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At least 523 records · Page 29Linked to original sources
PubMed1987

Antigenic variation in rabies and rabies-related viruses: cross-protection independent of glycoprotein-mediated virus-neutralizing antibody.

Immunization experiments with vaccines prepared from the PM and ERA strains of rabies virus demonstrated that in mice, only ERA vaccine primes for an anamnestic response to the rabies-related strain Duvenhage (DUV6); in rabbits, both ERA and PM vaccines induced immunologic memory to DUV6 virus. In mice, ERA vaccine, but not an equal concentration of PM vaccine, conferred protection against a lethal challenge infection with DUV6 virus. This result indicated that the protective activity correlated with the vaccine's ability to induce immunologic memory. A vaccine prepared from a sequentially selected, neutralization-resistant, multiple-variant virus conferred protection against challenge with the parental strain, a result indicating that antigenic variation of the glycoprotein may not be the sole factor in determining the relative efficacy of rabies prophylaxis. We found no correlation between titers of neutralizing antibody and mortality rates in mice immunized with purified glycoprotein from these viruses.

Animals↗
PubMed1997

Recombinant Listeria monocytogenes as a live vaccine vehicle and a probe for studying cell-mediated immunity.

The ability of Listeria monocytogenes (L. monocytogenes) to enter the cytosol of host cells allows secreted proteins to efficiently enter the endogenous antigen-processing pathway leading to presentation by MHC class I molecules. L. monocytogenes has recently been exploited as a live vaccine vehicle for the induction of immunological memory against heterologous antigens. We have established a genetic system for site-specific integration of antigen expression cassettes into the Listeria genome which allows regulated expression and secretion of heterologous proteins. The ability of recombinant strains to stimulate long-term immunological memory and CD8+ T-cell-mediated protective immunity was investigated using the lymphocytic choriomeningitis virus (LCMV) murine infection model. Vaccination of mice with recombinant Listeria strains expressing LCMV antigens induced LCMV-specific CD8+ T cells which protected mice against LCMV challenge. We have also used a cottontail rabbit papillomavirus model to test the ability of recombinant Listeria strains to stimulate protective antitumor immunity in domestic rabbits. These studies have demonstrated the protective efficacy of recombinant L. monocytogenes vaccines and have established an experimental system for systematic analysis of cytotoxic T-cell induction by an intracellular bacterium.

Animals↗
PubMed2000

Immunogenicity of pneumococcal conjugate vaccines.

BACKGROUND: Prevention of pneumococcal infections is a public health priority because of the high impact of the disease and because of the increasing problems due to antimicrobial resistance. Traditional vaccines, consisting of purified capsular polysaccharides (PSs) of Streptococcus pneumoniae, are not immunogenic in young children. In addition they confer only limited protection in patients with immunodeficiencies and hematologic malignancies. IMMUNOGENICITY OF PNEUMOCOCCAL CONJUGATE VACCINES: Immunogenicity of the PS vaccine has been enhanced by coupling pneumococcal PSs to proteins to produce a conjugate vaccine. Conjugate molecules are designed to possess T cell dependent properties, such as immunogenicity in early infancy, stimulation of high levels of IgG isotype antibodies and enhanced immunologic memory responses. In the clinical studies multivalent pneumococcal conjugate vaccines have been shown to induce an IgG-dominating serum antibody response against common pneumococcal serotypes causing infections in children. A booster dose later in life creates a robust and rapid antibody response, indicating the existence of immunologic memory in primed children. Antibodies induced by conjugate vaccines are functionally active, as demonstrated by their high avidity and opsonophagocytic activity.

Bacterial Vaccines↗
PubMed1997

Modeling the lifespan of human T lymphocyte subsets.

T lymphocytes may be classified as naive or memory cells, depending on whether they possess immunological memory. The central tenet of this work is that memory lymphocytes revert to naive lymphocytes in vivo. This phenomenon is modeled by a mechanism qualitatively similar to Demoivre's law of human mortality. Additionally, both lymphocyte subsets undergo decay. Model parameters and their standard errors are estimated by maximizing a likelihood function constructed by Kalman filtering of the experimental data on the assumption that it is contaminated by measurement noise of constant relative error.

Cell Death↗
PubMed2001

Adolescent hepatitis B vaccination. A review.

Adolescents and young adults are at particular risk for HBV. Many countries with varying degrees of incidence now incorporate late childhood and/or adolescent HBV immunizations into their vaccine schedules. Available vaccines are highly effective in inducing long-term seroprotection and are considered of equivalent immunogenicity for most purposes. Immunologic memory maintains seroprotection in the absence of measurable HBsAb. Recent innovations have included the 2-dose, 10 mg Recombivax HB regimen for those 11-15 years old and Twinrix, a combination hepatitis A and B vaccine. The immunocompromised are at increased risk for hypo or non-response to HBV vaccine and loss of immunologic memory. These patients should have post vaccination testing for HBsAb titers as well as periodic testing thereafter. If their HBsAb titer decreases to less than 10 mIU/ml, they should receive a booster dose.

Adolescent↗
PubMed2004

Is chronic fatigue syndrome an autoimmune disorder of endogenous neuropeptides, exogenous infection and molecular mimicry?

Chronic fatigue syndrome is a disorder characterised by prolonged fatigue and debility and is mostly associated with post-infection sequelae although ongoing infection is unproven. Immunological aberration is likely and this may prove to be associated with an expanding group of vasoactive neuropeptides in the context of molecular mimicry and inappropriate immunological memory. Vasoactive neuropeptides including vasoactive intestinal peptide (VIP) and pituitary adenylate activating polypeptide (PACAP) belong to the secretin/glucagon superfamily and act as hormones, neurotransmitters, immune modulators and neurotrophes. They are readily catalysed to smaller peptide fragments by antibody hydrolysis. They and their binding sites are immunogenic and are known to be associated with a range of autoimmune conditions. Vasoactive neuropeptides are widely distributed in the body particularly in the central, autonomic and peripheral nervous systems and have been identified in the gut, adrenal gland, reproductive organs, vasculature, blood cells and other tissues. They have a vital role in maintaining vascular flow in organs, and in thermoregulation, memory and concentration. They are co-transmitters for acetylcholine, nitric oxide, endogenous opioids and insulin, are potent immune regulators with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system to toxic assault, promotion of neural development and the maintenance of homeostasis. This paper describes a biologically plausible mechanism for the development of CFS based on loss of immunological tolerance to the vasoactive neuropeptides following infection, significant physical exercise or de novo. It is proposed that release of these substances is accompanied by a loss of tolerance either to them or their receptor binding sites in CFS. Such an occurrence would have predictably serious consequences resulting from compromised function of the key roles these substances perform. All documented symptoms of CFS are explained by vasoactive neuropeptide compromise, namely fatigue and nervous system dysfunction through impaired acetylcholine activity, myalgia through nitric oxide and endogenous opioid dysfunction, chemical sensitivity through peroxynitrite and adenosine dysfunction, and immunological disturbance through changes in immune modulation. Perverse immunological memory established against these substances or their receptors may be the reason for the protracted nature of this condition. The novel status of these substances together with their extremely small concentrations in blood and tissues means that clinical research into them is still in its infancy. A biologically plausible theory of CFS causation associated with vasoactive neuropeptide dysfunction would promote a coherent and systematic approach to research into this and other possibly associated disabling conditions.

Autoimmune Diseases↗
PubMed1966

Enhancement of antibody synthesis by 6-mercaptopurine.

The administration of 6-MP to rabbits led to either suppression or enhancement of antibody production, depending on when the drug was given in relation to the antigenic challenge. Maximum enhancement of antibody synthesis was found when a small dose of BGG was administered 5 days after the last dose of a 1 wk course of 6-MP. There were no indications that the macrophage system or immunological memory was affected in animals with augmented antibody synthesis. It was proposed that enhancement of antibody production by 6-MP was due to nucleic acids released from cells killed or injured by the drug. It was suggested that lymphocytes incorporating these nucleic acids were transformed into specialized cells capable of direct and immediate stimulation by antigen and lacking immunological memory (hemocytoblasts). A relatively small dose of antigen was apparently capable of stimulating all the hemocytoblasts representing a given clone) with the result that large amounts of antibody rapidly appeared in the serum.

Animals↗
PubMed2006

Killing of normal melanocytes, combined with heat shock protein 70 and CD40L expression, cures large established melanomas.

Previously, we showed that nine intradermal injections of a plasmid in which the HSVtk suicide gene is expressed from a melanocyte-specific promoter (Tyr-HSVtk), combined with a plasmid expressing heat shock protein 70 (CMV-hsp70), along with systemic ganciclovir, kills normal melanocytes and raises a CD8+ T cell response that is potent enough to eradicate small, 3-day established B16 tumors. We show in this study that, in that regimen, hsp70 acts as a potent immune adjuvant through TLR-4 signaling and local induction of TNF-alpha. hsp70 is required for migration of APC resident in the skin to the draining lymph nodes to present Ags, derived from the killing of normal melanocytes, to naive T cells. The addition of a plasmid expressing CD40L increased therapeutic efficacy, such that only six plasmid injections were now required to cure large, 9-day established tumors. Generation of potent immunological memory against rechallenge in cured mice accompanied these therapeutic gains, as did induction of aggressive autoimmune symptoms. Expression of CD40L, along with hsp70, increased both the frequency and activity of T cells activated against melanocyte-derived Ags. In this way, addition of CD40L to the hsp70-induced inflammatory killing of melanocytes can be used to cure large established tumors and to confer immunological memory against tumor cells, although a concomitant increase in autoimmune sequelae also is produced.

Animals↗
PubMed2001

Controlled local delivery of interleukin-2 by biodegradable polymers protects animals from experimental brain tumors and liver tumors.

PURPOSE: The purpose of our study was to develop an injectable polymeric system for the long-term localized delivery of bioactive interleukin-2 for antitumor immunotherapy. METHODS: IL-2 was encapsulated into gelatin and chondroitin-6-sulfate using an aqueous-based complex coacervation. CTLL-2 cells were used to measure the bioactivity of released IL-2 and radiolabeled IL-2 was used for release studies in the rat brain and mouse liver. Antitumor efficacy studies were carried out in primary (9L gliosarcoma) and metastatic (B16-F10 melanoma) brain tumor models in rats and mice, respectively, as well as a murine liver tumor model (CT26 carcinoma). Survivors of the metastatic brain tumor challenge were rechallenged with tumor in the opposite lobe of the brain to confirm that antitumor immunologic memory had developed. RESULTS: Bioactive IL-2 was released for over 2 weeks in vitro and in vivo IL-2 release showed significant IL-2 levels for up to 21 days. Polymeric IL-2 microspheres injected intratumorally were statistically more effective in protecting animals challenged with fatal tumor doses in the brain and the liver than placebo or autologous tumor cells genetically engineered to secrete IL-2. Immunologic memory was induced following IL-2 microsphere therapy in the B16-F10 brain tumor model that was capable of protecting 42% of animals from a subsequent intracranial tumor challenge, suggesting that tumor destruction was mediated by the immune system. CONCLUSIONS: Local IL-2 therapy using novel polymeric carriers. aimed at stimulating long-lasting antitumor immunity, may provide an improved method of treating a variety of cancers.

Animals↗
PubMed2004

Scientific challenges for the quality control and production of group C meningococcal conjugate vaccines.

Recommendations (formerly known as requirements) for meningococcal polysaccharide vaccines were adopted by the World Health Organisation (WHO) Expert Committee on Biological Standardisation in 1976 and amended in 1978 and 1981. In clinical studies, these vaccines have been shown to have efficacy of at least 90% and have proved to be highly effective in vaccination programmes. Nevertheless, their inability to elicit protective responses in young infants or to induce good immunological memory has prevented their implementation in national infant immunisation schedules. Following the successful introduction of the Haemophilus influenzae type b conjugate (Hib) vaccines, considerable progress has been made in the development of similar conjugate vaccines based on meningococcal group C capsular polysaccharide. Controlled clinical trials have demonstrated that they induce protective levels of antibodies to group C polysaccharide in all age groups and, as T-cell dependent antigens, induce immunological memory and affinity maturation of anti-capsular antibodies. Such vaccines have been shown to offer protective immunity following the introduction of group C conjugates in the UK. The World Health Organisation has produced recommendations for the production and control of these new vaccines.

Meningococcal Vaccines↗
PubMed1977

Induction of avian immunological responsiveness following cloacal drinking of immunogen.

A solution of human serum albumin which has been cloacally ingested can cause effective development of immunological memory with minimal or no immediate production of antibody in 4 to 6 week old chickens. Such memory production was not accompanied by the generation of circulating rosette-forming ABC (antigen binding cells) and thus the peripheral appearance of such cells as a part of the normal primary response to HSA (human serum albumin) does not accord with the interpretation that they represent memory B cells. The cloacal route may be important for the maturing chick in initiating immunity to the food and micro-organisms of its external environment and gut flora.

Animals↗
PubMed2003

Innate defence: evidence for memory in invertebrate immunity.

Acquired immunity in vertebrates is characterized by immunological memory and specificity, whereas the innate defence systems of invertebrates are assumed to have no specific memory. Here we use a model system of a copepod, which is a minute crustacean, and a parasitic tapeworm to show that the success of reinfection depends on the antigenic resemblance between the consecutively encountered parasites. This finding indicates that an invertebrate defence system may be capable of specific memory.

Animals↗
PubMed1994

Immunotherapy of cancer using cytokine gene-modified tumor vaccines.

Distant metastasis is the major cause for therapeutic failures in clinical oncology. Active immunotherapy of patients with low tumor burden would not only contribute to further reduction of the remaining tumor burden to subclinical levels, but it would also establish a constant state of immunity, i.e. immunological memory, that could protect the patient from recurrence of disease. Studies employing rodent tumor models with little or no intrinsic immunogenicity have shown that genitically modified tumor cell preparations consisting of irradiated tumor cells transduced with and expressing cytokines such as IL-2, IL-6, IFN-gamma or GM-CSF were capable of inducing the regression of a preexisting tumor burden and cure animals from their disease. Moreover, in some instances the cured animals have retained immunological memory, as indicated by the fact that such animals have resisted a second challenge with the parental tumor cells. Induction of potent immune responses in tumor bearing animals against non-immunogenic tumors supports the view that active immunization of cancer patients deserves consideration despite lack of demonstrable immunogenicity in many human tumors.

Animals↗
PubMed1990

Localized memories in idiotypic networks.

The present paper investigates conditions under which immunological memory can be maintained by stimulatory idiotypic network interactions. The paper was motivated by the work of (De Boer & Hogeweg, 1989b, Bull. math. Biol. 51, 381-408.) which claimed that idiotypic memory is not possible because of percolation within the network. Here we reinvestigate the issue of percolation using both the previous model and a simpler one (Weisbuch, 1990, J. theor. Biol. 143, 507-522.) that allows analytic analysis. We focus on network topologies in which each Ab1 is connected to several Ab2s, which in turn are connected to several Ab3s. It is demonstrated that, for a considerable range of parameters, both models account for the existence of localized memory-states in which only the Ab1 and the Ab2 clones are activated and the clones of the Ab3 level remain virgin. The existence of localized memory-states seems to contradict the previous percolation result. This discrepancy will be shown to depend on the system dynamics. By simulation we explore the parameter regimes for which one finds percolation and those for which localized memory-states exists. We show that the conditions required for attaining the localized memory-state are considerably more stringent than those required for its existence and local stability. We conclude that both localized memory and percolation are possible in stimulatory idiotypic networks.

Animals↗
PubMed2003

Pneumococcal vaccination and revaccination of older adults.

As individuals advance in age, the risk of infection, bacteremia, and mortality caused by Streptococcus pneumoniae rises. Retrospective data demonstrate that the licensed penumococcal polysaccharide vaccine (PPV) is effective in older persons in reducing serotype-specific invasive disease. PPV demonstrates good immunogenicity in older adults, generally comparable to that in younger subjects, although certain cohorts respond less well. The response to PPV is T cell independent, however, and does not elicit immunologic memory. The duration of the anti-capsular polysaccharide antibody response appears to wane as early as 3 years after vaccination. In older persons, revaccination induces an antibody response, although it may not be as strong as that from the initial vaccine. While revaccination of older adults has been recommended, clinical efficacy has not yet been proven. Measures of antibody function may be at least as important in determining protection as are quantitative antibody levels. Additional studies of immunogenicity, particularly regarding revaccination, will facilitate the design of an optimal pneumococcal vaccination policy. Research into conjugate- and protein-based pneumococcal vaccines, which elicit T-cell-dependent responses and induce immunologic memory, is needed in older persons. In the meantime, administering to PPV to recommended groups should be a public health priority.

Adult↗
PubMed2006

A critical role for TNF receptor-associated factor 1 and Bim down-regulation in CD8 memory T cell survival.

The mechanisms that allow the maintenance of immunological memory remain incompletely defined. Here we report that tumor necrosis factor receptor (TNFR)-associated factor (TRAF) 1, a protein recruited in response to several costimulatory TNFR family members, is required for maximal CD8 T cell responses to influenza virus in mice. Decreased recovery of CD8 T cells in vivo occurred under conditions where cell division was unimpaired. In vitro, TRAF1-deficient, antigen-activated T cells accumulated higher levels of the proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bim(S). In the presence of excess IL-15, memory phenotype T cells with similar surface phenotype and comparable levels of Bcl-2 family members could be generated from WT or TRAF1-deficient T cell receptor transgenic OT-I T cells. However, when the memory CD8 T cells were allowed to compete for survival signals in the absence of antigen in vivo, the TRAF1-deficient T cells showed decreased recovery compared with TRAF1-sufficient T cells. This defect in T cell recovery in vivo was alleviated by introduction of siRNA to down-modulate Bim in TRAF1-deficient memory T cells. These studies identify the TRAF1 signaling axis and Bim down-regulation as critical for CD8 memory T cell survival in vivo.

Animals↗
PubMed1998

IgA antibody-forming cell responses in the nasal-associated lymphoid tissue of mice vaccinated by intranasal, intravenous and/or subcutaneous administration.

Effects of a single intranasal (i.n.), subcutaneous (s.c.) or intravenous (i.v.) vaccination and their combined vaccination of priming and boosting on a primary and a secondary IgA antibody forming cell (AFC) response were examined in the nasal associated lymphoid tissue (NALT), spleen and popliteal lymph nodes (pLNs) of BALB/c mice. Mice were primed with the vaccine prepared from A/Yamagata/120/86 (H1N1) together with a cholera toxin-adjuvant and boosted with the same vaccine 3 weeks later. Three days after boosting, IgA-AFC responses in each lymphoid tissue were measured as an index of the immunological memory that mediates a secondary IgA-AFC response. Single i.n. vaccination induced a greater primary IgA-AFC response in the NALT not only than that in the spleen or pLNs, but also than that induced by single i.v. or s.c. vaccination. The combination of i.n. priming and i.n. boosting afforded a greater anamnestic IgA-AFC response in the NALT not only than that in the spleen or pLNs, but also than that induced by any other combinations of priming and boosting (i.n.-i.v., i.n.-s.c., s.c.-i.n., s.c.-i.v., and s.c.-s.c.). These results showed that i.n. priming induced a greater primary IgA-AFC response in the NALT and simultaneously induced the immunological memory that mediated a greater secondary-type AFC response following i.n. boosting in the NALT.

Administration, Intranasal↗
PubMed2000

Memory B-cell persistence is independent of persisting immunizing antigen.

Immunological memory in the antibody system is generated in T-cell-dependent responses and carried by long-lived memory B cells that recognize antigen by high-affinity antibodies. But it remains controversial whether these B cells represent true 'memory' cells (that is, their maintenance is independent of the immunizing antigen), or whether they are a product of a chronic immune response driven by the immunizing antigen, which can be retained in the organism for extended time periods on the surface of specialized antigen-presenting cells (follicular dendritic cells). Cell transfer experiments provided evidence in favour of a role of the immunizing antigen; however, analysis of memory cells in intact animals, which showed that these cells are mostly resting and can persist in the absence of detectable T-cell help or follicular dendritic cells, argued against it. Here we show, by using a genetic switch mediated by Cre recombinase, that memory B cells switching their antibody specificity away from the immunizing antigen are indeed maintained in the animal over long periods of time, similar to cells retaining their original antigen-binding specificity.

Alleles↗