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Biomedical subjects

D W Scott

Publications and source records attributed to D W Scott.

At least 271 records · Page 15Linked to original sources
PubMed1976

Effect of carrier-specific tolerance on the generation of helper cell function.

The effect of carrier-specific tolerance on the development of helper cell function was studied in irradiated rats reconstituted with normal or carrier-tolerant bone marrow. Bone marrow (BM) from normal rats or rats tolerant to sheep IgG (SGG) was transferred to lethally irradiated syngeneic recipients, which were challenged 3 to 5 weeks later when immunocompetence to T-dependent antigens was shown to have recovered. When recipients were challenged with the 2,4,6-trinitrophenyl (TNP) hapten coupled to SGG in adjuvant, groups which received SGG-tolerant BM were 70-80% unresponsive in terms of anti-TNP plaque-forming cells compared to recipients of normal BM. This effect was carrier (SGG)-specific and was reversed when normal thymocytes were transferred with tolerant BM. Moreover, neither tolerant BM nor tolerant thymocytes were able to suppress the responsiveness of normal BM at a 1:1 ratio. These cell-mixing experiments imply that the reduction in helper cell function is due neither to suppressor cells nor antigen carryover in the tolerant BM. It is suggested that a BM precursor of the helper T cell may be rendered tolerant and therefore already possesses antigen specificity prior to thymic migration.

Animals↗
PubMed1976

Effect of lipopolysaccharide on the induction of tolerance to polymerized flagellin.

The effect of bacterial lipopolysaccharide (LPS) on the induction of tolerance to the T-independent polymerized flagellar protein (POL) of Salmonella adelaide strain SW1338 was studied in vitro. In contrast to published results with T-dependent antigens, LPS failed to prevent or reverse tolerance induction to POL under conditions in which tolerance was reversible by other means. Moreover, the addition of high doses of LPS to slightly supra-immunogenic concentrations of POL augmented-tolerance induction. These results suggest that the mitogenic properties of LPS are insufficient to convert a tolerogenic dose of POL into an immunogenic one and, therefore, that LPS may act only on T-dependent B cell responses. Since both POL (1338) and LPS are T-independent, mitogenic and so-called "polyclonal B cell activators," these data have implications for signal discrimination in the immune response.

Animals↗
PubMed1975

A lectin model for unresponsiveness. I. Reversible effects of high doses of concanavalin A on spontaneous and induced DNA synthesis.

A mitogen model for unresponsiveness has been studied. In 72-hr cultures the lowest supraoptimal dose of Concanavalin (Con A) showing no stimulation of rat thymocytes above background was 160 mug/ml. This dose was also found to inhibit substantially (50%) the high spontaneous DNA synthesis by thymocytes during the first 24 hr of culture. This effect was most significant 12 to 24 hr after addition of high-dose Con A. It was not necessary for the cells to remain continuously with high-dose Con A, since washing out unbound Con A after 1 hr still led to reduced 3-H-thymidine incorporation at 24 or 72 hr. Furthermore, high-dose Con A treatment suppressed DNA synthesis when added at 48 hr to cultured optimally stimulated with Con A. Interaction with high-dose Con A appears to inhibit the ability of cells to initiate new rounds of DNA synthesis without blocking ongoing DNA replication. Removal of Con A with alpha-methyl-D-mannopyranoside (mannose) led to only partial reversal of these effects after 1 hr although "unresponsiveness" was reversible at 15 min. Suppression was not due to cytotoxic or agglutinating effects of the high-dose Con A. Two times 10-6 thymocytes exposed to 160 mug of Con A for 1 hr bound 1.7 mug, 86% of which was elutable with mannose. There was no reduction in the ability of high-dose treated cells to bind a subsequent optimal dose of Con A. Since Con A binds to essentially all thymocytes, this system is useful in following early events in the induction of lectin "unresponsiveness" as a model for immunologic tolerance.

Animals↗
PubMed1975

Rheumatoid arthritis in a dog.

Rheumatoid arthritis was diagnosed in a 5-year-old Golden Retriever. Diagnosis was made on the basis of historoclinical, laboratory, and radiographic findings, a positive rheumatoid factor titre, and compliance with the American Rheumatism Association criteria for diagnosis of rheumatoid arthritis in man. Satisfactory remission was obtained with buffered aspirin.

Agglutination Tests↗
PubMed1975

Receptors for antigen on lymphoid cells. II. The nature of the molecule responsible for plaque-forming cell adherence.

The nature of specific adherence of rat anti-TNP PFC to TNP-GRBC has been investigated with PLL-fixed antigen monolayers as cellular immunoadsorbents and as plaque indicators. The immunoglobulin nature of the molecule responsible for PFC adherence is suggested by the fact that pretreatment of the PFC with rabbit anti-rat Ig antisera, but not anti-histocompatibility antisera, inhibits adherence. Removal of the adherence capacity of early PFC with the proteolytic enzymes papain and pronase, or by "capping" with anti-Ig is followed by slow regeneration of the ability to adhere, suggesting that adherence is due to membrane rather than secreted immunoglobulin, the latter being detectable within minutes after enzyme treatment. Several time-related events relating to PFC adherence were observed. 1) Both direct and indirect PFC are capable of specific adherence; the ability to adhere, however, tends to decline with time, especially after secondary immunization. 2) Although early PFC adherence is unaffected by trypsin treatment, later populations become increasingly sensitive. 3) Pretreatment of PFC at various times after primary immunization with antisera specific for rat mu-chain indicates that IgM and possibly early IgG-secreting PFC have mu heavy chains on their surface. These data suggest that the PFC membrane is progressively changing during the maturation of the antibody response.

Adsorption↗