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B R Clark

Publications and source records attributed to B R Clark.

90 records · Page 5Linked to original sources
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Fate of intercellular MHC-peptide-T-cell receptor complexes during T-cell activation.

Antigen-specific T-cell activation requires the formation of a transient cell-cell conjugate between a T cell and an appropriate antigen presenting cell (APC). Focal aggregation of T-cell receptor (TCR) molecules at the T-cell-APC membrane interface accompanies formation of multiple non-covalent intercellular bridges consisting of TCRs on the T cell and cognate MHC-peptide complexes on the APC. Enhanced adhesiveness and T-cell activation follow the T-cell signalling that results from crosslinking of T-cell receptors (TCR). Models of T-cell activation propose that the APC and activated T cell separate following a decline in the enhanced adhesiveness. The rate of intercellular TCR-(MHC-peptide) complexes formed during T-cell activation is unknown. Based on the reported CD4-positive T-cell internalization of the peptide moiety of preformed cognate MHC II-peptide complexes, it is proposed here that translocation of the peptide moiety leads to destabilization and decomposition of intercellular trimolecular TCR-(MHC-peptide) complexes in the T-cell-APC interface. This decomposition accompanies or results in the decline in enhanced adhesiveness leading to separation of the APC and activated T cell.

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Effect of methionine replacement by homocystine in cultures containing both malignant rat breast carcinosarcoma (Walker-256) cells and normal adult rat liver fibroblasts.

When malignant W-256 rat breast carcinosarcoma cells are mixed with an equal number of normal adult rat liver fibroblasts and allowed to grow in a medium containing sufficient L-methionine and an excess of vitamin B12 and of folic acid, the malignant cells outgrow the normal cells, and within 2 weeks the tissue culture flasks contain only neoplastic cells. However, when ample DL-homocystine or homocysteine replaces methionine in the medium containing the same amount of vitamin B12 and folic acid, and seeded with the same type and number of malignant and normal cells, the malignant cells die and the normal cells thrive. Substantiating this conclusion are the results of injections into rats of comparable numbers of cells from each group after 3 weeks of growth in tissue culture. Fatal malignancies are produced by the homocystein-cultivated cells.

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