This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ghanta, V. K. Articles by Hiramoto, R. N. Search for Related Content PubMed PubMed Citation Articles by Ghanta, V. K. Articles by Hiramoto, R. N.

Effect of Immune Response to Sheep Red Blood Cells on Plasmacytoma MOPC 104 E¹

Department of Microbiology, University of Alabama in Birmingham, Birmingham, Alabama 35294

BALB/c mice were given 1 x 10⁶ MOPC 104E plasmacytoma cells i.v. to disseminate the neoplasm to various organs. Twenty-five days after implantation and at a time when the neoplastic B-cell clone was in the exponential growth phase, the mice were given i.p. injections of a mixture of antigens containing sheep red blood cells and levan. Each mouse was monitored simultaneously for immunoglobulin M (IgM) anti-dextran myeloma protein produced by the plasmacytoma and anti-sheep red blood cell hemolysin. The increase and decrease of these markers permit assessment of the expansion of the abnormal B-cell clone during the rise and fall of a normal B-cell clone in response to a specific antigen. The model was used to determine (a) the extent of the suppression of myeloma protein, (b) how long inhibition can be maintained, and (c) how soon it occurs after antigen is administered. The results showed that, as the IgM antibody response to sheep red blood cells begins to peak, it exerts a transient suppressive effect on either the MOPC 104E growth or on the cellular release of MOPC 104E IgM. The suppressive effect was noticeable 4 days after antigen administration for only 24 hr. These results indicated that plasmacytoma cells in vivo can recognize signals for either suppression of growth or release of the idiotypic MOPC 104E IgM and were not inconsistent with the view that myeloma may be the result of a defect in B-cell regulation.

¹ Supported by USPHS Research Grants CA16699 and CA25965 from the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 10/28/80. Accepted 2/27/81.