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Results for “immunization”

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PubMed1989

Immune adherence and the processing of soluble complement-fixing antibody/DNA immune complexes in mice.

We have examined in mice the immune adherence (IA) reactivity and the fate (clearance kinetics and organ distribution) of a variety of preformed and nascent soluble antibody/125I-DNA immune complexes prepared at antibody excess. Parallel studies of the clearance kinetics and organ deposition of free DNA were also conducted. Preformed immune complexes prepared with large dsDNA bound to mouse platelets in vivo and exhibited clearance kinetics in general agreement with our previous observations in rabbits. Very little kidney deposition was evident for these immune complexes, but three to four times as many counts were found in the kidneys when free DNA was injected. Nascent immune complexes did form in the circulation, but in contradistinction to our previous studies of nascent immune complexes in rabbits and rhesus monkeys, these immune complexes did not demonstrate IA and had clearance kinetics and organ distributions intermediate between the preformed immune complexes and free DNA. Thus, complement-fixing antibody/DNA immune complexes that could form in the circulation might be cleared both via immune complex recognition mechanisms and via DNA recognition mechanisms. The role of IA in modulating the organ deposition of complement-fixing immune complexes is also discussed.

Animals↗

PubMed2005

Induction of serum and mucosal FIV-specific immune responses by intranasal immunization with p24Gag.

We examined the ability of FIV p24Gag to induce systemic and mucosal FIV-specific immune responses when delivered as a nasal immunogen alone, or with a mucosal adjuvant, Escherichia coli heat labile toxin LT(R192G). Nasal immunization with p24Gag alone induced FIV-specific immune responses but overall responses were weak, transient, and/or present only in a few animals. Co-administration of LT(R192G) resulted in strong FIV-specific serum IgG and enhanced salivary IgA responses. Moreover, FIV-specific IgA was detected in vaginal wash fluid from 6/6 cats co-immunized with LT(R192G) and p24Gag versus 1/6 immunized with p24Gag alone. This is the first report detailing induction of systemic or mucosal FIV-specific immune responses by nasal immunization alone. As such, this study demonstrates that nasal immunization of cats can be a relevant and effective route for the delivery of candidate vaccines. However, while nasal immunization of cats with p24Gag induces antigen-specific systemic immune responses, development of strong systemic and mucosal immune responses requires co-administration of a mucosal adjuvant, such as LT(R192G).

Adjuvants, Immunologic↗

PubMed1987

Quantitative analysis of the interaction between immune complex and C1q complement subcomponent. The role of interdomain interactions in rabbit IgG in binding of C1q to immune precipitates.

A novel method was developed for the analysis of the interaction of large multivalent ligands with surfaces (matrices) to analyse the binding of complement subcomponent C1q to immune precipitates. Our new evaluation method provides quantitative data characteristic of the C1q-immune-complex interaction and of the structure of the immune complex as well. To reveal the functional role of domain-domain interactions in the Fc part of IgG the binding of C1q to different anti-ovalbumin IgG-ovalbumin immune complexes was studied. Immune-complex precipitates composed of rabbit IgG in which the non-covalent or covalent bonds between the heavy chains had been eliminated were used. Non-covalent bonds were abolished by splitting off the CH3 domains, i.e. by using Facb fragments, and the covalent contact was broken by reduction and alkylation of the single inter-heavy-chain disulphide bond. The quantitative analysis of the binding curves provides a dissociation constant (K) of 200 nM for the interaction between C1q and immune precipitate formed from native IgG. Surprisingly, for immune precipitates composed of Facb fragments or IgG in which the inter-heavy-chain disulphide bond had been selectively reduced and alkylated, stronger binding (K = 30 nM) was observed. In this case, however, changes in the structure of the immune-complex matrix were also detected. These structural changes may account for the strengthening of the C1q-immune-complex interaction, which can be strongly influenced by the flexibility and the binding-site pattern of the immune-complex precipitates. These results suggest that domain-domain interactions in the Fc part of IgG affect the segmental mobility of IgG molecules and the spatial arrangement of the immune-complex matrix rather than the affinity of individual C1q-binding sites on IgG.

Animals↗

PubMed2002

Development of mixed Th1/Th2 type immune response and protection against Mycobacterium tuberculosis after rectal or subcutaneous immunization of newborn and adult mice with Mycobacterium bovis BCG.

Cell-mediated immunity plays a key role in containing the growth of Mycobacterium tuberculosis in the host. The induction of an antibody response or a mixed cell-mediated and humoral response is frequently associated with tuberculosis disease or a decrease in the ability to control M. tuberculosis load. We recently reported the induction of similar immune responses and protection by rectal, subcutaneous (SC) or intradermal administration of Mycobacterium bovis BCG in adult mice, guinea pigs and macaques. The rectal immunization, which did not induce the side-effects associated with parenteral routes (axillary adenitis) and which could be used to reduce the risks of viral transmission associated with unsafe injections in the developing world, was analysed and compared in newborn and adult BALB/c mice. The rectal and SC immunization induced, in mice immunized as newborns or as adults, a mixed T helper 1/T helper 2 (Th1/Th2) immune response; however, particularly in adult mice, after SC administration of BCG, the level of Th2 immune response is significantly higher than it is by the rectal route. Six months after immunization with BCG, rectal and SC delivery induced similar levels of protective immunity against a virulent challenge with M. tuberculosis strain (H37Rv) in mice immunized as adults, but the rectal BCG delivery triggered stronger protection than the SC delivery if mice were immunized as newborns.

Administration, Rectal↗

PubMed1980

Molecular structure of the immunity gene and immunity protein of the bacteriocinogenic plasmid Clo DF13.

The nucleotide sequence of the Clo DF13 DNA region comprising the immunity gene has been determined. We also elucidated the aminoacid sequence of the 40 N-terminal and 7 C-terminal aminoacids of the purified immunity protein. From analysis of the data obtained we were able to locate the immunity gene between 11.7 and 14.5% on the Clo DF13 map, and to determine the complete aminoacid sequence of the immunity protein. It was observed that the Clo DF13 immunity gene encodes an 85 aminoacid protein and is transcribed in the same direction as the cloacin gene. These experimental data support our model, presented elsewhere, which implicates that the cloacin and immunity genes of Clo DF13 are coordinately transcribed from the cloacin promoter. We also present DNA sequence data indicating that an extra ribosome binding site precedes the immunity gene on the polycistronic mRNA. This ribosome binding site might explain the fact that in cloacinogenic cells more immunity protein than cloacin is synthesized. The comparison of the complete aminoacid sequence of the Clo DF13 immunity protein, with the aminoacid sequence data of the purified, comparable Col E3 immunity protein revealed that both proteins have extensive homologies in primary and secondary structure, although they are exchangeable only to a low extent in vivo and in vitro. It was also observed that a lysine residue was modified in immunity protein isolated from excreted bacteriocin complexes.

Amino Acid Sequence↗

PubMed2006

Serum immune responses predict rapid disease progression among children with Crohn's disease: immune responses predict disease progression.

BACKGROUND AND AIM: Crohn's disease (CD) is a heterogeneous disorder characterized by diverse clinical phenotypes. Childhood-onset CD has been described as a more aggressive phenotype. Genetic and immune factors may influence disease phenotype and clinical course. We examined the association of immune responses to microbial antigens with disease behavior and prospectively determined the influence of immune reactivity on disease progression in pediatric CD patients. METHODS: Sera were collected from 196 pediatric CD cases and tested for immune responses: anti-I2, anti-outer membrane protein C (anti-OmpC), anti-CBir1 flagellin (anti-CBir1), and anti-Saccharomyces-cerevisiae (ASCA) using ELISA. Associations between immune responses and clinical phenotype were evaluated. RESULTS: Fifty-eight patients (28%) developed internal penetrating and/or stricturing (IP/S) disease after a median follow-up of 18 months. Both anti-OmpC (p < 0.0006) and anti-I2 (p < 0.003) were associated with IP/S disease. The frequency of IP/S disease increased with increasing number of immune responses (p trend = 0.002). The odds of developing IP/S disease were highest in patients positive for all four immune responses (OR (95% CI): 11 (1.5-80.4); p = 0.03). Pediatric CD patients positive for > or =1 immune response progressed to IP/S disease sooner after diagnosis as compared to those negative for all immune responses (p < 0.03). CONCLUSIONS: The presence and magnitude of immune responses to microbial antigens are significantly associated with more aggressive disease phenotypes among children with CD. This is the first study to prospectively demonstrate that the time to develop a disease complication in children is significantly faster in the presence of immune reactivity, thereby predicting disease progression to more aggressive disease phenotypes among pediatric CD patients.

Adolescent↗

PubMed1985

Suppression of immune response to Listeria monocytogenes: mechanism(s) of immune complex suppression.

We have investigated possible mechanisms underlying immune complex suppression of resistance to Listeria monocytogenes. Inhibition of resistance was found when immune complexes were formed in vivo in immune mice or in nonimmune mice adoptively transferred with specific antibody. Suppression was also found when nonimmune mice were injected with immune complexes preformed in vitro. We investigated the role of complement by decomplementing mice with cobra venom factor purified by high-pressure liquid chromatography. Complete depletion of serum C3 did not eliminate immune complex suppression of resistance to L. monocytogenes, suggesting that complement activation is not required for immune complex suppression. Infection-induced changes in the surface phenotype and functional properties of macrophages from normal and immune complex-suppressed mice were also investigated. Macrophage expression of both H-2K and Ia molecules increased during the response of normal mice to L. monocytogenes. However, these changes were not found in immune complex-suppressed mice. In contrast, membrane interleukin 1 expression was increased in macrophages from suppressed mice compared with macrophages from normal mice. Macrophages from L. monocytogenes-infected normal and immune complex-suppressed mice expressed cytotoxicity against tumor cells in vitro. We conclude that immune complexes do not inhibit resistance to L. monocytogenes by activation of complement or decreasing macrophage cytotoxic activity. Rather, defects in Ia expression by macrophages from suppressed mice might be one component responsible for immune complex suppression of resistance to L. monocytogenes.

Animals↗

PubMed1986

Immune responses to the lipopolysaccharides and capsular polysaccharides of Haemophilus pleuropneumoniae in convalescent and immunized pigs.

The immunologic responses to a smooth-type lipopolysaccharide (LPS) (HpS-LPS), a rough-type LPS (HpR-LPS), and a capsular-enriched polysaccharide preparation (HpC-PS) purified from Haemophilus pleuropneumoniae were determined in pigs immunized with a commercial H. pleuropneumoniae cellular vaccine, in pigs experimentally infected with H. pleuropneumoniae, in control pigs, and in immunized rabbits. The ability of the preparations to induce lymphocyte blastogenesis and B-cell activation was determined in the pigs and compared with the responses induced by the LPS of Escherichia coli O111:B4 and the LPS of Salmonella minnesota Re595. All the LPS preparations acted to induce proliferation of peripheral blood lymphocytes (PBL) from all pigs. The blastogenic response of PBL from H. pleuropneumoniae-infected pigs to HpS-LPS and HpR-LPS was significantly (P less than 0.05) greater than that of PBL from immunized and control pigs. HpC-PS did not induce a blastogenic response in the PBL of control pigs but did in PBL from H. pleuropneumoniae-infected pigs and to a greater degree in immunized pigs. An increase in the response of PBL to the S. minnesota LPS occurred only in the H. pleuropneumoniae-infected pigs. Significantly more (P less than 0.05) immunoglobulin-secreting cells (ISC) were induced in a reverse hemolytic plaque assay by stimulation with HpS-LPS and HpC-PS of PBL isolated from pigs infected with H. pleuropneumoniae than of PBL from immunized pigs. Increasing the number of T cells increased the number of ISC induced by HpS-LPS in control and immunized pigs, but not in convalescent pigs. The presence of macrophages reduced activation of ISC by HpS-LPS in control pigs and to a lesser degree in immunized pigs, whereas in H. pleuropneumoniae-infected pigs macrophages enhanced the induction of ISC by HpS-LPS. In immunized pigs, macrophages acted to inhibit the ability of HpC-PS to induce ISC. Serologic studies indicate that HpC-PS contains strain- and serotype-specific antigens; that HpS-LPS has both serotype-specific and cross-reacting species-specific antigens; and that HpR-LPS does not contain detectable serotype-specific antigens but does have both non species- and species-specific antigens. These studies show that the serotype-specific protection provided by immunization of pigs with an H. pleuropneumoniae cellular vaccine is principally the result of immunity to capsular antigens and that a weak cellular immune response occurs as compared with that induced by infection with H. pleuropneumoniae.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

Single exposure of mice to Borrelia burgdorferi elicits immunoglobulin G antibodies characteristic of secondary immune response without production of interleukin-4 by immune T cells.

Borrelia burgdorferi antigen can elicit immunoglobulins (Igs) characteristic of the primary and secondary immune responses without the contribution of an interleukin-4-producing helper T-cell population. Single exposure of mice to soluble B. burgdorferi antigen elicited both Th1-type and Th2-type antispirochete antibodies. Production of the Ig classes showed different patterns with increasing time postinjection (IgM levels decreased; IgG1, IgG2a, IgG2b, and IgG3 levels increased; IgE was not detected), and Ig patterns were similar to those produced in infected mice. Upon infectious challenge, immunized mice achieved maximal titers of all antispirochete IgG subclasses more quickly than unimmunized mice did. In contrast to the antibody responses which showed both Th1- and Th2-type patterns, T-cell immune response to either immunization or infection was characterized by interleukin-2 and gamma interferon production; interleukin-4 and interleukin-5 were undetectable. Injection with whole spirochetes induced a pattern of antibodies and cytokine production similar to those obtained by injection with soluble antigen. In addition, mouse strains of different major histocompatibility complex backgrounds produced similar patterns of Ig in response to immunization. None of the various parameters of immunization tested resulted in detectable interleukin-4 production by primary or secondary immune T cells. The production of both IgM and IgG1 at early times following a single exposure to spirochete antigen clearly differs from immune responses to haptens or model protein antigens. Production of similar Ig classes in infected and immune mice implies that antigen-specific antibody is responsible for passive immunizing activity found in immune sera.

Adjuvants, Immunologic↗

PubMed2000

Mycobacterium bovis BCG induces similar immune responses and protection by rectal and parenteral immunization routes.

We compared cellular immune responses to rectal, subcutaneous, and intradermal administration of Mycobacterium bovis BCG for 5 to 20 weeks in mice, guinea pigs, and macaques. Strong lymphoproliferative responses were induced in spleen cells after in vitro stimulation with purified protein derivative in guinea pigs and macaques, whatever the route of immunization. Comparable high numbers of gamma interferon- and tumor necrosis factor alpha-producing cells were found in the spleen after rectal, subcutaneous, and intradermal immunization of mice and macaques. Similar levels of precursors of cytotoxic T lymphocytes specific for mycobacterial antigens were observed in mice for all immunization routes. In macaques, cytotoxic activity, determined only at the end of the experiment (20 weeks), was similar after rectal and intradermal immunization. Six months after immunization, rectal and subcutaneous routes induced in mice similar levels of protective immunity against challenge with a virulent Mycobacterium tuberculosis strain (H37Rv). Rectal immunization gave immune responses and protective capacity similar to those for parenteral immunization and seemed to be a promising new route of vaccination against tuberculosis; in our study, immunization via the rectal route never induced side effects associated with parenteral routes (axillary adenitis) and could also effectively reduce the risks of viral transmission associated with unsafe injections in the developing world.

Administration, Rectal↗

PubMed2001

Immunization with the Chlamydia trachomatis mouse pneumonitis major outer membrane protein can elicit a protective immune response against a genital challenge.

Infertility, ectopic pregnancy, and chronic abdominal pain are frequent complications of genital infections with Chlamydia trachomatis. In an attempt to produce a vaccine to protect against this pathogen we purified and refolded the C. trachomatis mouse pneumonitis (MoPn) major outer membrane protein (MOMP). This preparation, mixed with Freund's adjuvant using vortexing or sonication, was used to immunize BALB/c mice that were subsequently challenged in the upper genital tract. Vaginal cultures were taken on a weekly basis, and mice were mated 6 weeks after the challenge. Gels of the vortexed MOMP showed a predominant band with a molecular size of 62 kDa and weaker bands at 42 and 132 kDa, while the sonicated MOMP had a single band with a molecular size of 42 kDa. Following immunization with these two preparations, strong humoral and cell-mediated immune responses were detected in the mice inoculated with the vortexed MOMP. On the other hand, mice immunized with the sonicated MOMP had a strong humoral immune response but a relatively weak cell-mediated immune response, as determined by a T-cell lymphoproliferative assay and level of cytokine production by splenocytes. Vaginal cultures showed that the mice immunized with the vortexed MOMP were significantly protected, as determined by a decrease in the number of animals with positive cultures, the length of time the mice shed viable organisms, and the number of inclusion-forming units recovered per mouse. Animals immunized with the sonicated MOMP, on the other hand, showed a weaker level of protection based on the same three parameters. After mating, the number of fertile animals and number of embryos per mouse were significantly higher for the mice immunized with vortexed MOMP, but not for the mice immunized with sonicated MOMP, compared to those of the control groups. In conclusion, immunization with a purified and refolded preparation of the C. trachomatis MoPn MOMP confers a significant level of protection in mice against a genital challenge.

Animals↗

PubMed1986

Growth inhibition of a B cell leukemia: evidence implicating an anti-idiotype immune response for protective tumor immunity.

BCL1, a spontaneous surface IgM (mu lambda)-positive (sIgM+) B cell leukemia of BALB/c (Igha) origin rarely grows in the Ig heavy chain (Igh) congenic mouse C.B-20 (Ighb) but is highly metastatic and lethal in the host strain of origin. Previous studies indicated that BCL1 tumor immunity in C.B-20 mice was associated with a T cell-mediated immune response against H-40, a minor histocompatibility (H) antigen controlled by a gene linked to the Igh locus. However, we observed that BCL1 leukemia grew progressively in BAB-14 (Igha/b) mice, a strain capable of generating an anti-H-40 immune response. This suggested that anti-H-40 immunity was insufficient for protection and implied that an Igh-V (variable) region gene product was also important for BCL1 growth inhibition. We therefore evaluated the role of two possible Igh-V region-linked gene products in BCL1 growth inhibition; namely, an Igh-V region-linked minor H antigen or alternatively the BCL1 IgM idiotype (Id). We could find no evidence for an Igh-V region-linked minor H antigen because immunosuppressed (500 R) CB-20 mice reconstituted with C.B-20 anti-BAB-14 splenocytes were susceptible to BCL1 growth, whereas recipients reconstituted with C.B-20 anti-BALB/c splenocytes were resistant to BCL1 challenge. In contrast, C.B-20 mice immunized against purified BCL1 IgM protein could adoptively confer BCL1 tumor immunity. C.B-20 mice immunized against other BALB/c IgM myeloma proteins containing either lambda or kappa light chains failed to protect C.B-20 mice suggesting that recognition of a unique determinant (Id) and not an allotype was crucial for tumor immunity. The BCL1 mu-chain appeared to make the major contribution to the idiotypic determinant because a hybridoma product composed of BCL1 mu-chains and BALB/c kappa-chains still elicited BCL1 immunity. Adoptive transfer of C.B-20 anti-BCL1 Id splenocytes into irradiated recipients that prevented an anti-H-40 response due to H-40 tissue expression failed to adoptively confer BCL1 immunity. Thus, these data suggest that BCL1 growth inhibition requires a T cell-mediated response against both H-40 and the BCL1 Id; these responses must be elicited concurrently in the tumor-bearing host to achieve protective BCL1 immunity.

Animals↗

PubMed1987

Monoclonal antibody characterization of Plasmodium falciparum antigens in immune complexes formed when schizonts rupture in the presence of immune serum.

When Plasmodium falciparum parasites are cultured with some immune sera, merozoites are agglutinated by antibodies to form immune clusters of merozoites and prevent their invasion into erythrocytes. Within these immune clusters of merozoites, several antigens that are normally found in the soluble fraction after detergent extraction accumulate in relatively insoluble immune complexes. From mice immunized with these immune complexes, we obtained hybridomas secreting monoclonal antibodies (mAb) that react with various immune clusters of merozoites antigens, including mAb 3D5, which recognizes a 101-kDa antigen (p101) and mAb, 5E3, which recognizes a 113-kDa antigen (p113). Both mAb reacted with antigens at the surface of schizonts, in the vacuolar space, and at the surface of merozoites before their release from schizont-infected cells. Both p101 and p113 were synthesized by mature trophozoites and young schizonts. In pulse-chase experiments, p113 was processed to 100-, 70-, 55-, and 50-kDa products. Both p101 and p113 appeared in the culture medium when schizont rupture occurred in normal culture medium but were found in immune complexes when schizont rupture occurred in the presence of immune serum. Antibodies in immune complexes, when dissociated with acid and used to probe immunoblots, reacted with affinity-purified p101 and p113. Antigens such as these, which are accessible at the parasite surface and react with antibodies present in immune serum that inhibits parasite invasion, are logical candidates to study in the search for a vaccine against the erythrocytic stages of malaria.

Animals↗

PubMed1997

Adoptive immunotherapy of murine lymphosarcoma: comparative study using allo-immune or tumor-immune T cells.

The antitumor effect of allosensitization with lymphocytes and skin graft of DBA/2 mice was evaluated using immunogeneic, transplantable Lymphosarcoma (LS-A) syngeneic to Swiss mice. A dose dependent tumor inhibitory effect in terms of tumor free mice was observed in mice sensitized i.p. with lymphocyte doses between 10-100 million per animal. Sensitization with allogeneic primary skin graft was more effective than lymphocyte immunization. The antitumor immunity could be adoptively transferred in syngeneic Swiss mice using either allo-immune or tumor-immune T cells. Analysis of T cell phenotypes using monoclonal antibodies against cell surface markers CD4 and CD8, indicated absolute dependence on the CD4+ T cells subset in tumor cure in case of allo-immune as well as tumor-immune T cells. CD8+ T cell subset was found essential only in case of allo-immune T cell therapy. Immunosuppression of mice with whole body gamma irradiation (4 Gy), 6 hr before transfer of allo-immune or tumor-immune T cells did not abrogate the therapeutic ability of allo-immune or tumor-immune T cells. Our results suggest that allosensitization could be an effective method of generating effector lymphocyte populations that might be used to treat tumors that exhibit detectable immunogenecity.

Animals↗

PubMed1983

Eradication of tumor cells after injection into immunized hosts compared with the eradication of tumor cells after transfer of immune peritoneal exudates into tumor-bearing recipients.

DBA/2 mice were immunized against the syngeneic SL2 lymphoma by two or five injections with irradiated lymphoma cells given IP or SC, respectively. The antitumor efficacy induced in immunized mice was tested by (a) IP injection of the immunized mice with nonirradiated tumor cells and (b) transfer of the total 'immune' peritoneal exudate, the cellular fraction only, or the cell-free fraction only, IP into tumor-bearing recipients, or (c) tumor neutralization tests (Winn assay). It was shown that immunized mice were able to reject 5 X 10(7) SL2 tumor cells (8 of 14 mice survived greater than 100 days), while in most transfer experiments 2 X 10(5) SL2 cells could be eradicated. In the tumor neutralization experiments a number of 10(6) SL2 cells were eradicated. When the immune exudates were given before the inoculations of SL2 tumor cells the number of survivors increased significantly. Further, it was shown that the cellular fraction is the major contributor to the antitumor effect in the transfer experiments, since there was no significant difference in tumor eradication after injection of a complete immune exudate and after injection of the isolated cellular fraction. Injection of the noncellular fraction had no measurable antitumor effect. An increase in the number of injections with total peritoneal exudates from immunized mice did not result in an increase in tumor eradication in the tumor-bearing recipients. Extra stimulation (IP) of immunized mice with 10(4) nonirradiated cells 6 days after the last immunization resulted in an increase of the antitumor efficacy of these peritoneal exudates of these mice when collected 4-24 h after this stimulation. Extra stimulation with 10(6) irradiated cells had no measurable effect.

Animals↗

PubMed1987

Aujeszky's disease vaccination and infection of pigs with maternal immunity: effects on cell- and antibody-mediated immunity.

SCC, ADV-SCC, ADV-ADCC and ADV-LYST as well as ND50-titres of neutralizing serum antibodies were examined in 36 passively immune pigs, 25 of which were vaccinated at 3 weeks of age and partly revaccinated 3 weeks later. Twenty-five vaccinated animals and 8 non-immune control pigs were challenged with infectious ADV. Independent of the state of maternal immunity the cytotoxic response of the white blood cells from all the animals was low at WPP 3 but rose with increasing age. ADV-LYST occurred only in some of the animals. A single vaccination evoked no significant effect on our immune parameters, but revaccination led to higher ADV-LYST and ADV-ADCC. In pigs vaccinated at WPP 3 the neutralizing serum titres decreased gradually, similar to unvaccinated animals, indicating that the antibodies were of maternal origin. However, after vaccination at WPP 6, no further decline of ND50-titres could be detected, pointing to a limited antibody production. Animals vaccinated at WPP 3 and revaccinated 3 weeks later showed a significant increase of serum neutralizing titres. Whereas the controls showed typical symptoms of Aujeszky's disease, the immune animals, especially the unvaccinated passively immune pigs, showed only elevated temperatures and most of them excreted small amounts of ADV. The development of cellular immunity after infection was rather similar within the maternally immune group independent whether the animals had been vaccinated or not, but ADV-ADCC and ADV-LYST showed a more rapid progress within the vaccinated group than in the non-vaccinated group and the non-immune control group. Infection resulted in significantly higher ND50 titres in vaccinated and revaccinated animals than in unvaccinated animals, indicating a secondary response in those pigs. Thus, ADV sensitization of lymphocytes had been evoked by vaccination despite the presence of maternal antibody. The interpretation of the results was complicated by great individual and litter-dependent variations of the immune parameters.

Animals↗

PubMed2006

Regulatory T cells and innate immune regulation in tumor immunity.

Innate and adaptive immunity play important roles in immunosurveillance and tumor destruction. However, increasing evidence suggests that tumor-infiltrating immune cells may have a dual function: inhibiting or promoting tumor growth and progression. Although regulatory T (Treg) cells induce immune tolerance by suppressing host immune responses against self- or nonself-antigens, thus playing critical roles in preventing autoimmune diseases, they might inhibit antitumor immunity and promote tumor growth. Recent studies demonstrate that elevated proportions of Treg cells are present in various types of cancers and suppress antitumor immunity. Furthermore, tumor-specific Treg cells can inhibit immune responses only when they are exposed to antigens presented by tumor cells. Therefore, Treg cells at tumor sites have detrimental effects on immunotherapy directed to cancer. This review will discuss recent progress in innate immunity, Treg cells, and their regulation through Toll-like receptor (TLR) signaling. It was generally thought that TLR-mediated recognition of specific structures of invading pathogens initiate innate and adaptive immune responses through dendritic cells. New evidence suggests that TLR signaling may directly regulate the suppressive function of Treg cells. Linking TLR signaling to the functional control of Treg cells opens intriguing opportunities to manipulate TLR signaling to control both innate and adaptive immunity against cancer.

Animals↗

PubMed2000

Induction of immune responses in newborn lambs following enteric immunization with a human adenovirus vaccine vector.

We investigated the antigen-specific mucosal and systemic immune responses of newborn lambs following enteric immunization, targeting jejunal Peyer's patches with a human adenovirus vector that expressed the glycoprotein D (gD) of bovine herpesvirus-1. Both humoral and cell-mediated gD-specific mucosal immune responses were detected in newborn lambs (1-4 days old) after a single immunization and these responses were qualitatively and quantitatively similar to those detected in 5-6-week-old lambs. Passively transferred gD-specific maternal antibody did not significantly alter either mucosal or systemic gD-specific immune responses. Furthermore, enteric immunization of newborn lambs primed mucosal immune responses in the lungs. These observations confirmed that gut-associated lymphoid tissue of a newborn ruminant is immune competent and that enteric immunization may be an effective approach for the induction of both mucosal and systemic immune responses in the neonate.

Adenoviruses, Human↗