Increased plaque-forming cell response to pneumococcal polysaccharide type III-coated sheep erythrocytes after priming with erythrocytes but not with polysaccharide

Byfield, Patricia

doi:10.1016/0008-8749(72)90123-2

Cited by 17 publications

(4 citation statements)

References 13 publications

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“…Cell source well (10-')~~~0 the administration of conjugate. The results obtained (Table 10) indicate that priming with carrier (horse erythrocytes) results in a substantial SSS-III-specific PFC response in mice immunized with a marginally immunogenic dose of conjugate (SSS-III-horse erythrocytes), as expected (Table 10; groups A versus B, P < 0.05); such a response is due to the generation of carrier-specific helper T cells (4,15,16,32). Treatment with 100 jig of MPL did not decrease the magnitude of the helper T-cell-dependent response produced (Table 10; groups B versus C, P > 0.05).…”

Section: Resultssupporting

confidence: 65%

“…Pretreatment or priming with a subimmunogenic dose of carrier (horse erythrocytes) then permits mice to generate an antibody response upon immunization with amounts of the conjugate (SSS-Ill-horse erythrocytes) that would otherwise not be immunogenic in unprimed mice (32). Such an antibody response has been shown to be both specific for SSS-III and dependent upon the presence of carrier-specific helper T cells generated as a result of priming with carrier (15,16).…”

Section: Methodsmentioning

confidence: 99%

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Inactivation of suppressor T-cell activity by nontoxic monophosphoryl lipid A

et al. 1988

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Treatment with nontoxic monophosphoryl lipid A (MPL), which was derived from a polysaccharidedeficient, heptoseless Re mutant of Salmonella typhimurium, was found to inactivate suppressor T-cell activity, as evidenced by a decrease in the degree of low-dose immunological paralysis expressed and an increase in the magnitude of the antibody response to type III pneumococcal polysaccharide. The effects produced, which could not be attributed to the polyclonal activation of immune B cells by MPL, were dependent upon the dose of MPL used, as well as the time when MPL was given relative to low-dose priming or immunization with type III pneumococcal polysaccharide. Neither amplifier nor helper T-cell activity was decreased by treatment with the same, or larger, doses of MPL. The significance of these findings to the use of MPL as an immunological adjuvant or an immunomodulating agent is discussed.

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Section: Resultssupporting

confidence: 65%

Section: Methodsmentioning

confidence: 99%

Inactivation of suppressor T-cell activity by nontoxic monophosphoryl lipid A

et al. 1988

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“…It must be stressed that not all polysaccharides indiscriminately possess this capacity. Pneumococcal polysaccharide Type III injected into mice 3 days before SRBC has been reported not to influence the eventual response to the erythrocytes (31).…”

Section: Discussionmentioning

confidence: 97%

Regulation of Immunoglobulin Synthesis by Dextran

Battisto

Pappas

1973

The Journal of Experimental Medicine

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Dextran, of the variety commonly used as plasma expander, markedly altered antibody synthesis to an unrelated antigenic stimulus, SRBC, in two animal species, guinea pig and mouse. The time at which dextran was administered relative to antigen was found to be most critical for increasing or decreasing the number of IgM and IgG PFC. Furthermore, these times differed for the two species studied. Typically, when given to guinea pigs 6 h before SRBC, dextran caused a 20-fold rise in IgM-producing cells but had little effect upon IgG synthesis. However, if dextran preceded antigen by 24 h the same magnitude of increase was seen in IgG-forming cells while a decrease in IgM-producing cells occurred. In mice, a short 2 h interval between dextran and antigen favored cells synthesizing IgG and not those producing IgM. A longer 6 to 24 h lapse between dextran and antigen resulted again in an inverted pattern, i.e., an increase in IgM and a decrease in IgG-producing cells. In both species, if dextran was given 48 h before antigen, synthesis of IgG markedly decreased. At the cellular level dextran activated those B cells already in the vascular compartment. In stimulating the IgM response to SRBC, dextran appears either to substitute for T cells or to amplify the effects of that small number of T cells still present in bone marrow preparations. Dextran-altered mouse B cells synthesized SRBC-specific IgG in the presence of normal T cells at an earlier time than did normal B and T cells. However, dextran was unable to cause blastogenesis in vitro of guinea pig lymph node cells or mouse B, T, and spleen cells. The data suggest at least two effects that T cells exert upon B cells. One is to stimulate more B cells to produce IgM, a function accomplished by endotoxins, PWM, PPD, and the simple polysaccharide dextran. The other is to trigger shifts in synthesis of immunoglobulins M and G. Our observations are compatible with the view that a single cell is capable of synthesizing both of these immunoglobulins and that the stimulating factor for one may cause cessation of the other.

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“…Thus, the primary response to purified type III pneumococcal polysaccharide may be accentuated by immunization with polysaccharide coated on sheep red cells if the recipient animals have received prior immunization with the sheep red cell carrier (50). Prior sensitization of the host with an unrelated bacterium such as Corynebacteriumt parzunt may also augment the antibody response to capsular polysaccharide (51), a phenomenon possibly related to the immunopotentiating effect of macrophages activated by intact bacteria.…”

Section: Of the 70 Children Admitted To The Children's Hospitalmentioning

confidence: 99%

Circulating polyribophosphate in Hemophilus influenzae, type b meningitis. Correlation with clinical course and antibody response.

O'Reilly¹,

Anderson²,

Ingram³

et al. 1975

J. Clin. Invest.

117

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A B S T R A C T In systemic infections caused by Hemophilus influenzae, type b, the capsular polysaccharide, polyribophosphate, is released into the circulation. Polyribophosphate was quantitated in serial serum and cerebrospinal fluid samples from 45 children with H. influenzae, type b meningitis by means of a radiolabeled antigen-binding inhibition assay. Polyribophosphate was regularly found in acute serum and cerebrospinal fluid samples and could be detected in unbound form for periods of 1-30 days after initiation of effective therapy. Complexes of polyribophosphate dissociable with acid and pepsin were detected in serum samples from 17 patients, in one case for a period of 145 days after hospitalization. Polyribophosphate levels and patterns of clearance were studied in relation to hospital course and antibody response. Patients with prolonged antigenemia had protracted fevers and severe neurological symptoms during hospitalization, frequently with focal complications. Antipolyribophosphate antibody responses were detected during the first 100 days of convalescence by radioimmunoassay in 79% of the patients studied, including 60% of the children 1 yr or less in age. The intensity of antibody response although clearly related to the age of the patient, was more reliably predicted by the efficiency of antigen clearance. Antibody responses were uniformly of low magnitude in patients with prolonged antigenemia, irrespective of age. Paients who failed to develop antibody to polyribophosphate after meningitis also exhibited impaired antigen clearance. These studies suggest that mechanisms necessary for clearance of polyribophosphate may influence

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Increased plaque-forming cell response to pneumococcal polysaccharide type III-coated sheep erythrocytes after priming with erythrocytes but not with polysaccharide

Cited by 17 publications

References 13 publications

Inactivation of suppressor T-cell activity by nontoxic monophosphoryl lipid A

Inactivation of suppressor T-cell activity by nontoxic monophosphoryl lipid A

Regulation of Immunoglobulin Synthesis by Dextran

Circulating polyribophosphate in Hemophilus influenzae, type b meningitis. Correlation with clinical course and antibody response.

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