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Biomedical subjects

W R Thomas

Publications and source records attributed to W R Thomas.

At least 145 records · Page 8Linked to original sources
PubMed1978

Vitamin C and immunity: an assessment of the evidence.

The high concentration of ascorbate in leucocytes and its rapid expenditure during infection and phagocytosis suggests a role for the vitamin in the immune process. Evidence published to date shows an involvement in the migration and phagocytosis by macrophages and leucocytes, as well as the induction and expression of delayed hypersensitivity. Its effect on antibody production and complement levels is controversial but probably minimal. This study suggests there is room for further investigation into the effect of ascorbate on immunity, particularly with defined populations, but cautions the use of megadose therapy.

Antibody Formation↗
PubMed1978

Induction and modification of anti-TNP reaginic and IgG antibody responses by reactive trinitrophenyl derivatives.

The anti-TNP antibody response of mice exposed to picryl chloride is a response where IgE antibody can be preferentially produced. Skin-painting with picryl chloride induces IgM, IgG and IgE antibody. After repeated painting the titre and persistence of the IgE but not IgG antibody is increased. Feeding picryl chloride does not induce antibody but it does produce unresponsiveness for IgG without affecting responsiveness for IgE. Injection of picryl sulphonic acid produces unresponsiveness for both classes. The unresponsiveness (induced by feeding or injection) is found for responses to picryl chloride but responses to TNP-KLH are barely affected. Both the IgE and IgG responses to picryl chloride are initiated in the lymph nodes and then develop in the spleen. IgE and IgG antibody production are both T-cell dependent but not influenced by adult thymectomy.

Animals↗
PubMed1978

Induction of contact sensitivity. Selective induction of delayed hypersensitivity by the injection of cells from draining lymph nodes into the footpads of normal recipients.

Cells taken from the draining lymph nodes of mice 1 day after painting with picryl chloride can induce contact hypersensitivity when injected into the footpads of normal recipients. Previous studies have presented evidence to show that this is an immunizing process rather than a transfer of sensitized cells. This study shows that footpad injection of 5 times 10(6) 1-day draining lymph node cells induces a similar degree of hypersensitivity to the original skin painting with picryl chloride but no antibody, as judged by anti-TNP splenic PFC and serum antibody, in contrast to the moderate antibody response found after skin painting. The apparent inability to induce a response did, however, correlate with the finding that the draining lymph nodes of mice painted with picryl chloride had few PFC. Some effect of the cells on antibody was noted in that after mice were challenged on the ear to produce contact sensitivity reactions they produced an antibody response larger than that of mice not injected with cells. This was not a large phenomenon but was unusual because 2-5 times 10(6) cells was more effective than either 10(6) or 5 times 10(6) cells, even though 5 times 10(6) cells produced the largest contact sensitivity reactions. The augmentation was antigen specific and the same dose-response effect could be obtained with irradiated cells (2000 rad). It is suggested that the ability of these cells to induce large contact sensitivity reactions without antibody indicates that they may have an important role in the immunogenicity of contact sensitizing agents, which can induce large delayed-type hypersensitivity reactions accompanied only by moderate antibody responses.

Animals↗
PubMed1978

Reaginic antibody to contact sensitizing agents. Occurrence of cells which supress IgG and not reagin responses.

Mice painted with the contact sensitizing agent picryl chloride produce IgG and reaginic or IgE-type antibody. They concomitanly produce suppressor cells which can inhibit IgG responses of normal mice to picryl chloride. These cells were produced between 3 and 7 days after primary sensitization (skin painting) and were T cells, as evidenced by their sensitivity to anti-theta serum and by their passage through nylon wool columns. Although they inhibited IgG responses they did not significantly change IgE titres. This correlates with a previous observation that repeated painting with picryl chloride increased IgE and not IgG responses.

Animals↗
PubMed1977

Inhibition of antibody responses by cells from mice treated with picryl sulphonic acid.

Cells from mice inoculated with picryl sulphonic acid (PSA cells), which contain suppressor T cells for contact sensitivity to picryl chloride, were examined for their ability to alter antibody responses of normal mice. These cells did not influence antibody or plaque-forming cell (PFC) production accompanying contact sensitivity reactions produced by painting with picryl chloride but reduced IgG antibody and indirect PFC responses to conjugates of trinitrophenyl (TNP) bovine serum albumin and ovalbumin. IgG responses to TNP or new antigenic determinants of TNP-mouse serum albumin were not affected by PSA cells. The PSA cells required several weeks to produce reductions of responses and only reduced responses to optimal doses of antigen. When the injection of antigen was delayed until several weeks after the injection of PSA cells rapid reductions of responses were found but these were short-lived. The inhibition was specific for TNP proteins although responses to hapten and carrier were reduced. Evidence is presented to show that the inhibition was mediated by an adherent macrophage-like cell rather than a T cell. The inhibitory activity was resistant to irradiation and anti-theta treatment but was removed by glutaraldehyde treatment and cotton wool filtration.

Animals↗
PubMed1976

Reaginic antibody produced in mice with contact sensitivity.

Mice produced reaginic antibody within 1 wk of painting with the contact sensitizing agent picryl chloride. The titers, measured by passive cutaneous anaphylaxis in rats, increased after repeated applications of picryl chloride. In contrast, serum agglutinins did not increase after two applications of picryl chloride. Reagin was also elicited by another contact sensitizing agent, oxazolone. Some strain variation of the response to picryl chloride was found, with CBA mice being good responders and BALB/c and C57BL/10 mice being poor responders.

Animals↗
PubMed1975

Humoral immune response of mice with long-term exposure to cigarette smoke.

Mice were exposed to fresh cigarette smoke for 1,17, and 38 weeks. After each period the primary and secondary humoral immune response to intraperitoneal inoculation of sheep erythrocytes was studied. Direct and indirect plaque forming cell responses in the spleen and in a pool of cervical and mediastinal lymph nodes, as well as serum hemolytic and hemagglutinating antibodies were examined. Primary plaque forming cell and antibody response to sheep erythrocytes was first enhanced and then depressed by continual cigarette smoke exposure, while the secondary response was unaffected. Serum antibody response to polyvinylpyrrolidone, an immunogen independent of thymus-derived lymphocytes, was not impaired by 41 weeks of cigarette smoke exposure.

Animals↗
PubMed1974

The growth of transplanted tumours in mice after chronic inhalation of fresh cigarette smoke.

The subcutaneous growth of the Lewis lung tumour in C57BL mice chronically exposed to fresh cigarette smoke was increased above that in age-matched control mice. When murine sarcoma virus (Harvey) induced tumour cells were introduced to the lungs of groups of BALB/c mice, only mice chronically exposed to fresh cigarette smoke died with tumour cells in the lungs. Tumour cell growth in mice during short term cigarette smoke exposure was indistinguishable from that in controls.

Animals↗