Passive Transfer Of Immune Serum Research Articles

Adoptive Transfer of Protective Immunity in Experimental Schistosomiasis in the Mouse

Passive transfer of immune serum alone did not confer protection to recipient mice irrespective of the routes of serum transfer or cercarial challenge of Schistosoma mansoni. Mice that received both sensitized cells and immune serum were protected against challenge by subcutaneous injection of cercariae but not by percutaneous exposure. The immune serum could be transferred as late as 8 days after subcutaneous challenge, suggesting that the protection was afforded in part by a late parasite killing mechanism which functions after the schistosomula have migrated through the lungs.

PASSIVE IMMUNISATION WITH SERUM AND IMMUNOGLOBULINS AGAINST DENTAL CARIES IN RHESUS MONKEYS

Active immunisation with Streptococcus mutans induced protection against dental caries in rhesus monkeys, and this was associated with serum antibodies. Passive transfer of immune serum with IgG, IgM, and IgA antibodies to Strep. mutans failed to induce protection against dental caries. However, when separated IgG, IgM, and IgA sera were given, IgG induced significant protection but IgA or IgM antibodies to Strep. mutans did not. IgA and IgM may compete or interfere with the protective effect of IgG antibodies, and the ratio of IgG/IgA and IgG/IgM antibodies might be an important factor in immunisation against dental caries.

ANAPHYLACTIC REACTIONS TO ENDOTOXIN IN GUINEA‐PIG TISSUES: RELATIONSHIP TO ENDOTOXIN TOXICITY

1 A lipopolysaccharide extract of Escherichia coli 026:B6 cells (026:B6(B) endotoxin) was shown to be toxic to normal adult guinea-pigs. 2 The agent had no action on isolated preparations of ileum and heart taken from normal adult guinea-pigs. 3 Ileal segments from animals actively immunized against 026:B6(B) endotoxin showed dose-dependent contractions when exposed to endotoxin. Desensitization phenomena were demonstrated. 4 Reactivity of 026:B6(B) endotoxin was transferred to isolated preparations of ileum and heart from normal animals by passive transfer of immune serum. 5 Tissue responses to 026:B6(B) were associated with release of ileal spasmogen into the bath medium. Mepyramine blocked the effects of this spasmogen at bath concentrations which caused little change in ileal responses to carbachol. 6 It is concluded that E. coli endotoxin can elicit anaphylactic reactions, and that this process may potentiate endotoxin toxicity in sensitized animals. However, endotoxin toxicity in guinea-pigs does not appear to depend on this kind of allergic process.

Autoimmune murine thyroiditis VII: Induction of the thyroid lesions by passive transfer of immune serum

Early granulocytic and later mononuclear infiltration of the thyroid was produced in mice by injection of mouse antisera to mouse thyroid extract. The lesions were first seen 4 days after injection and persisted as long as 40 days. Similar effects resulted from injection of antigen-antibody mixtures produced in antigen excess. The biphasic cellular response to immune serum suggests a two-phase mechanism in the induction of passive autoimmune thyroiditis in the mouse.

Specific and Non-Specific Immunosuppression in Chickens

Specific immunosuppression, caused by the passive transfer of immune sera, and non-specific immunosuppression, caused by ACTH, were investigated for possible interactions. The data confirm earlier studies which show that both types of suppression when administered independently cause reductions in humoral immune responsiveness. However, when both suppressive methods were administered simultaneously a level of suppression occurred which was not greater than that caused by either method alone. Additionally, when ACTH-induced non-specific immunosuppression was established in donors, passive transfers of sera from these donors did not cause suppression in the recipients.

Enhanced Immunosuppression in Bursectomized Chickens by Passive Transfer of Antibody ,

Three trials were conducted using commercial broiler cockerels to determine the immunological consequences of passive transfers of immune sera to bursectomized chickens. The data illustrate that passive transfers of immune sera to juvenile chickens which had been surgically bursectomized immediately after hatching caused a suppression of the primary hemagglutination response which was greater than that caused by bursectomy or passive transfer of immune sera alone. However, when these same birds were given a secondary challenge of antigen the resulting secondary hemagglutination response was normal. These data indicate that the passive transfer of immune sera to bursectomized chickens greatly limits their ability to mount primary humoral responses, while not affecting the ability to develop anamnestic immunity.

Immunity to exoerythrocytic forms of malaria. II. Passive transfer of immunity to exoerythrocytic forms

The passive transfer of heat-inactivated or nonheat-inactivated convalescent serum, from turkeys inoculated with Plasmodium fallax exoerythrocytic forms and treated with chloroquine to suppress the development of erythrocytic forms and the development of immunity to them, delayed the exoerythrocytic-form infection in turkeys inoculated intravenously with exoerythrocytic forms. The degree of exoerythrocyticform parasitization in cerebral tissue was significantly less in the experimental groups than the degree of parasitization in control groups, and the experimental birds continued gaining weight for a longer period than the control birds. The passive transfer of immune serum had an effect on the course of the exoerythrocytic-form infection equivalent to killing 90% of the exoerythrocytic-form inoculum. The immunity to exoerythrocytic forms is form-specific, since the infected, chloroquine-treated, serum donors were just as susceptible to an erythrocytic-form challenge infection as normal turkeys. In vitro studies demonstrated that heat-inactivated serum from turkeys immune to exoerythrocytic-form infections caused a precipitate to form at the small end of exoerythrocytic merozoites. This precipitate was not observed on merozoites mixed with control serum.

Sporozoite-induced immunity in mammalian malaria. A review.

SummaryBased on experimental evidence the following fundamental characteristics of sporozoite-induced immunity have, so far, been established. 1. The sporozoite stage of malaria parasites is strongly immunogenic. The intravenous injection of small numbers of attenuated, X-irradiated sporozoites induces a high degree of protective immunity and formation of anti-sporozoite antibodies. 2. Sporozoite-induced immunity is highly stage-specific. Its effects are mainly directed against the sporozoite stage. The erythrocytic stages of the parasite are not affected by this immune mechanism. 3. Considerable cross-protection and serologic cross-reactivity occur among sporozoites of different rodent malaria strains and species. 4. Sporozoites undergo antigenic changes during their process of maturation. These might possibly be correlated with the development of sporozoite infectivity. 5. The spleen does not play an essential role in sporozoite-induced protective immunity. The immunization of splenectomized animals renders them resistant to sporozoite challenge in the absence of antibodies detectable by the CSP reaction. 6. Sporozoite-induced immunity is, at least in part, serum-mediated. The incubation of sporozoites with immune serum considerably reduces their infectivity. The passive transfer of immune serum considerably increases the rate of sporozite clearance observed in normal animals. 7. The non-specific stimulation of the reticulo-endothelial system which occurs during sporozoite immunization is very shortlived. This reticulo-endothelial system stimulation does not play an important role in protection against sporozoite challenge.

Specificity of the inflammatory response in viral encephalitis. I. Adoptive immunization of immunosuppressed mice infected with Sindbis virus.

The viral-induced perivascular inflammatory response in Sindbis virus encephalitis of mice was shown to be immunologically specific. Mice were inoculated intracerebrally with Sindbis virus, and 24 hr later a single dose of cyclophosphamide was given which ablated the inflammatory response. 3 days after virus inoculation, cells and/or sera from specifically and nonspecifically sensitized donor mice were given, and the inflammatory reactions, virus content, and antibody response of recipients were examined 5 days later. Reconstitution of the viral inflammatory response required virus-specific sensitized lymph node cells and was enhanced when these lymph node cells were combined with bone marrow cells. Reconstitution was not achieved with Sindbis virus immune serum even when combined with nonspecifically sensitized cells. Combination of immune serum with Sindbis virus-sensitized cells did not produce an accentuation of the reaction. In distinction, reconstitution of the inflammatory reaction surrounding the stab wound was reconstituted with bone marrow cells from mice inoculated with Sindbis virus or control antigens. Reconstitution of the perivascular reaction was associated with a reduction in brain virus content. Although the transfer of Sindbis virus-sensitized lymph node cells and bone marrow cells resulted in the limited production of neutralizing antibody in the immunosuppressed recipient, the reduction in virus was significantly greater with the transfers of Sindbis virus-sensitized lymph node cells than with the passive transfer of immune serum alone.

Variants of Plasmodium berghei resistant to passive transfer of immune serum

Antiserum from infected rats suppressed stock strain P. berghei infections in mice, the degree of suppression depending in part on the nature and amount of antiserum used. Relatively large amounts of antiserum did not, however, produce more than a transient suppression of parasitemia, which eventually increased rapidly and killed the host. Parasites multiplying in antiserum-treated hosts were subinoculated into normal mice; although these parasites showed no apparent alteration in virulence, they did show a decreased susceptibility to the same antiserum. The present work suggests that there is some biological variability in populations of mouse P. berghei and that rat antiserum can change the immunological nature of these populations, i.e., render them relatively antiserum resistant.