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E Möller

Publications and source records attributed to E Möller.

At least 325 records · Page 18Linked to original sources
PubMed1970

Rapid lymphocytic recognition of histoincompatibility. Changes of the deoxyribonucleoprotein complex in mixed cultures of allogeneic human lymphocytes.

The mechanism of growth stimulation in allogeneic lymphocytes mixed in vitro was studied at the cell level by means of cytophotometric techniques. A pronounced increase in fluorescence intensity of fixed and acridine orange (AO) stained lymphocytes was observed as soon as after 1-3 hr in mixed culture. No increase in the amount of DNA took place during this time. The higher fluorescence intensity was due to an increased accessibility of AO binding sites in the deoxyribonucleoprotein (DNP) complex, most probably as a result of weakened bonds between the DNA and the protein moiety in the DNP complex. Similar DNP changes have been found in other systems of growth stimulation and may be one prerequisite for later induction of cellular synthetic processes. Increased AO binding only occurred when the lymphocyte donors were incompatible at the major histocompatibility locus (HL-A); there was no change in AO binding in cases of HL-A identity. The AO binding reaction probably reflects a specific recognition of HL-A antigens, whereas other antigenic discrepancies between the individuals do not seem to cause an analogous response.

Acridines↗
PubMed1967

Cytotoxicity by nonimmune allogeneic lymphoid cells. Specific suppression by antibody treatment of the lymphoid cells.

Nonimmune lymphoid cells were capable of causing cytotoxicity of H-2 incompatible mouse tumor cells in vitro in the presence of PHA, whereas syngeneic cells were not. Semisyngeneic and X-irradiated (1500-3000 R) F(1) hybrid lymphoid cells were cytotoxic for target cells derived from one of the parental strains. In addition, parental nonimmune and X-irradiated lymphoid cells damaged hybrid target cells. It was concluded that one component of cytotoxicity was not related to an induction of a primary immune response in vitro, since F(1) hybrid cells are not capable of reacting immunologically against parental type target cells. It seemed probable that cytotoxicity was caused by target cell confrontation with antigenically and/or structurally incompatible lymphoid cells. This conclusion was strengthened by the demonstration that isoantibodies produced in the target strain and directed against the allogeneic lymphoid cells specifically suppressed cytotoxicity. Isoantibodies reacting against some but not all of the antigenic determinants of the lymphoid cells differentiating them from the target cells did not suppress cytotoxicity. The specific suppression of cytotoxicity by specific isoantibodies against the lymphoid cells support the allogeneic inhibition concept.

Animals↗