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At least 793 records · Page 44Linked to original sources
PubMed2001

Low-dose intradermal administration of recombinant hepatitis B vaccine in children: 5-year follow-up study.

Several studies have documented the efficacy of low-dose intradermal administration of hepatitis B vaccine. However, little is known about the duration of protection provided by low-dose intradermal administration of hepatitis B vaccine. This study reports results from a 5-year follow up period of 200 healthy children (100 infants and 100 preschool children) immunized intradermally with 2 microg doses of recombinant hepatitis B vaccine (GenHevac B) at months 0,1, and 6. In the 8th week after the third vaccine dose, 97% of the children developed anti-HBs antibodies higher than or equal to 10 mlU ml(-1), and the antiHBs geometric mean titre (GMT) was 676 mlU ml(-1). In month 18 and year 5, the anti-HBs GMT decreased to approximately one-third (220 mlU ml(-1)) and one-tenth (68 mlU ml(-1)) of the initial levels, respectively. However, 87% of the children had protective levels of anti-HBs (> or =10 mlU ml(-1)) after 5 years. Among 156 children followed for 5 years, none became positive for anti-HBc and/or HbsAg. Seven children who were seronegative after 5 years developed anti-HBs antibodies higher than 1000 mlU ml(-1) after an additional 10 microg intramuscular hepatitis B vaccine. Persistent immunologic memory over periods of 5 years or more is evident, the anamnestic antibody response to a booster dose of vaccine, even in these children who have lost antibody. We conclude that intradermal administration of 2 microg recombinant hepatitis B vaccine provides long-term protection against hepatitis B virus in infants and preschool children.

Child↗
PubMed2000

Human immunosenescence: the prevailing of innate immunity, the failing of clonotypic immunity, and the filling of immunological space.

According to the remodeling theory of aging we proposed several years ago, the current data on human immunosenescence depicts a complex scenario where clonotypical immunity deteriorates, while ancestral innate/natural immunity is largely conserved or even up-regulated with age. Under an evolutionary perspective, antigens are the cause of a persistent life-long antigenic stress, responsible for the accumulation of effector CD8+/CD28- T cells, the decrease of naive T cells (CD95-) and the marked shrinkage of T cell repertoire with age. Concomitantly, NK cytotoxicity, chemotaxis, phagocytosis and complement activities remain unaffected or negligibly affected, in comparison to clonotypical immunity. Thus, immunosenescence is not a random deteriorative phenomenon but appears to inversely recapitulate an evolutionary pattern. On the whole, immunosenescence can be envisaged as the result of the continuous challenge of the unavoidable exposure to a variety of potential antigens (viruses, bacteria, but also food and self molecules among others). From this perspective antigens are nothing else than a particular type of stressor and immunosenescence appears to be the price paid to immunological memory, i.e. one of the main characteristics of the most evolutionary recent and sophisticated type of immunity. Together with the age-related thymic involution, and the consequent age-related decrease of thymic output of new T cells, this situation leaves the body practically devoid of virgin T cells, and thus likely more prone to a variety of infectious and non infectious diseases.

Aged↗
PubMed1998

Programming for responsiveness to environmental antigens that trigger allergic respiratory disease in adulthood is initiated during the perinatal period.

Allergy to airborne environmental antigens (allergens) is a major cause of asthma in children and adults. This review argues that the development of allergen-specific immunologic memory of the type that predisposes to allergy development is the end result of a T-cell selection process operative during infancy, which is triggered via encounters between the immature immune system and incoming airborne allergens from the environment. In normal individuals this process leads to the development of allergen-specific T-memory cells that secure the T helper (Th)-1 pattern of cytokines, which actively suppress the growth of their allergy-inducing Th-2 cytokine-secreting counterparts. However, these protective allergen-reactive Th-1 memory cells fail to develop in some individuals, permitting the subsequent proliferation of allergen-specific Th-2 cells that can trigger allergic reactions. Recent evidence suggests that genetic predisposition to allergy may be due in part to hyperactivity of control mechanisms operative in utero and which normally protect the fetoplacental unit against the toxic effect of Th-1 cytokines.

Adult↗
PubMed2004

A nonclassical MHC class I molecule restricts CTL-mediated rejection of a syngeneic melanoma tumor.

Although CTL and polymorphic, classical MHC class I molecules have well defined roles in the immune response against tumors, little is currently known regarding the participation of nonpolymorphic, nonclassical MHC class I in antitumor immunity. Using an MHC class I-deficient melanoma as a model tumor, we demonstrate that Q9, a murine MHC class Ib molecule from the Qa-2 family, expressed on the surface of tumor cells, protects syngeneic hosts from melanoma outgrowth. Q9-mediated protective immunity is lost or greatly diminished in mice deficient in CTL, including beta(2)-microglobulin knockout (KO), CD8 KO, and SCID mice. In contrast, the Q9 antitumor effects are not detectably suppressed in CD4 KO mice with decreased Th cell activity. Killing by antitumor CTL in vitro is Q9 specific and can be blocked by anti-Q9 and anti-CD8 Abs. The adaptive Q9-restricted CTL response leads to immunological memory, because mice that resist the initial tumor challenge reject subsequent challenges with less immunogenic tumor variants and show expansion of CD8(+) T cell populations with an activated/memory CD44(high) phenotype. Collectively, these studies demonstrate that a MHC class Ib molecule can serve as a restriction element for antitumor CTL and mediate protective immune responses in a syngeneic setting.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

Intracranial paracrine interleukin-2 therapy stimulates prolonged antitumor immunity that extends outside the central nervous system.

To explore the potential efficacy of local cytokine delivery against tumors in the central nervous system (CNS), C57BL6 mice were simultaneously given intracranial injections of tumor challenge and of irradiated B16F10 melanoma cells transduced to secrete interleukin-2 (IL-2). Intracranial IL-2 therapy generated antitumor responses capable of extending the survival of animals that received simultaneous intracranial tumor challenge either locally or at distant sites in the brain. Nontransduced melanoma cells had little effect. Animals that survived intracranial IL-2 therapy and tumor challenge showed prolonged survival compared with controls when challenged with a second tumor dose 70 days after initial treatment. In addition, animals that rejected intracranial tumors were also protected from tumor growth upon rechallenge at sites outside the CNS (i.e., subcutaneous tumor challenge). Conversely, identical or 10-fold larger doses of IL-2-transduced cells administered by subcutaneous injection failed to generate protection against intracranial tumor challenges. Elimination of T-cell and natural killer (NK) subsets using gene knockout mice and antibody-depletion techniques demonstrated that NK cells were most important for the initial antitumor response, whereas CD4+ T-cells were not necessary. These studies demonstrate that local IL-2 therapy in the brain not only generates an immediate local antitumor immune response, but also establishes long-term immunologic memory capable of eliminating subsequent tumor challenges within and outside of the CNS. Furthermore, the antitumor response to paracrine IL-2 in the brain differed significantly from that in the flank, suggesting that the intrinsic CNS cells involved in initiating immunity within the brain have different cytokine requirements from their peripheral counterparts.

Adjuvants, Immunologic↗
PubMed1993

The application of biotechnology to the diagnosis and control of animal diseases.

Methodologies for animal disease diagnosis and the analysis and control of animal health currently make much use of immunoassay techniques, in particular ELISA, and tests based on nucleic acid measurement (nucleic acid hybridisation, polymerase chain reaction [PCR]). In the latter area, the recently developed PCRs have become most useful. Recombinant technologies have yielded defined and extremely pure antigens, which can give more accurate interpretations of results obtained using diagnostic tests; in addition, such antigens obviate the need to handle live pathogens, except where these may be contained within the sample for diagnosis. The application of monoclonal antibodies (MAbs) to many tests, in particular those which use immunoassay bases or perform molecular fingerprinting of isolates, has increased the specificity and usefulness of these methodologies. Modern technology has permitted a considerable reduction in the use of animals for MAb generation through in vitro immunisation methods and the application of serum-free media with bio-reactors. These in vitro immunisation procedures have an additional application in the analysis of vaccine efficacy without recourse to animal experimentation. Furthermore, in vitro methods can be used to monitor the immune response in an animal and, in particular, to measure the development of immunological memory. It is now possible to estimate more accurately the quality and duration of an induced immune response without using animals for testing. Not only are the assay systems developed through biotechnology more sensitive and less hazardous than previous techniques (especially with regard to the necessity of handling live pathogens), but they can also determine more accurately the immune responsiveness or immune status of the animals under study.

Animal Diseases↗
PubMed1995

Considerations for the use of cytokine-secreting tumor cell preparations for cancer treatment.

Limited efficacy of chemotherapy in most solid tumors has revived interest in immunotherapeutic approaches for cancer. One novel form of immunotherapy is the use of cancer vaccines consisting of tumor cells genetically engineered to secrete cytokines. The rationale for this immunization strategy is based on the existence of tumor-specific antigens, on the importance of the cellular arm of the immune system in mediating an effective antitumor response, and on the role of cytokines in regulating the cellular immune response. Such tumor vaccines showed considerable promise in various animal models and induced potent antitumor immunity in the host, which led to regression of established tumors and, moreover, produced immunological memory protecting animals from a subsequent tumor challenge at a distant site. Translated to the human patient, this implies that genetically modified tumor vaccines may be able to eradicate or reduce existing tumor deposits to subclinical levels as well as provide long-term protection from regrowth of tumor cells. This report will review and discuss the concept and rationale for the use of cytokine-secreting tumor vaccines for the treatment of human malignancies.

Animals↗
PubMed1994

CD23/IgE-mediated regulation of the specific antibody response in vivo.

We have recently reported that IgE Abs specific for TNP are able to enhance the specific IgG response in mice via the low affinity receptor for IgE, Fc epsilon RII, or CD23. In this study we show that IgE can up-regulate IgM, IgG1, IgG2a, and the IgE response, thereby indicating the possibility of a viscious circle in the maintenance of an allergic response. One of the suggested modes of action of IgE/CD23 is to increase the ability of B cells to present Ag to T cells. The involvement of T cells in IgE-mediated enhancement of the Ab response was studied in several ways: nude mice were resistant to the effect of IgE and a dramatic effect on the induction of immunologic memory was seen, both by in situ secondary immunizations and in adoptive transfer systems. Basic conditions for the ability of IgE to induce enhancement were established, demonstrating critical importance of factors such as type of Ag and temporal relationship between administration of IgE and Ag. Finally, no evidence for the requirement for CD23 for a normal (non-IgE induced) Ab response was found, although modulation of the receptor completely abrogated the IgE-induced Ab response.

Animals↗
PubMed1979

A role for clonal dominance in the maintenance of allotype suppression?

The establishment of immunological memory during the early and complete phase of allotype suppression in the young rabbit has been shown to lead to the preferential production of antibodies with the nonsuppressed allotypic specificity in response to recall injections given after spontaneous or induced release from suppression. It is suggested that this manifestation of clonal dominance, applied to stimulation by environmental antigens, may contribute to the long lasting persistence of allotype imbalance in allotype suppressed rabbits.

Animals↗
PubMed1979

Immunosuppression in murine malaria. IV. The secondary response to bovine serum albumin.

The anamnestic antibody response of CBA mice to bovine serum albumin was characterized by a rapid production of high-avidity antibody. After 3 weeks both the total amount of antibody and its avidity declined but still remained above those seen in the primary response for at least 6 weeks. The effects of acute Plasmodium berghei and Plasmodium yoelii yoelii infections upon the induction and the expression of this anamnestic response were studied. Mice infected with these malaria parasites responded poorly to primary immunization and the immunological memory generated was quantitatively subnormal. In addition, presence of the infection during a period between approximately the second and third weeks of the primary response prejudiced the development of high-avidity memory. Optimally primed mice, challenged during a subsequent acute infection, responded well initially, but were unable to maintain the secondary response at a normal level in terms of both quantity and avidity of the antibody. However, if challenge was delayed until after recovery from the infection, a normal secondary response ensued. Antibody concentrations in the sera of primed animals declined rapidly during infection. This was at least partly due to increased catabolism.

Acute Disease↗
PubMedDate not supplied

[Comparative study of cellular and humoral immunity as well as of resistance to the rabies virus in rabies vaccination].

Experiments in CBA and BALB/c mice showed that after vaccination against rabies alongside with humoral immune response there developed a clone of cells sensitized to rabies antigen which, upon a secondary exposure to it, responded by increased blast formation. The immunological memory to the rabies antigen was found to be specific and to persist for up to 100 days (the observation period). Immunization of mice with rabies vaccine using various schedules and in combination with interferon inducers revealed no correlation between the lymphocyte blastogenesis parameters and virus-neutralizing antibody levels or the intensity of immunity to street rabies virus. The lymphocyte blasttransformation test with nonspecific mitogens may also be used for evaluation of the toxicity of new preparations.

Animals↗
PubMed1976

Immunosuppressive activity of submaxillary gland extracts of the mouse. I. Effect on antibody formation in response to sheep red blood cells.

Aqueous extracts of mouse submaxillary glands yield six peaks on Sephadex G-75 columns, each containing several molecular species. Two of these fractions (III and IV) have a profound effect on the immune response. When given a day before immunization with sheep erythrocytes, the number of antibody-producing cells is reduced ten-fold or more, and the switch from IgM to IgG is virtually absent. Administration two days before or on the day of immunization results in about 50% depression; outside this range there is no effect. The dose-response curve is of sigmoid shape, with the median at about 0.5 mg of fraction III/40 g mouse, reaching an asymptote after doses of greater than or equal to 5 mg at about 5% of the response of untreated mice. Depression of the primary response does not prevent the development of immunological memory: the secondary response is typical in the early and predominant appearance of IgG-producing cells, although their numbers are somewhat lower than in the controls which received no treatment before primary immunization. Treatment on the day before boosting abrogates the secondary response. The immunotranquilizer from mouse submaxillary glands acts equally well on syngeneic and allogeneic recipients, affecting the earliest stage of the immune response. The results are compatible with the induction of a temporary block in the development of helper T cells.

Animals↗
PubMed1975

Cell-mediated and humoral immunity in mice: cross reaction between lysozyme and S-carboxymethylated lysozyme studied by a modified footpad test.

The mouse sensitized by subcutaneous (sc) injection of lysozyme in emulsion of Freund's complete adjuvant (FCA) was shown by a modified footpad test to develop three kinds of hypersensitivities. Injecting lysozyme in 2.5-mul emulsion of Freund's incomplete adjuvant (FIA) into the footpad elicited strong footpad swelling in 30 min (anaphylactic reaction), in 3 hr (Arthus-type reaction) and in 24 hr (delayed-type hypersensitivity; DTH). The mice showing anaphylactic reaction in the footpad test manifested severe active systemic anaphylaxis, and the sera of these animals showed high IgG1 antibody titers with only sparingly detectable or no IgE antibody titers. In the sensitizing system with the use of FCA, the antigenicity of S-carboxymethylated lysozyme (CM-lysozyme) devoid of the three-dimensional conformation of lysozyme was compared with that of the native molecule. CM-lysozyme and lysozyme completely cross-reacted to each other in DTH, but not at all in the anaphylactic or Arthus-type reaction or in IgG1 antibody production. CM-lysozyme was shown also to have the ability to bestow immunological memory for the induction of humoral immunity against lysozyme; intravenous (iv) injection of lysozyme in saline or sc injection of CM-lysozyme-FCA alone failed to induce immediate hypersensitivities and IgG1 antibody production against lysozyme, but pre-sensitization by sc injection of CM-lysozyme-FCA enabled the animal to induce these responses to significant levels when iv injection of lysozyme in saline was given as a booster.

Anaphylaxis↗
PubMed1998

Normal cerebrospinal fluid suppresses the in vitro development of cytotoxic T cells: role of the brain microenvironment in CNS immune regulation.

The regulatory role of cerebrospinal fluid (CSF) in brain physiology is well established, while our understanding of its role in brain immunity is undefined. We demonstrate that normal rat CSF suppresses the in vitro development of mastocytoma-specific CTL activity in restimulated splenocytes from Balb/c mice, a strain unable to reject this tumor from the brain. Suppression is dependent on TGF-beta, revealed by reversal of suppression with specific neutralizing antibody. In contrast, mice which can reject this tumor from the brain, such as Balb/c mice with immunological memory to the tumor or CD-1 mice with major histo-incompatibility with the tumor, have populations of precursor CTL which are resistant to CSF-induced suppression, in the in vitro restimulation protocol. We propose that the susceptibility to CSF-induced suppression of peripherally generated immune cells that traffic to the brain plays an important role in determining whether growing tumor cells survive in the brain.

Animals↗
PubMed1985

Resistance to listeriosis in two lines of mice genetically selected for high and low antibody production.

Infection by the intracellular parasite Listeria monocytogenes was studied in two inbred lines of mice genetically selected for high and low antibody production against xenogeneic red blood cells. It was revealed that, during the early non-specific phase of infection, bacterial growth in tissues was significantly enhanced in high responder (HR) mice, as opposed to low responder (LR) mice. This is interpreted as the in vivo expression of a genetic impairment of the bactericidal activity of resident macrophages in this line of mice. After Day 2 of infection, the kinetics of bacterial growth in the spleen and the liver was almost identical in the two lines, indicating that mice from both lines generated efficient anti-Listeria immunity. This was confirmed by the fact that no interline difference could be detected in the expression of T-cell mediated immunity, as estimated by the production of protective T cells and delayed sensitivity T cells, and by the level of immunological memory. The genetic impairment in the bactericidal activity of resident macrophages resulted in a significant increase of anti-Listeria antibody production in HR mice and did not prevent T-dependent activation of effector macrophages mobilized in infectious sites. This explains that the overall resistance to listeriosis was similar in LR and HR mice, as shown by the LD50 values respectively estimated as 2.2 X 10(5) and 3.8 X 10(5) bacteria per mouse. This natural resistance was expressed at the same level as that of C57BL/6 mice.

Animals↗
PubMed2001

Generation of experimental allergic airways inflammation in the absence of draining lymph nodes.

The objective of this study was to investigate the contribution of secondary lymphoid organs in the generation and maintenance of experimental allergic airway inflammation. We employed a previously reported murine model of respiratory mucosal allergic sensitization, induced by repeated aerosolizations of ovalbumin in the context of a GM-CSF airway environment. We executed this protocol in wild-type (WT) and lymphotoxin-alpha-deficient mice (LTalpha-KO) mice, which are devoid of lymph nodes (LNs) and possess rudimentary spleen structures. Despite the lack of pulmonary LNs draining the airway compartment, LTalpha-KO mice were fully capable of mounting a robust inflammatory response in the airways, consisting of Th2 polarized CD4+ T cells and eosinophils. This was accompanied by IL-5, IL-13, and IFN-gamma production by splenocytes and generation of ovalbumin-specific serum IgE. Exposure to the same antigen 7 weeks after complete resolution of airway inflammation once again induced a Th2 polarized infiltrate, demonstrating intact immunological memory. To investigate inherent plasticity in establishing antigen-specific immunity, mice were splenectomized before sensitization. Allergic sensitization was completely abrogated in splenectomized LTalpha-KO mice, compared with eusplenic LTalpha-KO controls. These data demonstrate that secondary lymphoid organs, either LN or spleen, are essential for the generation of allergic airway responses.

Administration, Intranasal↗
PubMed2000

Paracrine delivery of IL-12 against intracranial 9L gliosarcoma in rats.

OBJECT: Interleukin-12 (IL- 12) has potential for the treatment of tumors because it can stimulate an antitumor immune response and possesses antiangiogenic properties. In the study reported here, the authors investigated the therapeutic role of locally delivered IL-12 in a malignant brain tumor model. METHODS: After genetically engineering 9L gliosarcoma cells to express IL-12 (9L-IL12 cells), the authors used these cells as a source of locally delivered cytokine. First, they investigated the behavior of these cells, which were implanted with the aid of stereotactic guidance into the rat brain, by using serial magnetic resonance imaging and histopathological examination. Second, they assessed the antitumor efficacy of proliferating, as well as nonproliferating (irradiated), 9L-IL12 cells by implanting these cells in animals challenged by wild-type 9L gliosarcoma (9Lwt) cells. The IL-12 expression in brain regions injected with 9L-IL12 was confirmed by reverse transcription-polymerase chain reaction. Last, the authors explored whether animals treated with 9L-IL12 cells developed an antitumor immunological memory by rechallenging the survivors with a second injection of 9Lwt cells. The authors demonstrated that local delivery of IL-12 into the rat brain by genetically engineered cells significantly prolongs survival time in animals challenged intracranially with a malignant glioma. CONCLUSIONS: These findings support continued efforts to refine local delivery systems of IL-12 in an attempt to bring this therapy to clinical trials.

Animals↗
PubMed2006

Gamma interferon production in response to Mycobacterium bovis BCG and Mycobacterium tuberculosis antigens in infants born to human immunodeficiency virus-infected mothers.

In utero sensitization to infectious pathogens can establish immunological memory and may influence the immune response to unrelated antigens. Little is known about the influence of intrauterine human immunodeficiency virus (HIV) exposure on the cellular immune response to mycobacterial antigens. Whole-blood culture gamma interferon (IFN-gamma) production in response to mycobacterial antigens was measured at birth and 6 weeks of age to determine the characteristics of the IFN-gamma response in HIV-exposed infants to Mycobacterium bovis BCG and mycobacterial antigens. At birth, we observed an increased immune activation in response to phytohemagglutinin among HIV-exposed, uninfected infants. In a proportion of these infants, we also observed an increased immune activation in response to purified protein derivative, BCG, and early secreted antigen target 6. Increases in the IFN-gamma response to the four antigens between birth and 6 weeks of age, observed in all HIV-unexposed infants, was absent in a substantial proportion of HIV-exposed, uninfected infants. The immunological differences persisted at 6 weeks of age, suggesting a sustained impact of in utero immune priming by HIV. Intrauterine exposure to HIV affects the infants' cellular immune response to mycobacterial antigens, either specifically or as a consequence of nonspecific, broadly reactive immune activation. Further studies will be important to help determine optimal vaccination and disease prevention strategies for this vulnerable population group.

Antigens, Bacterial↗