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PubMed1998

Analysis of the persistence of humoral and cellular immunity in children and adults immunized with varicella vaccine.

The persistence of humoral and cellular immunity to varicella-zoster virus (VZV) was evaluated in 60 children and 18 adults immunized with live attenuated VZV vaccine. At a mean of 5 years after vaccination, 93% of children and 94% of adults had IgG antibodies to VZV as determined by ELISA. VZV antibody concentrations were significantly higher at 5 years than at 1 year after immunization in children and adults. Cell-mediated immunity to VZV was detected in 87% of children and 94% of adults at 5 years. The mean stimulation index was significantly higher at 5 years than at 1 year among children and adults. Cytokine responses to VZV, including interleukin-2, interferon-gamma, and interleukin-10 were equivalent between children and adults at 5 years. In summary, varicella immunization induced long-term humoral and cellular immunity, and initial differences between cell-mediated responses in children and adults diminished over time.

Adolescent↗
PubMed2002

Age-related differences in the immune response to immunization with human Abeta42 peptide.

Several studies show that plaque burden is resolved in young to middle-aged amyloid precursor protein transgenic mice after rigorous immunization with Abeta42 peptide. We determined if wild-type 20-month-old and 3-month-old animals could produce high-titer antibody against Abeta42 with a less strenuous immunization protocol. All treated young animals mounted a high-titer (20,000-50,000) response after two immunizations and sustained a strong response for 6 months following the initial treatment with Abeta42. However, 6 of 8 immunized aged animals did not respond after three immunizations. The 2 responding aged mice produced low-titer antibody (5,000-10,000), which rapidly declined to control levels within 5 weeks after the third immunization. Aged animals may require alternate strategies for successful vaccination, such as inclusion of stimulatory cytokines or better adjuvants. If tolerance to Abeta42 underlies the poor response observed in aged animals, then a mechanism to overcome this response will have to be investigated.

Age Factors↗
PubMed1976

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines. II. Kinetics of neutralizing antibody responses in donors and adoptively immunized recipients.

Lymphoid cell responses to immunization with various formalin-inactivated Venezuelan equine encephalomyelitis (VEE) virus vaccines were monitored in mice by assessment of the development of both the neutralizing antibody response in sera of spleen cell donors and the adoptive neutralizing antibody response induced by spleen cell transfer in recipients. Donors immunized intraperitoneally with formalin-inactivated VEE vaccine (a single dose or a dose on three consecutive days) developed early serum neutralizing antibody responses (larger than or equal to 1:88-1:100) by seven days after immunization. Recipients of spleen cells from such mice were, however, incapable of eliciting a neutralizing antibody response (less than or equal to 1:10). Only spleen cells from donors immunized with inactivated VEE vaccine plus adjuvants (particularly complete Freund's adjuvant and Bordetella pertussis) were consistently capable of producing early, high-titer serum neutralizing antibody responses in adoptively immunized recipients (larger than or equal to 1:50-1:120 on day 4). The magnitude of neutralizing antibody responses of donors to inactivated VEE vaccines did not serve as a useful indicator of whether spleen cells from such mice could adoptively induce antibody responses in recipients. Finally, treatment of immune spleen cells with rabbit antiserum to mouse thymocytes, but not with rabbit antiserum to mouse gamma-globulin or normal rabbit serum, abolished the capacity of such cells to transfer an antibody response adoptively.

Adjuvants, Immunologic↗
PubMed2000

Synthetic oligodeoxynucleotide containing CpG motif induces an anti-polysaccharide type 1-like immune response after immunization of mice with Haemophilus influenzae type b conjugate vaccine.

Synthetic oligodeoxynucleotides containing CpG motifs [immunostimulatory sequences (ISS)] have been described as potent adjuvants of type 1 immune responses when co-administered with protein or peptide vaccines. To investigate their role in the immune response to polysaccharides (CHO), different preparations of anti-Haemophilus influenzae type b (Hib) conjugate vaccine were administered to mice. The unconjugated CHO did not induce the synthesis of specific antibodies even in the presence of ISS. On the other hand, anti-CHO-specific antibodies significantly increased in the presence of ISS, when tetanus (TT) or diphtheria [cross-reacting material (CRM)] toxoid-conjugated CHO were used to immunize mice. The adjuvant effect was also observed for the immune response against the carrier protein (TT and CRM). ISS insured an early and long-lasting specific IgG production. The effects of ISS on the anti-CHO immune response could be attributed to the amplification of the T help provided by the carrier. The analysis of anti-CHO IgG subclasses showed a significant increase of IgG2a and IgG3 in the presence of ISS. ISS caused a rapid release of IL-12 and IFN-gamma in sera from treated mice. This data provide a first evidence for the ability of ISS to induce an anti-CHO type 1-like immune response and demonstrate that ISS have the potential to increase host antibody response against both the CHO and the protein component of a conjugated vaccine.

Adjuvants, Immunologic↗
PubMed1996

The association between lung innate immunity and differential airway antigen-specific immune responses.

The mechanisms involved in the differential regulation of airway immune responses in atopic versus non-atopic individuals are poorly understood. In this study, the association between non-specific immunity and the differential airway antigen-specific immune responses was examined in a murine model. The disparity in antigen-specific IgE and IgG2a productions between the two strains of mice was observed to be significant. C57BL/6J mice were much more efficient than BALB/cJ mice in making IgE antibody to inhaled ovalbumin (OVA) antigen. On the contrary, BALB/cJ mice did make more IgG2a antibodies than C57BL/6J mice to inhaled OVA. These findings suggest that in C57BL/6J mouse strain a predominant Th2 type of immune response develops in response to inhaled OVA antigen. In contrast, BALB/cJ mice mount a Th1 type of immune response to aerosolized OVA antigen. Furthermore, after lipopolysaccharide (LPS) stimulation, the IL-12 mRNA expression of lung-derived cells from BALB/cJ mice was higher than that from C57BL/6J cells. However, the lung-derived cells of C57BL/6J mice stimulated by LPS produced higher levels of IL-10 and prostaglandin E2 than BALB/cJ lung-derived cells did. Therefore, our study demonstrated that the difference of lung-derived cells in their ability to produce cytokine and prostaglandin between BALB/cJ and C57BL/6J mice correlates well with the type of the airway antigen-specific immune effector functions.

Animals↗
PubMed2005

Early life immune challenge alters innate immune responses to lipopolysaccharide: implications for host defense as adults.

Fever is the most common manifestation of the innate immune response to invading pathogens. Animals prevented from developing fever have increased morbidity and mortality to infection. We now show that early life events can program this innate immune response, in that rats that have been challenged neonatally with the immune stimulant lipopolysaccharide (LPS) have both suppressed febrile responses to LPS as adults and significantly reduced nuclear factor (NF)-kappaB activation in peripheral immune organs. This was associated with reduced levels of proinflammatory cytokines tumor necrosis factor (TNF)-alpha, and interleukin-6 (IL-6) in the plasma after adult LPS challenge, compared with animals that have received saline neonatally. In contrast, adult LPS challenge elicited higher corticosterone levels in the animals that had been treated neonatally with LPS. When this increased corticosterone response was negated by adrenalectomy or by administration of the glucocorticoid receptor antagonist RU-486, both the cytokine and febrile responses were normalized. This study indicates that the innate immune response can be programmed by a neonatal LPS challenge, whereby an amplified hypothalamic-pituitary-adrenal response causes reduced cytokine synthesis and an attenuated febrile response to an adult immune challenge. In light of the importance of fever in the host defense response, these alterations may have deleterious consequences on an individual's ability to combat disease later in life.

Adrenalectomy↗
PubMed1993

Mechanisms in immune recovery after bone marrow transplantation. Management of posttransplant immune deficiency.

PURPOSE: Bone marrow transplantation usually entails the ablation of the recipient's immune system. The recovery of immunity post-marrow transplantation is a complex process dependent on a number of pre- and posttransplant factors. This knowledge has led to the development of novel approaches to supportive care of the patient, as well as to methods of augmenting immunity. DESIGN: Hematopoietic growth factors are now used to speed neutrophil recovery. Certain lymphokines are being investigated for the enhancement of cell-mediated immunity, and gamma globulin preparations are used to support the deficiency in humoral immunity. CONCLUSIONS: This review summarizes the basic concepts of immune reconstitution posttransplant and discusses some of the therapeutic interventions that have been investigated. In addition, some general recommendations are offered regarding supportive care.

Anti-Infective Agents↗
PubMed1982

The immune response of the mouse to lymphocytic choriomeningitis virus. II. Active suppression of cell-mediated immunity by infection with high virus doses.

Infection of CBA/J mice with low doses of strain WE lymphocytic choriomeningitis (LCM) virus resulted in high cell-mediated and relatively low humoral virus-specific immune phenomena; anamnestic responses were marked. In contrast, infection with high doses of this virus induced no or low degrees of cell-mediated immune phenomena but higher antibody concentrations. Subsequent challenge of these mice did not reveal cell-mediated immunity. However, transfer of spleen cells from mice suppressed as to cell-mediated immunity together with virus into X-irradiated recipients led to marked anamnestic responses. Furthermore, when spleen cells from mice previously infected with low virus doses were injected into mice previously infected with high virus doses, cell-mediated immune phenomena could not be induced by concomitantly inoculated virus, although in controls anamnestic responses were readily evoked. Thus, infection with high doses of LCM virus actively suppressed LCM virus-specific cell-mediated immune responses but led to increased production of antibodies. suppressor cells could not be demonstrated.

Animals↗
PubMed2006

Humoral and cellular immune responses in sheep immunized with a 22 kilodalton exported protein of Mycobacterium avium subspecies paratuberculosis.

An immunogenic 22 kilodalton exported Mycobacterium avium subspecies paratuberculosis (MAP) lipoprotein (P22) was previously identified, and found to belong to the LppX/LprAFG family of mycobacterial lipoproteins. N-terminal polyhistidine-tagged P22 was produced and purified from Escherichia coli. Antibody recognition of P22, and interferon-gamma (IFN-gamma) responses in vitro using blood from a sheep vaccinated with Neoparasec, confirmed its immunogenicity. To evaluate the immunogenicity of P22 in vivo, five sheep were immunized with a single dose containing 0.8 mg recombinant P22 protein in adjuvant. Blood was collected at 4, 13 and 29 weeks post-immunization (p.i.) and tested for anti-P22 antibodies and P22-specific IFN-gamma production. P22-specific antibodies were detected by Western blot analysis in all five Neoparasec-immunized sheep at the three time points. Three out of five P22-immunized sheep produced P22-specific antibodies for up to 13 weeks p.i., and two gave a response at 29 weeks p.i. Recombinant P22 was able to stimulate significant IFN-gamma production in blood of P22-immunized sheep at 13 and 29 weeks p.i. Recombinant P22 also elicited an IFN-gamma response in blood of sheep immunized with Neoparasec.

Adjuvants, Immunologic↗
PubMed1993

Immunization of mice with baculovirus-derived recombinant SV40 large tumour antigen induces protective tumour immunity to a lethal challenge with SV40-transformed cells.

In this study, we examined the humoral immune responses and in vivo tumour immunity induced by baculovirus recombinant simian virus 40 (SV40) large tumour antigen (rSV40 T-ag). BALB/c mice immunized with rSV40 T-ag produced antibody responses that recognized SV40 large tumour antigen (T-ag) by ELISA. Analysis of these anti-SV40 T-ag responses indicated that the antibodies recognized epitopes associated with both the carboxy and amino terminus of SV40 T-ag. This pattern of SV40 T-ag epitope recognition was similar to that observed in anti-SV40 T-ag responses induced by inoculation with irradiated SV40-transformed cells. Mice immunized with either rSV40 T-ag or with the inactivated transformed cells were protected from a subsequent in vivo lethal tumour challenge with live SV40-transformed cells. These studies suggest that humoral immune responses induced by rSV40 T-ag are similar in epitope specificity to that induced by inactivated SV40-transformed cells. In addition, recombinant tumour-specific antigens from papovaviruses, such as SV40, can be used to induce tumour immunity which protects from a subsequent lethal tumour challenge. This study may provide insight into the use of recombinant tumour antigens as putative tumour vaccines and in the development of active immunotherapeutic strategies for treating virus-induced cancers.

Animals↗
PubMed1986

Genetic control of immunity to Trichinella spiralis in mice. Response of rapid- and slow-responder strains to immunization with parasite antigens.

Slow-responder C57BL/10 (B10) mice responded poorly to immunization with muscle larval antigen of Trichinella spiralis showing no accelerated loss of worms from a subsequent challenge infection. In contrast, rapid-responder NIH mice and (B10 X NIH) F1 mice developed high levels of immunity after immunization. Lymphocyte proliferation studies showed that immunized B10 mice did respond to in vitro restimulation with antigen, though less well than NIH mice. Failure of B10 mice to respond to immunization did not therefore reflect a failure to recognize larval antigen, a view confirmed by the fact that immunization was achieved using abbreviated enteral infections and, to a smaller extent, by parenterally administered muscle larvae.

Animals↗
PubMed1988

Protective immunity to malaria: studies with cloned lines of Plasmodium chabaudi chabaudi in CBA/Ca mice. III. Protective and suppressive responses induced by immunization with purified antigens.

The protective effect of affinity purified antigen has been investigated in an experimental model for malaria which shows a well marked recrudescence of parasitaemia, a feature of the disease in man. A monoclonal antibody (MoAb) recognizing an epitope common to two genetically distinct cloned lines of Plasmodium chabaudi (AS and CB), was used to purify a Mr250,000 polymorphic schizont antigen (PSA) from these parasites. The purified preparations were then examined for the presence of specific and cross-reactive epitopes by immunoprecipitation with a panel of MoAb raised against P. chabaudi AS. When tested previously on smears of parasitized blood by immunofluorescence, or against lysates of parasitized erythrocytes by immunoprecipitation, most of these MoAb had been found to be AS specific. When either AS or CB affinity purified Mr250,000 PSA was used as the target, these same MoAb immunoprecipitated both antigens, and in some cases, a number of associated polypeptides (AP) which copurify with the Mr250,000 PSA. Subsequently, mice were immunized with either the purified AS or CB antigens in Freund's complete adjuvant (FCA). Prechallenge sera were compared by indirect immunofluorescence and immunoprecipitation. Sera from mice immunized with AS antigen reacted strongly with AS and cross-reacted with CB parasite preparations. Pre-challenge serum from CB antigen immunized mice reacted well with CB, but only faintly with AS preparations. In mice immunized with the AS antigen and then challenged with either AS or CB parasites, the initial parasitaemias were delayed in appearance and the height of the peak parasitaemia reduced, an effect which was most pronounced after challenge with homologous parasites. Only homologous challenge of the mice immunized with CB antigen produced statistically significant modification of the initial parasitaemia. In the immunized mice challenged with homologous parasites, the delayed appearance and slightly reduced peak of the primary parasitaemia was associated with delayed resolution of the patent parasitaemia and significant enhancement of the recrudescence.

Animals↗
PubMed1995

Protective immunity against malaria: cellular changes in the liver vary according to the method of immunization.

Characterization of cells present in the extravascular compartment of murine liver was performed after different immunization procedures against the malaria parasite Plasmodium yoelii. Mice were immunized with live or irradiated sporozoites or with parasitized erythrocytes. Whatever the immunization protocol used, the mice were protected against a sporozoite challenge but each immunization procedure induced a specific profile of cell types. Immunization with irradiated sporozoite induce a significant increase in CD8+ lymphocytes, parasitized erythrocytes stimulates production of monocytes/macrophages and CD8+ lymphocytes while, after live sporozoites immunization, polymorphonuclear cells, macrophages/monocytes, B cells and a range of T cell subsets were increased in number.

Animals↗
PubMed1997

Antigen localisation regulates immune responses in a dose- and time-dependent fashion: a geographical view of immune reactivity.

This review summarises experimental evidence to illustrate that induction of immune reactivity depends upon antigen reaching and being available in lymphoid organs in a dose- and time-dependent manner. If antigen reaches lymph organs in a localised staggered manner and with a concentration gradient, a response is induced in the draining lymph node. Antigen-presenting cells are of critical importance to transport antigen from the periphery to local organised lymphoid tissue. If antigen is all over the lymphoid system, then it deletes all specific cells in the thymus or induces them within a few days; because of their limited life-span they then die off, leaving the repertoire depleted of this specificity. If antigen does not reach lymphoid organs it is ignored by immune cells. Once a response is induced, activated but not resting T cells will reach antigen outside lymphoid organs, whereas activated B cells differentiate into plasma cells in an inducing environment, mostly in lymphoid tissue including bone marrow, but also in chronic lymphoid-like infiltrations in peripheral organs. In immunopathology (when the infectious agent is known) or in autoimmunity (when the triggering infectious agent is not known or not recognised) lymphoid tissue may become organised close to the antigen (e.g. in organ-specific autoimmune diseases) and may thereby maintain an autoantigen-driven disease-causing immune response for a long time. The notion that native T cells get induced or silenced in the periphery may be questioned because induction can only occur in lymphoid organs providing anatomical structures where critical cell-cell interactions are properly guided and where, therefore, cells are likely to meet sufficiently frequently and in a critical milieu. Since overall immune reactivity critically depends upon the localisation of antigens in a dose- and time-dependent manner, it seems more likely-but this remains to be shown-that activated T cells may get exhausted in non-lymphoid peripheral tissues, whereas they are usually maintained in lymphoid organs. The critical role of antigen in regulating immune responses also has relevance for our understanding of immunological defence against epithelial and mesenchymal tumours, against many infectious diseases and for understanding autoimmunity and immunological memory. Collectively the data indicate that antigen, dependent upon localisation, dose and time, seems to be the simplest regulator of immune responses.

Adjuvants, Immunologic↗
PubMed1978

Mechanisms of immunity in typhus infection: some characteristics of intradermal Rickettsia mooseri infection in normal and immune guinea pigs.

Rickettsia mooseri infection in skin at sites of intradermal inoculation was studied in nonimmune and immune guinea pigs with respect to dynamics of infection, localization of rickettsiae within tissues, and gross and microscopic pathology. Intradermal inoculation of R. mooseri into nonimmune guinea pigs resulted in gross lesions which, in magnitude, were directly related to the number of rickettsiae inoculated. The lesions progressively enlarged through 3 or 4 days and remained enlarged through at least 7 days. Histological examination revealed an early acute inflammation which progressed to a predominantly monocyte-macrophage inflammation and subsequently condensed into lymphocyte-containing granulomatous foci. Rickettsiae in the skin at sites of inoculation increased in numbers from 6 h through 3 days, in parallel with the increasing diffuse monocyte-macrophage inflammatory response, and then declined markedly on days 4 or 5 as ganulomatous foci appeared. Some rickettsiae, however, persisted through at least day 7. Fluorescent-antibody studies suggested that R. mooseri infected only a subset of cells available, i.e., cells associated with the microvascular system. Dissemination of infection was demonstrated by the presence of rickettsiae in the skin at sites distant from the point of inoculation. Immune guinea pigs, made immune by intradermal infection with R. mooseri 12 days before intradermal challenge, displayed an accelerated response. The lesions were maximal by 24 to 48 h and subsequently regressed. The inflammatory response of immune guinea pigs was a greater magnitude than the response of similarly challenged nonimmune guinea pigs, and the respose from acute inflammation through the formation of granulomatous lesions was accelerated. The number of rickettsiae in the skin of immune guinea pigs declined steadily from the time of inoculation, until no rickettsiae were recovered on or after day 3. Furthermore, dissemination of rickettsiae to sites in skin distant from the site of inoculation was not demonstrable. The results are discussed in terms of pathogenesis and of immunity to typhus.

Animals↗
PubMed1992

Maternal immunization with gametocyte antigens as a means of providing protective immunity against Eimeria maxima in chickens.

In the present study, we wished to demonstrate the ability of surface gametocyte antigens to induce protective immunity against Eimeria maxima infections in chickens. In order to accomplish this goal, we employed maternal immunization as a means of providing large amounts of specific antibodies to offspring chicks. Upon challenge with sporulated E. maxima oocysts, chicks from hens immunized with affinity-purified gametocyte antigens showed greatly reduced oocyst production compared with chicks from sham-immunized hens. These results suggest that maternal immunization with gametocyte antigens can be used as a means to provide transmission-blocking immunity against E. maxima infections.

Animals↗
PubMed1993

Protective immunity induced in Aotus monkeys by a recombinant SERA protein of Plasmodium falciparum: adjuvant effects on induction of protective immunity.

We report the results of vaccination trial 2 of Panamanian Aotus monkeys with a recombinant blood-stage antigen, SERA 1, of the malaria parasite Plasmodium falciparum. Monkeys were immunized with SERA 1, a 262-amino-acid fragment (amino acids 24 to 285) of the 989-amino-acid SERA protein produced by the Honduras 1 strain of the parasite. Immunization mixtures contained 100 micrograms of recombinant SERA 1 protein per dose mixed with one of five different adjuvants. The protein mixed with either Freund's adjuvant or MF75.2 adjuvant stimulated protective immunity. When other P. falciparum antigens were included in the SERA 1-Freund's adjuvant mixture, no protective immunity was observed, although high anti-SERA 1 antibody titers were produced. Three other adjuvants mixed with SERA 1 failed to induce a protective immune response. These results, their relationship to those reported previously in the first vaccination trial (trial 1), and their relationships to the quantitative measurement of anti-SERA 1 antibodies in enzyme-linked immunosorbent assays provided insights into the induction of a protective immune response in vaccinated monkeys.

Adjuvants, Immunologic↗
PubMed1996

Susceptibility to Pneumocystis carinii infection: host responses of neonatal mice from immune or naive mothers and of immune or naive adults.

Mice from either naive or immunized dams were given intranasal inoculations of Pneumocystis carinii as neonates (24 to 48 h old). Lung P. carinii burdens increased through day 13 postinoculation in all pups and declined to nearly undetectable numbers by day 23 in pups from immune mothers. However, P. carinii numbers in pups from naive mothers did not begin to decline significantly until after day 33, and P. carinii organisms were still detectable in low numbers through day 45. In contrast, the lungs of naive or immunized adult mice contained detectable numbers of P. carinii organisms only up to 9 or 3 days, respectively, after inoculation. The onset of clearance of P. carinii organisms from the lungs of neonatal mice and naive adults was coincident with infiltration of neutrophils and CD4+ CD45RBlo cells into the alveolar spaces and increased titers of P. carinii-specific antibody in sera. Immunized dams had high levels of P. carinii-specific antibody in both their sera and milk, and pups from these dams had higher titers of P. carinii-specific antibody than did pups from naive dams. These data indicate that P. carinii survives for a much longer period in neonates than in adult mice, which is the result of a delay in the onset of the immune response in neonates. Furthermore, immunized mothers contributed to an early clearance of P. carinii organisms by their offspring presumably because of the transfer of P. carinii-specific antibody. However, the passively acquired antibody did not seem to have an effect until the neonates began to mount their own responses.

Animals↗