Biomedical subjects

C Corbel

Publications and source records attributed to C Corbel.

74 records · Page 5Linked to original sources

PubMed1980

Intracellular distribution of antibodies in rat lymph node cells during primary response. A kinetic study.

The kinetics of appearance of immunoglobulin- and antibody-containing cells in rat lymph nodes was studied by immunoenzymatic techniques between days 12 and 90 after a single injection of horse-radish peroxidase. Three distinct phases appeared during the primary repsonse. Between days 8 and 17, essentially no antibody-containing cells were detectable, while non-specific immunoglobulin-containing cells amounted to up to 9% of the total cell population. The peak of antibody-forming cells was observed between days 18 and 24, and their number decreased slowly during the last phase. Days 18-20 were marked by a sharp peak of a distinct category of cells containing antibodies in a limited area of their cytoplasm. One day before this event, the percentage of immunoglobulin-forming cells decreased drastically, and remained very low throughout the response. These results are discussed on the basis of a previously published model, which proposes that non-specific immunoglobulin-containing cells are precursors to antibody-containing cells, and that the transformation between these two categories of cells involves a stage where antibody synthesis is restricted to a few endoplasmic reticulum vesicles.

Animals↗

PubMedDate not supplied

Studies on B-cell activation in vitro.

When antigen activates B cells with the help of T cells, factors are produced by T cells which induce proliferation and maturation to Ig-secreting cells. T-cell lines and T-cell hybridomas have been obtained which, upon stimulation by antigen or by concanavalin A, produce these B-cell replication and maturation factors. However, their ability to produce these but not other factors, such as the T-cell growth factor, appears to be unstable even upon repeated recloning of the T hybridoma cells. Mitogens are known to replace some of the signals required in T-cell-dependent, antigen-specific activation of B cells. Depletion of cells, however, abolishes the mitogen responsiveness of the B-cell population from spleen. This responsiveness can be repaired when accessory cells such as peritoneal cells, irradiated spleen cells, cells of the macrophage line P388D1 or those from macrophage colonies grown from bone marrow cells with colony-stimulating factor are added back. Soluble factors obtained from different activated macrophages as well as from activated T cells also restore responsiveness. These results argue against a single, non-specific signal model of mitogenic activation of B cells and indicate that this activation is T-cell- but not macrophage-independent.

Animals↗