Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immunization”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,243 records · Page 69Linked to original sources
PubMed1998

Deficiency of the humoral immune response to measles vaccine in infants immunized at age 6 months.

CONTEXT: Measles causes serious morbidity in infants, with the highest risk among those who are 6 to 12 months of age. In the United States, measles vaccine has been given at age 12 to 15 months to minimize interference by passive antibodies and to achieve the high seroprevalence required for herd immunity. Infants of mothers with vaccine-induced immunity may lose passively acquired antibodies before 12 months, leaving them susceptible to measles infection. OBJECTIVE: To assess the immunogenicity of measles vaccine in infants younger than 12 months. DESIGN: Cohort study conducted before and after measles immunization. SETTING: Pediatric clinic in Palo Alto, Calif. PARTICIPANTS: Infants 6 (n = 27), 9 (n = 26), and 12 (n = 34) months of age were enrolled; 72 provided both initial and follow-up samples. MAIN OUTCOME MEASURES: Evaluation of immunogenicity before and 12 weeks after measles vaccination, including measles neutralizing antibody titers, measles-specific T-cell proliferation, and cytokine profiles. RESULTS: Measles neutralizing antibodies were present before vaccination in 52% (12/23), 35% (7/20), and 0% (0/22) of 6-, 9-, and 12-month-old infants, respectively. In the absence of detectable passive antibodies, geometric mean titers after vaccination were significantly lower in 6-month-old infants compared with 9-month-old infants (27 vs 578, P = .01) and 12-month-old infants (27 vs 972, P=.001). The seroconversion rate, defined as a 4-fold rise in antibody titer, in these 6-month-old infants was only 67%, and only 36% of these infants achieved seroprotective neutralizing antibody titers of 120 or higher after vaccination compared with 100% of 9- and 12-month-old infants lacking detectable passive antibody prior to vaccination. T-cell proliferation and cytokine responses to measles did not differ with age. CONCLUSIONS: Humoral immunity was deficient in 6-month-old infants given measles vaccine, even in the absence of detectable passively acquired neutralizing antibodies. Comparison of their responses with those of 9- and 12-month-old infants indicates that a developmental maturation of the immune response to measles may occur during the first year of life, which affects the immunogenicity of measles vaccine.

Age Factors↗
PubMed2001

Decreased generation of anti-tumor immunity after intrasplenic immunization.

The localization of antigen and the nature of the host antigen-presenting cells (APC) that present it to T cells are two major determinants of antigen immunogenicity. While lymph nodes appear to be the major site for T cell priming, recently the spleen was shown to provide an optimal microenvironment for direct CD8+ cytotoxic T cell (CTL) priming by tumor cells even in the absence of known costimulatory molecules on tumor cells. We analyzed whether the splenic microenvironment would support T cell priming also when host APC are involved (cross-priming) which is probably the major pathway during the generation of anti-tumor immunity. We performed immunization/challenge experiments using different tumor cells (B7.1+, B7.1- and/or beta-gal+, beta-gal-) known to induce CTL to a variable extent either exclusively by cross-priming (B7-) or at least partially by direct priming (B7+). Our results demonstrate that tumor take in the spleen required much less cells than at a subcutaneous injection site. Additionally, intrasplenic immunization was invariably ineffective compared to subcutaneous immunization. We further showed that B cells were not responsible for the inefficient intrasplenic immunization. Therefore delivering the tumor cell antigens inside the spleen by intrasplenic immunization did not improve but rather decreased the efficacy of tumor cell vaccines.

Adenocarcinoma↗
PubMed1997

Immunization with immune complex alters the repertoire of antigen-reactive B cells in the germinal centers.

The differentiation of memory B cells in germinal centers (GC) is selectively enhanced upon administration of antigen-antibody complexes. To characterize the repertoire of this response, we examined the rearranged immunoglobulin heavy chain variable (V(H)) genes from mouse splenic GC after a single immunization with either antigen, nitrophenyl (NP) hapten coupled to keyhole limpet hemocyanin, or with a preformed complex of antigen with a monoclonal anti-NP antibody of gamma1 isotype. Among antigen-immunized mice, NP-reactive GC B cell populations in the antigen-induced GC consisted mostly of cells expressing the canonical V186.2 gene which contained, on average, 0.8 point mutations/V(H) gene by day 8 after immunization. These results are indicative of the beginning of somatic hypermutation and consistent with previously published analyses of NP antigen-driven GC. In contrast, the NP-specific B cells in GC that were elicited by administration of immune complex represented a heterogeneous cell population expressing nine different germ-line segments of the V186.2/V3 (J558) gene family, i.e. V23, V24.8, C1H4, V3, CH10, V165.1, V102, V671.5 and V186.2. Moreover, the average frequency of mutations in these genes was 1.7, reaching up to 4 mutations/V(H) in some GC. Administration of the antigen NP in complex with specific antibody apparently alters the process of interclonal competition in the GC and results in loss of dominance by V186.2+ cells and nearly stochastic representation of diverse clonotypes. These results suggest an important feedback regulation of the B cell repertoire by antibody and indicate a role for immune complexes in the activation of somatic hypermutation.

Animals↗
PubMed2003

Generation and characterization of the humoral immune response to DNA immunization with a chimeric beta-amyloid-interleukin-4 minigene.

Active immunization with fibrillar beta-amyloid peptide (Abeta(42)) as well as passive transfer of anti-Abeta antibodies significantly reduces Abeta plaque deposition, neuritic dystrophy, and astrogliosis in the brain of mutant amyloid precursor protein (APP)-transgenic mice. Although the mechanism(s) of clearance of Abeta from the brain following active or passive immunization remains to be determined, it is clear that anti-Abeta antibodies are critical for clearance. DNA immunization provides an attractive alternative to direct peptide and adjuvant approaches for inducing a humoral response to Abeta. We constructed a DNA minigene with Abeta fused to mouse interleukin-4 (pAbeta(42)-IL-4) as a molecular adjuvant to generate anti-Abeta antibodies and enhance the Th2-type of immune responses. Gene gun immunizations induced primarily IgG1 and IgG2b anti-Abeta antibodies. Fine epitope analysis with overlapping peptides of the Abeta(42) sequence identified the 1-15 region as a dominant B cell epitope. The DNA minigene-induced anti-Abeta antibodies bound to Abeta plaques in brain tissue from an Alzheimer's disease patient demonstrating functional activity of the antibodies and the potential for therapeutic efficacy.

Amyloid beta-Peptides↗
PubMed1984

Immune rejection mechanisms in murine leukemia. I. Timing of tumor cell rejection process relative to the development of humoral and cell-mediated cytotoxic immune responses.

Studies were undertaken to investigate the relationship between cell-mediated and humoral immune responses in the rejection of L1210/MTX-Rev (LR) leukemia cells in CD2F1 mice. The anti-LR antibody (humoral) response was defined by both its cytotoxic antibody titer and isotype composition, assessed by a complement-dependent cytotoxicity assay and radioimmune assay, respectively. The cytotoxic thymus (T)-derived lymphocyte response in the spleen was quantitated by 125I release by 125I-IUdR-labelled target cells. Analysis of the sera of tumor-bearing mice indicated that the LR leukemia cells elicited a wide spectrum of anti-tumor antibody isotypes. In mice that mounted a rejection response, the IgM anti-LR response was transient, while in those that did not, the IgM response persisted. Antibody titers for all isotypes remained low until the onset of LR rejection. At that time, high titers of IgG anti-LR antibodies, predominantly of the IgG2a subclass, were detected in sera of tumor-free mice. Thus, the LR rejection response coincided best with the appearance of high titers of IgG2a anti-LR antibodies. A single i.p. injection of viable LR cells elicited a potent cell-mediated immune response; neither the appearance nor the magnitude of the cell-mediated immune response as measured in the spleen correlated well with the onset or the strength of the LR rejection response in the peritoneal cavity. The LR peritoneal cell population grew unabated in the presence of an intense spleen cell-mediated immune response, and the rejection process began at a time when little cellular immunity could be detected. These results suggest that in the rejection response IgM antibodies contribute little, if any, to the process, and the role of cytotoxic T lymphocytes is questionable (uncertain). The rejection of LR cells appears to be primarily mediated by IgG2a antibodies.

Animals↗
PubMed1981

Active immunization of mice with porcine zonae pellucidae: immune response and effect on fertility.

Female mice were heteroimmunized with varying dosages of intact and heat-solubilized porcine zonae. Mouse immune response was monitored by radioimmunoassay and the effect on mouse fertility of circulating antibodies to pig zonae was observed. Porcine zonae were a potent heteroimmunogen in the mouse and, for all dosages studied, the immune response was characterized by a rapid rise in titer, culminating in a peak which was followed by a plateau period of extended duration and of significantly high anti-zona activity. Maximum immune response was achieved using a dosage of 4000 heat-solubilized zonae per mouse. Studies involving alteration of immunization regimes, but use of a constant zonae dosage, indicated that maximal response to this antigenic target was obtained intact zonae applied over a series of injections rather than in a single application. In vitro studies involving proteolytic lysis or of sperm attachment to mouse zonae pretreated with either antibodies to mouse zonae (homologous system) or pig zonae (heterologous system) demonstrated that zona antibodies are considerably more biologically effective in the homologous system. Immunization of mice with pig zonae had no significant effect upon altering mouse fertility. The significance of these fertility results is discussed with respect to the information obtained from the in vitro studies and in respect to the continued consideration of the zona as an immunocontraceptive antigenic target.

Animals↗
PubMed2000

Effect of RNA from brain of immunized mice on the specific immune response.

The objective of the investigation was to study the influence of RNA isolated from the brains of immunized mice on the immune response in syngeneic recipients. (CBAxC57BL/6)F1 male mice immunized by SRBC and RRBC were used for isolation of experimental RNA. Mice injected with medium 199 were used for isolation of control RNA. Experimental and control RNA was injected into syngeneic mice recipients immunized by SRBC, RRBC or rat RBC preliminary. It was shown that experimental RNA stimulate the specific immune response only.

Animals↗
PubMed1997

Mucosal immunity induced by parenteral immunization with a live attenuated Venezuelan equine encephalitis virus vaccine candidate.

Induction of a mucosal immune response is generally thought to require introduction of an immunogen directly onto the mucosal surface. It has been observed, however, that live, attenuated mutants of the alphavirus, Venezuelan equine encephalitis virus (VEE), induce protection from virulent challenge at the respiratory mucosa even after parenteral inoculation. In this report, we propose a mechanism by which subcutaneous immunization with a molecularly cloned, attenuated double mutant of VEE is able to stimulate the production of mucosal anti-VEE IgA. Our results showed that the immunizing virus spread to, and replicated within, lymphoid tissues throughout the mouse. Several tissues known to be inductive sites of the mucosal immune system were found to be positive for the presence of VEE RNA by 48 hr postimmunization. Moreover, this mucosal lymphotropism resulted in the production of virus-specific IgA antibody detectable in vaginal secretions of immunized mice.

Administration, Intranasal↗
PubMed1997

E7 oncoprotein of human papillomavirus type 16 expressed constitutively in the epidermis has no effect on E7-specific B- or Th-repertoires or on the immune response induced or sustained after immunization with E7 protein.

A line of FVB (H-2q) mice transgenic for the E6/E7 open reading frames of Human Papillomavirus type 16 driven from the alpha-A crystallin promoter expresses E7 mRNA in lens and skin epithelium. E7 protein is detectable in adult skin, coinciding with the development of inflammatory skin disease, which progresses to papillomata and squamous carcinomata in some mice. By examining the outcome of parenteral immunization with E7 protein, we sought to determine whether endogenous expression of E7 in skin had induced a preexisting immune outcome, i.e., specific immunity or tolerance, or whether the mice remain naive ("ignorant") to E7. Our data show that the antibody response to defined E7 B-epitopes, the proliferative response to Th epitopes, and the delayed-type hypersensitivity (DTH) response to whole E7 did not differ between groups of young and old E6/E7 transgenic mice (likely having different degrees of lifetime exposure to E7 protein) or between E6/E7-transgenic and nontransgenic parental strain control mice. Although an E7-specific CTL response could not be induced in the H-2q background of these mice, incorporation of a Db allele into the genome allowed comparison of Db-restricted CTL responses in E6/E7 transgenic and nontransgenic mice. Experiments indicated that the E7-immunization-induced CTL response did not differ significantly between E6/E7 transgenic and nontransgenic mice. We interpret these results to indicate that in spite of expression of E7 protein in adult skin, E6/E7 transgenic mice remain immunologically naive (ignorant) of E7 epitopes presented by immunization.

Amino Acid Sequence↗
PubMed1999

Immune responses and protection obtained by oral immunization with rotavirus VP4 and VP7 DNA vaccines encapsulated in microparticles.

Protective immune responses in mice were obtained after oral immunization with rotavirus DNA vaccines encapsulated in poly(lactide-co-glycolide) (PLG) microparticles. The DNA vaccines used encoded outer capsid proteins VP4 and VP7; proteins that are the basis for rotavirus serotyping and the generation of virus neutralizing antibodies. One dose of vaccine was given to BALB/c mice by oral gavage (75 microg DNA/mouse). Rotavirus-specific serum antibodies and intestinal IgA antibodies were detectable by 6 weeks postimmunization. After challenge with homologous murine rotavirus at 12 weeks postimmunization, fecal rotavirus antigen was reduced significantly in immunized mice compared with controls. Protective immunity also was generated by oral delivery of unencapsulated VP 7 DNA vaccine but to a lesser degree. These results demonstrate that the oral route is effective for generating protective immune responses with rotavirus DNA vaccines targeting neutralization antigens.

Administration, Oral↗
PubMed2000

Innate immune therapy for cancer. Screen for molecules capable of activating the innate immune system.

Tumor cells usually express antigens which are distinguishable from normal "self" antigens and are thereby recognized by the host immune system. However, the host immune system barely responds to tumors in patients. Supplementation with adjuvant (such as BCG-CWS) in patients with cancer contributes to regression of intrinsically growing cancer. The adjuvant targets antigen-presenting cells, i.e. innate immunity, but not lymphocytes, and promotes up-regulation of MHC, co-stimulators and initial cytokines in antigen-presenting cells. We hypothesized that the role of the adjuvant is to provide conditions suitable for antigen-presentation where antigens are available and the lack of adjuvant-induced priming of antigen-presenting cells results in unresponsiveness to tumor antigens. Here, we report innate immune therapy applicable to cancer patients by supplementation with adjuvants for induction of potent immune responses against tumors.

Humans↗
PubMed2001

Immunization of the elderly to boost immunity against varicella-zoster virus (VZV) as assessed by VZV skin test reaction.

The utility of the VZV skin test in detecting individual susceptibility to varicella and zoster was determined. Its specificity particularly with regard to herpes simplex was also established. The VZV skin test was negative or weakly positive during the early stage of herpes zoster, and strongly positive during recovery from that disease. A small-scale clinical trial to immunize elderly individuals has been performed for the purpose of preventing herpes zoster, and, perhaps, severe post-herpetic neuralgia as well. Sixty individuals > or = 50 years old were screened for VZV antibodies by IAHA test and were given a VZV skin test for cell-mediated immunity. All were seropositive, but eight were skin-test negative. Thirty-seven individuals including the eight with negative skin tests were immunized with one dose of varicella vaccine (3.0 x 10(4) PFU/dose). After 5-7 weeks, the skin test reaction showed increased positivity, with a change in score from (-) to (+, ++) in 7/8 subjects, from (+) to (++, +++) in 3/5 subjects, and from (++) to (+++) in 6/10 subjects. Enhancement of the VZV antibody titer (defined as twofold or greater) was observed in all 15 vaccine recipients with a prevaccination titer of < or = 1:16, and in 19 of 24 subjects with a prevaccination titer of > or = 1:32. These results indicate that giving live varicella vaccine with a high viral titer can induce a good boost immunity particularly cell-mediated immunity to VZV in the elderly.

Aged↗
PubMed1983

Specific immune responses after booster immunization with tetanus toxoid in man: study of kinetics, family segregation, and linkage to HLA of in vitro lymphocyte proliferative responses and serum-antibody responses.

Kinetics and family transmission of antigen-specific in vitro cell-mediated responses were investigated in 68, and serum-antibody responses to tetanus toxoid (TT) in 73 individuals from a total of 12 families. Proliferative responses to highly purified TT monomer were studied in 6- to 7-day lymphocyte cultures. The effect of booster immunization was detectable 7 (D7) and 30 (D30), but not 120 days (D120) later. The sex of donors was not found to have any influence. A significant influence of the time interval since the last immunization was found for the responses at D7 and D30. Data were correspondingly adjusted for segregation and linkage analyses. Several transmission hypotheses for the data obtained at D7 and D30 were evaluated by likelihood ratio tests. Observations at D30 were compatible with the hypothesis of a control by a dominant genetic determinant for high responses closely linked to the major histocompatibility complex region. No such evidence could be found for D7. After booster immunization, mean antibody levels determined on D7, D30 (peak of response), and D120 were found to be higher than those prior to immunization (D0). The sex of the donors was found to have no influence on antibody responses. The time interval since the last immunization and the age of donors both had a slight influence, and data were correspondingly adjusted for segregation and linkage analyses, which showed no evidence of genetic control of the antibody responses or of linkage to HLA.

Adolescent↗
PubMed1992

Systemic immune response after mucosal immunization in patients with IgA nephropathy.

Increased IgA production has been proposed as a portion of the etiology of IgA nephropathy. Indirect human data suggest that IgG and complement may be equally important. We have immunized 17 patients with IgA nephropathy and 27 controls with tetanus toxoid. They were nasally immunized and, 2 weeks later, received an im booster immunization. This protocol has been shown to result in an increased serum IgA1 antibody response to tetanus toxin (TT). Patients had higher serum IgG antibodies to TT before and after the im immunization than did controls (pre, 42 vs 13 U; post, 155 vs 71 U; P = 0.004). Patients also had a greater increase in serum IgG antibodies (118 vs 58; P = 0.02). After the im TT, patients had lower levels of serum IgA1 antibody to TT (115 vs 180; P = 0.005) but the change in IgA1 antibodies was not significant. These data suggest that patients with IgA nephropathy may produce inappropriately large amounts of serum IgG antibodies to antigens encountered in the upper respiratory tree. Such antigens also induce a serum IgA1 response. Such a response could result in the formation of potentially nephritogenic immune complexes containing IgG, IgA1, and C3.

Administration, Inhalation↗
PubMedDate not supplied

Cell-mediated immunity and immune complexes in the pathogenesis of type 1 (insulin-dependent) diabetes.

Evidence for a role of the immune system in the pathogenesis of insulin-dependent (Type 1) diabetes is now plentiful. In the light of the lymphocytic infiltration in the islets of Langerhans, different autoaggressive mechanisms have been suggested in the initiation of B-cell damage. Lymphocytes characterized by cytotoxic properties (K cells) and having receptors for the Fc of IgG are increased in newly diagnosed Type 1 diabetics. Circulating immune complexes are also raised in these patients at the time of clinical diagnosis and there is evidence that K cells bind immune complexes which can modulate the activity of these cells. Here we propose a possible interrelationship between K or Fc gamma receptor+ T lymphocytes and immune complexes which could have a 'key' role in the mechanism of activation of cell-mediated immunity towards B-cells.

Antigen-Antibody Complex↗
PubMed1999

The immune system in the elderly: III. Innate immunity.

The capability to cope with infectious agents and cancer cells resides not only in adaptive immune responses against specific antigens, mediated by T and B lymphocytes clonally distributed, but also in natural immune reactions. These innate defence mechanisms include chemotaxis, phagocytosis, natural cytotoxicity, cell interactions, and soluble mediators or cytokines. However, specific and natural immune mechanisms are always closely linked and interconnected, providing the primary defense against pathogens. The Authors discuss the main changes observed with advancing age in granulocytes and natural killer (NK) cell activity, in the expression and function of adhesion molecules, and in the pattern of cytokine production. Since phagocytic function is the primary mechanism through which the immune system eliminates most extracellular pathogenic microorganisms, analysis of this function is of clinical importance. Neutrophils from aged subjects often exhibit a diminished phagocytic capacity, as well as a depressed respiratory burst, notwithstanding an activated state. The activity of NK cells during aging has been studied extensively and different results have been reported. The most consistent data indicate an increase in cells with high NK activity with advancing age. Cells from healthy centenarians can efficiently kill target cells. This finding seems to suggest that innate immunity and in particular NK cell activity, is not heavily deteriorated with age. Conversely, a low NK activity is a predictor of impending morbidity. Immunosenescence is associated with increased expression of several cell adhesion molecules (CAM) resulting in an augmented capacity to adhere. Finally, also the cytokine network, responsible for differentiation, proliferation, and survival of lymphoid cells, undergoes complex changes with age. The main findings are a Th1 to Th2 cytokine production shift and an increased production of proinflammatory cytokines, which could explain many aspects of age-associated pathological events, such as atherosclerosis and osteoporosis.

Aged↗
PubMed2003

Genomic analysis of immunity in a Urochordate and the emergence of the vertebrate immune system: "waiting for Godot".

Genome-wide sequence analysis in the invertebrate chordate, Ciona intestinalis, has provided a comprehensive picture of immune-related genes in an organism that occupies a key phylogenetic position in vertebrate evolution. The pivotal genes for adaptive immunity, such as the major histocompatibility complex (MHC) class I and II genes, T-cell receptors, or dimeric immunoglobulin molecules, have not been identified in the Ciona genome. Many genes involved in innate immunity have been identified, including complement components, Toll-like receptors, and the genes involved in intracellular signal transduction of immune responses, and show both expansion and unexpected diversity in comparison with the vertebrates. In addition, a number of genes were identified which predicted integral membrane proteins with extracellular C-type lectin or immunoglobulin domains and intracellular immunoreceptor tyrosine-based inhibitory motifs (ITIMs) and immunoreceptor tyrosine-based activation motifs (ITAMs) (plus their associated signal transduction molecules), suggesting that activating and inhibitory receptors have an MHC-independent function and an early evolutionary origin. A crucial component of vertebrate adaptive immunity is somatic diversification, and the recombination activating genes (RAG) and activation-induced cytidine deaminase (AID) genes responsible for the Generation of diversity are not present in Ciona. However, there are key V regions, the essential feature of an immunoglobulin superfamily VC1-like core, and possible proto-MHC regions scattered throughout the genome waiting for Godot.

Animals↗
PubMed2004

Effective immunotherapy against cancer: a question of overcoming immune suppression and immune escape?

During the last decade, the breakthroughs in understanding of the molecular mechanisms responsible for immune activation and the advent of recombinant DNA technologies have changed the view on immunotherapy from "a dream scenario" to becoming a clinical reality. It is now clear that both cellular immunity comprising T and NK cells, as well as strategies based on antibodies, can provide strong antitumoral effects, and evidence is emerging that these strategies may also cure patients with previously incurable cancers. However, there are still a number of issues that remain unresolved. Progress in immunotherapy against cancer requires a combination of new, improved clinical protocols and strategies for overcoming mechanisms of immune escape and tumor-induced immune suppression. This review discusses some of the salient issues that still need to be resolved, focusing on the role of oxidative stress and the use of antioxidants to alleviate the immune hyporesponsiveness induced by reactive oxygen species (ROS).

Animals↗