation. The data indicate that low molecular weight iron (as ferric citrate) in concentrations similar to those which have been reported in the serum of patients with iron overload diseases, can interfere with antigen-specific lymphocyte responses and this may have implications for the development of infections and neoplasia in diseases of iron-overload. [ABSTRACT FROM AUTHOR]

Limit dilution analysis (LDA) was used to determine the effect of initial treatment of chronic inflammatory periodontal disease on the frequency of periodontopathic bacteria-specific T-cells in peripheral blood. Eleven marginal gingivitis (MG) and 8 adult periodontitis (AP) subjects took part in the study. The proliferative T-Lymphocyte precursor (PTL-P) frequencies to Porphyromonas gingivalis and Actinomyces viscosus were determined using LDA and Poisson statistics both before and after treatment. Tetanus toxoid was used as a control antigen. Treatment resulted in a significant reduction in clinical disease parameters in both groups. The median peak PTL-P frequency for P. gingivalis was significantly higher in the AP group compared with the MG group before treatment. This was not the case after treatment nor with A. viscosus. In the MG group the median peak PTL-P frequency with both P. gingivaIis and A. viscosus declined as a result of treatment. Although this decline was not statistically significant it may indicate an antigen-specific response in this group. In the AP group the median peak PTL-P frequency with P. gingivalis before treatment was 83.76 × 10-6 (approximately 1 in 12,000) and after treatment it was 36.17 × (approximately 1 in 28,000) Dose-response relationships showed at each concentration of organisms/ well this trend lot a decline in PTL-P frequency after treatment, suggesting that any increased eased responsiveness to this organism in this group may be largely antigen- specific. However, there was no difference in this group in the median peak PTL-P frequency with A. viscosus before and after treatment. This, together with the low PTL-P frequency to A. viccosus, suggests that any increased responsiveness to this organism in this group may be non-specific. [ABSTRACT FROM AUTHOR]