The Role of Suppressor T Cells in the Development of Low-Dose Paralysis to Type Iii Pneumococcal Polysaccaride

Baker, Phillip J.; Burns, William H.; Prescott, Benjamin; Stashak, Philip W.; Amsbaugh, Diana F.

doi:10.1016/b978-0-12-401650-7.50048-x

Cited by 28 publications

(71 citation statements)

References 15 publications

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“…The procedure used for treating spleen cells with these monoclonal antibodies in the presence of complement (C'), as well as information concerning their specificity and immunologic characteristics, have been given (4). In all cell transfer experiments, mice were injected (i.v.)…”

Section: Treatment Of Cells With Monoclonal Antibodiesmentioning

confidence: 99%

Activation of antigen-specific suppressor T cells by B cells from mice immunized with type III pneumococcal polysaccharide.

Taylor¹,

Stashak²,

Caldes³

et al. 1983

The Journal of Experimental Medicine

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The transfer of B lymphocytes from mice immunized with type III pneumococcal polysaccharide (SSS-III) results in antigen-specific suppression of the antibody response of recipients immunized with SSS-III. Such suppression shares many features associated with low-dose paralysis, a phenomenon mediated by suppressor T cells; it reaches maximal levels 3 d after the transfer of viable or irradiated immune B cells and can be eliminated by the depletion of SSS-III-binding cells from spleen cell suspensions before transfer. In a two-step cell transfer experiment, purified T lymphocytes, isolated from recipients previously given immune B cells, caused suppression upon transfer to other mice immunized with SSS-III. Also, B-cell-induced suppression could be abrogated in a competitive manner by the infusion of amplifier T lymphocytes, as was previously demonstrated in the case of low-dose paralysis. These findings suggest that B cell surface components, presumably the idiotypic determinants of cell-associated antibody specific for SSS-III, are instrumental in activating suppressor T cells involved in regulating the magnitude of the antibody response to SSS-III.

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Section: Treatment Of Cells With Monoclonal Antibodiesmentioning

confidence: 99%

Activation of antigen-specific suppressor T cells by B cells from mice immunized with type III pneumococcal polysaccharide.

Taylor¹,

Stashak²,

Caldes³

et al. 1983

The Journal of Experimental Medicine

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“…The presence of free CPS in conjugate formulations is known to suppress the Thelper cell-dependent anti-CPS response after systemic immunization (2,43). In the present study, the small-M r conjugates prepared with either ADH or RA contained 50 and 66% free CPS, respectively.…”

Section: Discussionmentioning

confidence: 71%

Group BStreptococcusCapsular Polysaccharide-Cholera Toxin B Subunit Conjugate Vaccines Prepared by Different Methods for Intranasal Immunization

et al. 2001

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Group B Streptococcus (GBS) type III capsular polysaccharide (CPS III) was conjugated to recombinant cholera toxin B subunit (rCTB) using three different methods which employed (i) cystamine and N-succinimidyl-3-(2-pyridyldithio)propionate (SPDP), (ii) carbodiimide with adipic acid dihydrazide (ADH) as a spacer, or (iii) reductive amination (RA). The CPS III-rCTB conjugates were divided into large-and smallmolecular-weight (M r ) fractions, and the immunogenicities of the different preparations after intranasal (i.n.) immunization were studied in mice.

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“…The magnitude of the NCF-lgM antibody-induced suppression was comparable with that produced in low-dose paralysis' which has been attributed to the action of suppressor T cells (Baker, 1975;Baker et al, 1982). The latter workers have used doses of SIII ranging from 0-001-0-5 /ig to prime mice while a standard challenge dose of 0-5 /tg SIII was administered from between 2 to 25 days after priming.…”

Section: Discussionmentioning

confidence: 90%

“…The apparent failure to induce low-dose paralysis in athymic (nude) mice has also been used to support the notion that low-dose paralysis to SIII is mediated by suppressor T cells (Baker et al, , 1982. However, other reports have indicated that, on some occasions, low-dose paralysis can be produced in nude mice (Braley-Mullen, 1978).…”

Section: Discussionmentioning

confidence: 95%

“…Athymic (nude) mice do not produce the hybrid CF-IgM/A anti-SIII antibodies (Kearney and Johnstone, 1984). ALSinduced enhancement of direct PFC (Baker et ai, 1974) or inhibition of lowdose tolerance by treatment of adoptively transferred primed cells with monoclonal anti-Thy-1,2 antibody (Baker et al, 1982) may influence the relative proportions of the different cells producing direct plaques by mechanisms other than via suppressor T cells.…”

Section: Discussionmentioning

confidence: 99%

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THE ROLE OF A FUNCTIONALLY DISTINCT IgM ANTI‐TYPE III PNEUMOCOCCAL POLYSACCHARIDE (SIII) IN LOW‐DOSE PARALYSIS TO SIII IN MICE

Kearney¹,

Andrews²,

Johnstone³

1986

Aust J Exp Biol Med

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Summary.Prior treatment (priming) with a weakly immunogenic dose of TVpe 111 pneumococcal polysaccharide (SIII) results in the development of an antigen-specific state of unresponsiveness termed low-dose paralysis which is believed to be mediated by suppressor T cells. The present findings show that the passive administration of functionally distinct non-complement-fixing (NCF) IgM anti-SIII antibodies either in monoclonal form or from protein-A absorbed immune serum could significantly suppress the direct plaque-forming cell (PFC) response to an immunogenic dose of SIII administered concurrently. The degree of suppression was comparable with that induced by low-dose paralysis. Low-dose paralysis was consistently induced in athymic (nude) mice 4 days, but not 3 days, after priming with a low dose of SIII, and was associated with the delayed appearance of NCF-IgM anti-SIII in the serum of athymic mice. In contrast, low-dose paralysis was readily induced in normal BALB/c mice 3 days after priming when NCF-lgM anti-SlU antibodies were present. Comparable inhibiton of the direct anti-SIH PFC response was observed when Concanavalin A (Con A) or NCF-lgM anti-Sill serum was administered with Sill antigen. That Con A and NCF-lgM anti-SIII together did not produce additive suppression was attributed to the adsorption of NCF-lgM anti-SIII antibodies to Con A. Complement-dependent single radial haemolysis mediated by CF hybrid igM/A or CF-IgM anti-SIII serum was blocked by monoclonal NCF-lgM or IgA anti-SIII antibodies and indicated that each of the antibodies was specific for the same Slll-determinant. Evidence is presented to show that low-dose paralysis in the CF-IgM response to Sill is not mediated by suppressor T cells but can be attributed to highly avid NCF-lgM anti-SIII antibodies, formed preferentially to low doses of SIII, being able to reduce the immunogenicity of SIII administered subsequently.We propose that low-dose paralysis to Sill is the result of an immunobiological function of highly avid NCF-lgM anti-SIII antibodies which not only confer resistance against capsulated pneumococci but preferentially bind soluble Slll-antigen to reduce its immunogenicity and thereby protect specific CF-lgM positive B cells from being rendered tolerant by direct contact with higher doses of Sill antigen.

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The Role of Suppressor T Cells in the Development of Low-Dose Paralysis to Type Iii Pneumococcal Polysaccaride

Cited by 28 publications

References 15 publications

Activation of antigen-specific suppressor T cells by B cells from mice immunized with type III pneumococcal polysaccharide.

Activation of antigen-specific suppressor T cells by B cells from mice immunized with type III pneumococcal polysaccharide.

Group BStreptococcusCapsular Polysaccharide-Cholera Toxin B Subunit Conjugate Vaccines Prepared by Different Methods for Intranasal Immunization

THE ROLE OF A FUNCTIONALLY DISTINCT IgM ANTI‐TYPE III PNEUMOCOCCAL POLYSACCHARIDE (SIII) IN LOW‐DOSE PARALYSIS TO SIII IN MICE

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