The Journal of Immunology, Vol 130, Issue 4 1567-1572, Copyright © 1983 by American Association of Immunologists

ARTICLES

Inhibition of ongoing myeloma IgE synthesis in vitro by activated human T cells

A Hassner and A Saxon

The ability of activated T cells to suppress ongoing IgE synthesis in vitro was assessed using U266--a human myeloma cell line spontaneously producing IgE. T cells were able to inhibit U266 IgE synthesis in the presence of 10 micrograms/ml of Con A by 41.8% (p less than 0.01). T cells preincubated with 10 or 50 micrograms/ml of Con A and washed extensively were still able to inhibit U266 IgE synthesis in the absence of Con A by 41 and 46% (p less than 0.05 and p less than 0.02, respectively). The decrease in IgE measured was due to inhibition of newly formed IgE by U266, as shown by control experiments with cycloheximide. The inhibition was not due to the simple depletion of nutrient growth factors by the activated T cells, as it did not occur with MOLT-4, T cells that are very active metabolically; nor could it be reversed with medium containing IL 2 and B cell growth factors. Culture supernatants of Con A-activated T cells were also able to suppress IgE synthesis by U266 (21%; p less than 0.01), which suggests that upon appropriate activation, T cells secrete material(s) with inhibitory properties for IgE synthesis. Activation of T cells by mixed lymphocyte culture using puromycin-treated lymphoblastoid cell lines as stimulators also generated T cells that had suppressive activity for IgE synthesis. T cells activated with Con A and subsequently incubated with IgE demonstrated a diminished ability to suppress IgE synthesis. This observation is in agreement with the finding that patients with high levels of IgE may lack isotype-specific suppressor T cells for spontaneous IgE secretion. However, T cells from such patients have so far shown variable loss of IgE suppressive function. These results suggest that human IgE synthesis is susceptible to inhibition at a very differentiated stage, and this may be important in expression of allergic diseases.

This article has been cited by other articles:

				M. L. Reinagel, M. Gezen, P. J. Ferguson, S. Kuhn, E. N. Martin, and R. P. Taylor The Primate Erythrocyte Complement Receptor (CR1) as a Privileged Site: Binding of Immunoglobulin G to Erythrocyte CR1 Does Not Target Erythrocytes for Phagocytosis Blood, February 1, 1997; 89(3): 1068 - 1077. [Abstract] [Full Text] [PDF]