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Clinical and Experimental Immunology logoLink to Clinical and Experimental Immunology
. 1969 Jan;4(1):29–39.

Studies on immunological paralysis. I. A consideration of macrophage involvement in the induction of paralysis and immunity by type II pneumococcal polysaccharide

J G Howard, G W Siskind
PMCID: PMC1579057  PMID: 4389160

Abstract

Induction of paralysis with SII in mice was slightly facilitated by administration in ten injections during 5 weeks as compared with the equivalent total dose in a single injection. No improvement was afforded by repeated injection with regard to the degree of immunization.

Mice which had been hyperimmunized with type II pneumococcal vaccine were relatively resistant to the induction of paralysis with SII, while animals which had been immunized with purified SII were as readily or more readily made tolerant than were normal control animals.

SII in particulate form (complexed with methylated bovine serum albumin) (SII–MBSA) was indistinguishable from soluble SII with regard to its immunogenicity and capacity to induce paralysis.

Paralysis could be induced by the intravenous injection of normally paralytogenic doses of either SII–MBSA or soluble SII into splenectomized mice. Such mice were no less readily paralysed than normal animals.

Polysaccharide still circulating in mice 10 days after injection of paralysing doses (100–500 μg) of SII was strongly immunogenic on transfer of serum to normal recipients.

Five hundred rad whole body irradiation 24 hr before injection of varying doses of SII failed to lower the paralysis threshold.

It is concluded that SII does not exist in distinct immunogenic (particulate) and paralytogenic (soluble) forms; that the macrophage appears to play no essential role in the initiation phase of an immune response to SII; and that the major portion of SII which is phagocytosed is ultimately involved in the induction of paralysis. The apparent anomaly of the latter feature could be explained by a continual release of phagocytosed SII from macrophages by exocytosis.

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Selected References

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