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  • Title: Endogenous secretion of IL-4 maintains growth and Thy-1 expression of a transformed B cell clone.
    Author: Louie SW, Ramirez LM, Krieg AM, Maliszewski CR, Bishop GA.
    Journal: J Immunol; 1993 Jan 15; 150(2):399-406. PubMed ID: 8093458.
    Abstract:
    The CD5+ B cell lymphoma clone, CH12.LX, endogenously produces IL-4. Blocking the binding of this IL-4 to its cellular receptor inhibited the continuous proliferation of CH12.LX. mAb specific for either IL-4 or the IL-4R profoundly and specifically inhibited the proliferation of CH12.LX cells in a concentration-dependent manner, within 4 h after the addition of mAb. The addition of exogenous rIL-4 alone to CH12.LX cells had no effect on either proliferation or antibody secretion. However, exogenous rIL-4 was able to counteract the effects of anti-IL-4 antibody. Treatment of CH12.LX cells with antisense RNA oligodeoxynucleotides to IL-4 also specifically inhibited cell proliferation and decreased the levels of IL-4 secreted into the culture supernatants by more than 50%, without effect on total RNA or protein synthesis. Effects of antisense IL-4 were also blocked by addition of exogenous IL-4. Control oligodeoxynucleotides of equal size and base composition had no effect, and IL-4 antisense oligodeoxynucleotides did not effect the growth of a B cell lymphoma clone which does not produce IL-4. Blocking the binding of endogenously produced IL-4 to CH12.LX cells did not change the levels of membrane IL-4R or CD5 molecules. However, the constitutive expression of Thy-1 by these B cells was markedly decreased, and anti-Thy-1 antibodies decreased proliferation and PMA-induced aggregation of CH12.LX cells. Autocrine secretion of IL-4 thus appears to be required both for the continuous proliferation of CH12.LX B cells, as well as their expression of Thy-1, which may function either as a homotypic adhesion molecule or a signal transduction molecule for these cells. These findings indicate that endogenously produced lymphokines may play a critical role in the maintenance of B cell hyperproliferative disorders.
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