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Biomedical subjects

S Britton

Publications and source records attributed to S Britton.

At least 145 records · Page 8Linked to original sources
PubMed1976

Inability of normal and activated thymus-derived cells to act as cytotoxic effector cells against antibody-coated targets.

Thymus lymphocytes activated in vitro by a T cell mitogen (concanavalin A (Con A)) did not form Fc rosettes nor were they cytotoxic against untreated or antiserum-coated target cells. Con A activated spleen cells were cytotoxic against target cells, but they did not display an increased cytotoxic effect against antibody-coated YAC targets, when compared to normal spleen cells. Con A-activated spleen cells as well as cells activated by a mixed lymphocyte culture did not form Fc rosettes. Thus, activated cytotoxic T cells did not form Fc rosettes nor did they cause cytotoxicity on antibody-coated target cells. Antibody coating of the target cells did not suppress expression of cytotoxicity of activated T cells.

Animals↗
PubMed1975

The immunological hazard of Cushing's syndrome.

A 24-year-old woman was found to have cryptococcal meningitis and Cushing's syndrome due to an adrenal adenoma. Her meningitis was successfully arrested with fluorouracil. Treatment with metyrapone decreased her cortisol production and produced clinical remission of Cushing's syndrome. On admission her peripheral T lymphocytes were few and hyporeactive. When the overproduction of cortisol ceased the numbers of T lymphocytes and their reactivity returned to normal and she developed in-vitro lymphocyte responsiveness to the cryptococci.

Adenoma↗
PubMed1975

Experimental amyloidosis: the inducer is a polyclonal B-cell activator to which susceptibility is under genetic control.

Experimental amyloidosis in mice can be induced by repeated injections of casein. It has now been demonstrated that casein induces strong polyclonal antibody synthesis in mouse B spleen lymphocytes. This effect is much more pronounced in spleen cells from anyloid-susceptible mice (CBA/J) than amyloid-resistant mice (A/J). It is suggested that amyloidosis can be due in some instances to a constant exposure for molecules which induce polyclonal B-cell activation.

Amyloidosis↗
PubMed1975

Correction: mouse spleen cells cultured in homologous serum can indeed make primary antibodies to sheep erythrocytes.

Contrary to what I have reported in a previous article, I now present data that prove that spleen cells from various strains of mice can make primary antibodies to sheep erythrocytes in syngeneic adult serum. The reasons for this dichotomy of data are not clear. The present results indicate that it is possible to obtain an antibody response in the absence of demonstrable mitogens or polyclonal activators, suggesting activating signals only between antigen-specific cells. Primary IgG formation in vitro was demonstrable in cultures with normal mouse serum but not in fetal-calf-serum-substituted cultures. Since antigen has never induced antibody formation in vitro under serum-free conditions, it is now deduced that normal adult serum, in addition to containing suppressor molecules that restrain general lymphocyte proliferation, also contains material absolutely essential for antigen-induced specific cell proliferation to occur. These latter substances work even at very high dilutions.

Animals↗
PubMed1973

Heterogeneity of the effector cells in the cytotoxic reaction against allogeneic lymphoma cells.

The cytotoxic effect of spleen cells from H-2 allogeneic mice was tested in vitro against an A strain leukemia (YAC) labeled with [(125)I]iododeoxyuridine. After the mice were primed with tumor cells, significant and specific H-2 immunity was detected on day 3 and peak cytotoxicity was observed between 7 and 14 days after priming. Two effector cells appear to be involved in the host response, because spleens taken from mice soon after priming were not sensitive to antitheta sera and complement while those taken during the peak stages of the response showed a marked reduction in cytotoxicity after treatment. Macrophages were not involved, since removal of these cells by the carbonyl iron method did not result in any reduction in cytotoxicity. Immune serum that was capable of inducing cell-mediated cytotoxicity in normal spleen cell populations also augmented cytotoxicity of spleen cells taken from mice primed 3 days previously. However, when spleen cells were taken from mice during the peak phase of the immune response, the same serum at the same dilutions inhibited the preexisting cytotoxicity. A difference was also detected in the killing efficiencies between early and late immune cells.

Animals↗