Mechanisms of B cell tolerance. II. Evidence for inhibition of antigen receptor expression as a mechanism of unresponsiveness

Klaus, G.G.; Abbas, A.K.; McElroy, P.J.

European Journal of Immunology 7(6): 387-393

1977


ISSN/ISBN: 0014-2980
PMID: 19264
DOI: 10.1002/eji.1830070612
Accession: 068518141

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Abstract
The experiments reported examined the fate and properties of antigen-binding B cells (ABC) during the induction of hapten-specific tolerance by 2,4-dinitrophenyl (DNP)-conjugated type 3 pneumococcal polysaccharide (S3). [Rabbit anti-mouse immunoglobulin was raised against 5563 myeloma protein.] After short (nontolerogenic) pulses of DNP-S3, anti-DNP Ig receptors were physically blocked by cell-bound antigen. Removal of extracellular tolerogen led to full functional recovery of ABC. After more prolonged (tolerogenic) exposures to DNP-S3 the degree of recovery of ABC following antigen-free culture was inversely related to the dose of antigen given. Regardless of the dose or duration of exposure to DNP-S3, cells initially binding antigen effectively cleared it from their membranes; after tolerogenic exposures, cells neither carried cell-bound DNP-S3, nor expressed functional receptors. Under conditions where tolerized cells recovered near normal levels of ABC after removal of extracellular antigen, these ABC appeared to display fewer receptors per cell than normal. B cell inactivation by DNP-S3 may involve the progressive and eventually irreversible inhibition of Ig receptor expression on DNP-reactive B cells, and not be due to stable blockade of receptors by cell-bound antigen. The relationship of this effect to other models of B cell inactivation (especially the similar phenomenon seen in immature B cells exposed to anti-receptor antisera) is discussed. [Sheep erythrocytes were used.].