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IgA-binding factor suppresses synthesis of IgA in MOPC-315 plasmacytoma cells

Conference · · Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
OSTI ID:6966041
T cells with Fc receptors for IgA (T/sup ..cap alpha../ cells) and their products, IgA-binding factors (IgABF), have been implicated in the regulation of IgA expression by B cells. They have previously shown that an IgABF produced by IgA induced normal T cells or constitutively by the Fc/sup ..cap alpha../ R+ T cell lymphoma, BALENTL 8, is capable of suppressing the proliferation and the amount of secreted IgA by MOPC-315 cells. In the present studies, they demonstrate that: (a) suppression of proliferation and secretion requires surface membrane IgA on the target cell, (b) suppression exhibits rapid kinetics with maximal effect occurring by 3-4 hours, (c) suppression is reversible, and (d) suppression of secretion involves selective suppression of IgA synthesis as measured by /sup 3/H-leucine incorporation into immunoprecipitable IgA(non-IgA protein is unaffected). These findings indicate that IgA-isotype-specific effector molecules interact directly with their B cell targets through surface membrane immunoglobulin and cause a down regulation of immunoglobulin synthesis by the target. Current studies are underway to address whether this selective suppression of IgA is mediated at the transcriptional, translational or post-translational level. The use of MOPC-315 tumor cells as targets of T cell produced, isotype-specific, effector molecules should provide a unique model for the further analysis of isotype regulation at the molecular level.
Research Organization:
Univ. of Pennsylvania School of Medicine, Philadelphia
OSTI ID:
6966041
Report Number(s):
CONF-8604222-
Conference Information:
Journal Name: Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States) Journal Volume: 45:4
Country of Publication:
United States
Language:
English