Studies on the Control of Antibody Synthesis

Brody, Neil; Walker, Josephine G.; Siskind, Gregory W.

doi:10.1084/jem.126.1.81

Cited by 105 publications

(25 citation statements)

References 14 publications

(14 reference statements)

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“…Fc dependence was implicated by the finding that IgG-mediated suppression in many cases was nonepitope-specific (11, 12, 14 -16), i.e., that IgG specific for one epitope suppresses the response to other epitopes on the Ag. In contrast, epitope-specific suppression has also been observed (17,18). In a novel approach to study the Fc dependence of suppression, we recently showed that IgG can suppress the response to SRBC in mice lacking Fc␥RIIB (Fc␥RIIB Ϫ/Ϫ ), Fc␥RI and III (owing to the lack of the common ␥-chain (FcR␥), Fc␥RI, II, and III (Fc␥RIIB Ϫ/Ϫ ϫ FcR␥ Ϫ/Ϫ double knockouts) or the neonatal FcR, FcRn (owing to the lack of ␤ 2 -microglobulin, which constitutes part of the receptor).…”

mentioning

confidence: 84%

FcγRIIB in IgG-Mediated Suppression of Antibody Responses: Different Impact In Vivo and In Vitro

Karlsson

Getahun

Heyman

2001

The Journal of Immunology

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The suppressive effect of IgG on Ab responses to particulate Ags such as erythrocytes is well documented. IgG-mediated suppression is used clinically in rhesus prophylaxis to prevent RhD-negative mothers from becoming immunized against their Rh D-positive fetuses. We have recently shown that IgG anti-SRBC, passively administered together with SRBC, can induce efficient suppression of primary Ab responses to SRBC in mice lacking the known FcRs for IgG (FcγRI, FcγIII, and FcγRIIB or the neonatal FcR). The lack of a demonstrable effect of the inhibitory FcγRIIB was particularly surprising, and, in this study, the involvement of this receptor is further investigated during broader experimental conditions. The data show that SRBC-specific IgG administered up to 5 days after SRBC can induce suppression both in wild-type and FcγRIIB-deficient mice. Suppression of secondary Ab responses to SRBC in vivo was similar in the two strains. In contrast, IgG-mediated suppression of Ab responses in vitro was impaired in cultures with primed FcγRIIB-deficient spleen cells. In conclusion, inhibition of in vivo Ab responses to SRBC by passively administered IgG can take place via an FcγRIIB-independent pathway. This pathway causes >99% suppression and operates during all experimental conditions studied so far. The nature of the mechanism can at present only be hypothesized. Masking of epitopes and/or rapid elimination of IgG-Ag complexes would both be compatible with the observations.

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mentioning

confidence: 84%

FcγRIIB in IgG-Mediated Suppression of Antibody Responses: Different Impact In Vivo and In Vitro

Karlsson

Getahun

Heyman

2001

The Journal of Immunology

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“…This type of mechanism has been proposed by a number of workers in several experimental systems based on the ability of antiserum directed against certain determinants on a molecule or cell to specifically suppress the response to those determinants without affecting the response to other determinants on the same molecule or cell (29)(30)(31). The ability of T-cells to escape suppression may be explained in such a mechanism by their competing more efficiently than B-cells with the suppressing antiserum for the antigenic determinants or perhaps by their being directed against different determinants than the B-cells.…”

Section: Resultsmentioning

confidence: 99%

Regulation of the Immune Response

Kappler

Hoffmann

Dutton

1971

The Journal of Experimental Medicine

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The effect of passively transfered antiserum against sheep erythrocytes (SRBC) on the antigen stimulated increase of SRBC-specific plaque-forming cells (anti-SRBC-PFC) and SRBC-specific thymus-derived lymphocytes (SRBC-specific T-cells) in the mouse spleen was examined. A dose of antiserum which severely suppressed the development of anti-SRBC-PFC did not prevent the increase in SRBC-specific T-cells, as measured by their ability to cooperate in the in vitro response to trinitrophenylated (TNP) SRBC. It was shown that the insensitivity of these T-cells to antiserum could not be explained by their low antigen requirement as compared to that of PFC. In the in vivo response of mice to TNP-SRBC, antibody specific for TNP suppressed the appearance of both anti-TNP- and anti-SRBC-PFC. The presence of free SRBC specifically prevented the suppression of the anti-SRBC-PFC. These observations are consistent with opsonization by phagocytic cells as the primary means of the observed suppression of PFC development by antibody.

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“…The potential to modulate an immune response by systemic immunization with antigen bound by antibody has been recognized for some time (11,26,33,36,47,54,68,75,78,79). More recent work has begun to elucidate some of the underlying molecular mechanisms by which antibody may alter an immune response.…”

Section: Discussionmentioning

confidence: 99%

Monoclonal Antibody-Mediated Modulation of the Humoral Immune Response against Mucosally AppliedStreptococcus mutans

et al. 2000

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Systemic immunization with antigen coupled to monoclonal antibody (MAb) has been used by several investigators to increase the number of MAb-producing hybridomas against an antigen and to elicit antibodies specific for poorly immunogenic epitopes. This strategy has implications for vaccine design in that protective immunity is not necessarily directed at immunodominant epitopes of pathogens and may be improved by deliberately shifting the immune response toward subdominant epitopes. To our knowledge, no studies to date have addressed the potential for immunomodulatory activity mediated by MAbs bound to mucosally applied antigen. To test whether administration of an exogenous MAb directed against a streptococcal surface protein could influence the humoral immune response, BALB/c mice were immunized orally by gastric intubation or intranasally with Streptococcus mutans alone or S. mutans complexed with a MAb directed against the major surface protein P1. Significant changes in the subclass distribution, as well as the specificity, of anti-P1 serum immunoglobulin G antibodies were demonstrated in groups of mice which received S. mutans coated with the anti-P1 MAb versus those which received S. mutans alone. Alterations in the humoral immune response were dependent on the amount of anti-P1 MAb used to coat the bacteria. In addition, differences in the anti-P1 immune responses were observed between groups of mice immunized via oral versus intranasal routes. In summary, an exogenous MAb complexed with a streptococcal antigen prior to mucosal immunization can influence the immunoglobulin isotype and specificity of the host humoral immune response against the antigen.

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Studies on the Control of Antibody Synthesis

Cited by 105 publications

References 14 publications

FcγRIIB in IgG-Mediated Suppression of Antibody Responses: Different Impact In Vivo and In Vitro

FcγRIIB in IgG-Mediated Suppression of Antibody Responses: Different Impact In Vivo and In Vitro

Regulation of the Immune Response

Monoclonal Antibody-Mediated Modulation of the Humoral Immune Response against Mucosally AppliedStreptococcus mutans

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