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Biomedical subjects

C E Moody

Publications and source records attributed to C E Moody.

23 records · Page 2Linked to original sources
PubMed1979

Lymphocyte transformation induced by autologous cells. VIII. Impaired autologous mixed lymphocyte reactivity in patients with acute infectious mononucleosis.

The autologous mixed lymphocyte reaction (MLR) is severely impaired in patients with acute infectious mononucleosis. Reactivity returned during the course of convalescence. The allogeneic MLR was not impaired in these patients. B cells from patients with infectious mononucleosis do not stimulate autologous T-cell proliferation, and this observation appears to explain the cellular basis of the impaired autologous MLR in infection. Two explanations for the B-cell defect were considered: (a) the influence of serum factors on B-cell function and (b) the effect of Epstein-Barr virus infection.

Adolescent↗
PubMed1978

Tolerance induced by TNP-derivatized syngeneic erythrocytes: evidence for cooperation between hapten-specific T and hapten-specific B lymphocytes in the immune response.

Tolerance to the DNP haptenic determinant was induced with a single i.v. injection of trinitrophenylated syngeneic red blood cells. The tolerant state lasted 1 month and was stable on transfer to irradiated thymectomized syngeneic recipients. Suppressor activity was found soon after injection of tolerogen but was lost before the termination of tolerance. The unresponsive state could be reversed by adding normal thymus cells to tolerant spleen cells but not by normal bone marrow cells. LPS when given with immunogen restored the normal immune response in tolerant mice. Thus the injection of TNP-MRBC induced partial immune unresponsiveness which was characterized by the induction of T cell suppressor activity and by a hapten-specific helper T cells tolerance. Finally, these studies suggest a cooperative interaction between DNP-specific T lymphocytes and DNP-specific B lymphocytes in the immune response to DNP-BGG.

Animals↗
PubMed1977

Increased cell-mediated lysis of chicken erythrocytes following the addition of metabolic inhibitors.

The effect of a variety of metabolic inhibitors on the cell-mediated lysis of chicken erythrocytes by immune spleen cells was investigated using the Cr-release assay. The addition of cycloheximide, puromycin, emetine, pactamycin, actinomycin D or EDTA during the early stages of the reaction (0-2 h) produced partial to complete inhibition of the cytotoxic reaction, while the addition of these compounds at later time periods (2-4 h) resulted in the progressive loss of inhibitory effects. Later additions (4-6 h) of all compounds, except EDTA, resulted in a significant increase in target cell lysis. The ability of these compounds to induce increased cytotoxicity required complete inhibition of protein synthesis and the presence of reactive effector cells. It did not appear to be due to an increase in the rate of 51Cr release from previously damaged target cells, or inhibition of a target-cell repair mechanism dependent on protein synthesis. At least a portion of the increased reactivity was due to effector cell-target cell adhesions which formed after the addition of the inhibitor. The data suggests that the addition of metabolic inhibitors during the later stages of the reaction induced an increase in the efficiency or number of cytotoxic attacks.

Animals↗