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Mechanisms of B cell tolerance
Author(s) -
Klaus G. G. B.,
Abbas A. K.,
Mcelroy P. J.
Publication year - 1977
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830070612
Subject(s) - antigen , receptor , dinitrophenyl , biology , b cell , hapten , extracellular , microbiology and biotechnology , b cell receptor , cell , t cell , immunology , antibody , biochemistry , immune system
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). We found that (a) 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. (b) 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, (c) 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, (d) 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. We therefore propose that B cell inactivation by DNP‐S3 involves the progressive and eventually irreversible inhibition of Ig receptor expression on DNP‐reactive B cells, and is not 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.