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Biomedical subjects

D W Thomas

Publications and source records attributed to D W Thomas.

At least 289 records · Page 16Linked to original sources
PubMed1975

Activation of T-lymphocyte helper function by brief exposure to antigen-pulsed macrophages.

In this report we investigated the ability of macrophage-associated OVA to stimulate purified OVA-immune T-lymphocytes to produce nonspecific helper activity for antibody production. T-cell activation required only a brief contact between the antigen-pulsed macrophages and T-lymphocytes and was maximal after a 4-hr contact. T-cell activation occurred at 37 but not at 4 degrees C, indicating that the macrophages and/or lymphocytes must be metabolically active for efficient activation. In addition, we compared the ability of antigen-pulsed syngeneic or allogeneic macrophages to activate T-cells for helper function.

Animals↗
PubMed1975

Regulation of the immune response: production of a soluble suppressor by immune spleen cells in vitro.

The addition of ovalbumin-immune spleen cells (Ova ISC) to sheep erythrocytes-immune spleen cells (SRBC ISC) in Mishell-Dutton-type cultures resulted in a dramatic reduction of PFC to SRBC and was dependent upon the addition of soluble Ova at low concentrations of Ova ISC. The suppressing cells in the Ova ISC were shown to be irradiation sensitive, depleted by anti-theta antiserum and complement treatment, and did not absorb to glass bead columns. Ova ISC-induced inhibition also occurred in culture chambers across a cell-impermeable membrane and a soluble inhibitor was recovered in chambers opposite the Ova ISC. This suppressor factor was sensitive to trypsin treatment and to heating at 80 degrees C, but not to 70 degrees C, for 30 min. The molecular weight, as determined by sucrose gradient analysis, was between 55,000 and 60,000 daltons. This suppressor factor appears to be distinct from a T-cell "helper" factor which was found to be sensitive to heating at 70 degrees C for 30 min. We propose that this suppressor factor participates in the termination of most immunologic responses and is responsible for the antigenic competition phenomenon.

Animals↗
PubMed1975

Antibody synthesis in synchronized mouse spleen cells during the secondary response to sheep erythrocytes in vitro.

Immunoglobulin synthesis by mouse spleen cells during the secondary response to sheep erythrocytes in vitro was examined in cells synchronized by methotrexate and adenosine treatment. Antibody synthesis by the synchronized cells was discontinuous through the cell cycle and highest in the early S phase. Previous results from this laboratory indicated that antibody secretion, as measured by plaque production to sheep erythrocytes, was also greatest in early S, and taken together these results suggest little difference in the expression of antibody synthesis and secretion through the cell cycle. Actinomycin D was employed in several experiments in an attempt to determine if the variation in antibody synthesis was regulated by transcription of messenger RNA for immunoglobulin. Lower actinomycin concentrations (0.05 mug/ml) reportedly permitting messenger, but not ribosomal, RNA synthesis as well as higher concentrations (1 mug/ml) rapidly reduced immunoglobulin and total protein synthesis. These results indicated that actinomycin was not suitable for determining the stability of messenger RNA in mouse spleen cells. Therefore, the reasons for fluctuation in antibody synthesis during the cell cycle could not be determined, but several possibilities are suggested.

Adenosine↗
PubMed1975

Inhibiton of tumor cell proliferation: second role for suppressor cells?

An antimitotic factor for mouse tumor cells was isolated from the supernatant fluids of antigen-stimulated ovalbumin-immune mouse spleen cells. A similar antimitotic factor was obtained from the supernatant fluids of phytohemagglutinin-stimulated non-immune spleen cells. The inhibitor prevented the multiplication of mouse L929 fibroblast cells in vitro and the in vivo proliferation of Ehrlich ascites tumor cells. Inhibition was not due to cytotoxic effects and the antimitotic effects were reversible. The antimitotic activity may be species-specific since the purified factor obtained from mouse spleen cells had no effect on human or monkey cell lines. This factor appears to be the same as the T lymphocyte-dependent suppressor for antibody production that we described previously. Several implications for the production of the suppressor in response to tumor cells that may be beneficial or harmful to the host are discussed.

Animals↗
PubMed1974

Reversible encephalopathy possibly associated with bismuth subgallate ingestion.

Four patients who had undergone abdominoperineal resection for carcinoma of the colon and who had been taking oral bismuth subgallate developed a stereotyped recurrent and reversible neurological syndrome. This was characterized by confusion, tremulousness, clumsiness, myoclonic jerks, and an inability to walk. All patients were extensively investigated and no cause could be found, but symptoms regressed when the intake of bismuth was stopped. Postmortem examination in one patient failed to show any appreciable abnormality apart from a loss of Purkinje cells in the cerebellum. In the other three patients amino-acid chromatography performed on urine showed the presence of an abnormal unidentified constituent. It is thought that these four patients developed an encephalopathy associated with their bismuth subgallate ingestion.

Adult↗
PubMed1973

Interaction of gonococci with phagocytic leukocytes from men and mice.

The interaction of human and mouse phagocytic leukocytes with representative virulent (F62-T1) and avirulent (F62-T4, RD-5) strains of Neisseria gonorrhoeae was studied in vitro. Leukocyte monolayers were incubated with gonococci for 30 min at 37 C, washed repeatedly, reincubated with fresh medium, and sampled for viable bacteria at intervals. After the initial incubation period and washing, human leukocytes retained larger numbers of viable T1 than of T4. During the subsequent 120 min of incubation, the numbers of viable T1 remained approximately constant, whereas viable counts of T4 declined by about two-thirds. In contrast, mouse leukocytes under similar conditions destroyed 70% of both types of gonococci. When human bactericidal serum was applied to infected human leukocytes, it had no effect on T4 but inactivated over 50% of T1. It is concluded that T4 are phagocytized by human leukocytes and are thus exposed to internal digestion, but are protected from bactericidal serum. T1, on the other hand, either adhere to the surface of the leukocytes or remain located so that they are neither digested by the leukocytes nor protected from bactericidal serum.

Animals↗
PubMed1972

Response of mice to injection of ribosomal fraction from group B Neisseria meningitidis.

Ribosomes of strain NOR-7 of group B Neisseria meningitidis were isolated by a procedure that included treatment of the cells with sodium dodecyl sulfate, disruption in a French pressure cell, and differential centrifugation. These preparations consisted of 66% ribonucleic acid and 24% protein and sedimented as a single component with a constant of approximately 66S. When used in immunodiffusion tests with homologous rabbit antiserum, untreated ribosomes formed two precipitin lines, when treated with ribonuclease three lines, and when Pronase-digested only one distinct line. Qualitatively indistinguishable reactions were obtained with the same antiserum and ribosomes from group A meningococci, but no precipitation occurred with those of Escherichia coli. When injected into mice, group B ribosomes elicited an increase in the number of antibody-producing spleen cells demonstrable by the hemolytic plaque technique using unsensitized sheep erythrocytes. Sensitization of the erythrocytes with increasing amounts of supernatant fluid of meningococcal cultures progressively reduced the number of demonstrable plaque-forming cells. Neuraminidase treatment of the erythrocytes increased immune hemolysis, whereas Pronase digestion reduced it. Injected mice were protected against homologous and heterologous meningococcal challenge. Both hemolysis and protection-inducing activities of the ribosomes were unimpaired by ribonuclease, but were reduced by Pronase. It is concluded that the immunological response elicited by the meningococcal ribosomes does not involve the group-specific carbohydrate antigen. The immunological mechanism by which the mice are protected against meningococcal challenge remains unknown.

Animals↗