SEARCH · PubMed Health

Results for “immunization”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 91 records · Page 5Linked to original sources

PubMed2006

Immune stimulatory effects of CD70 override CD70-mediated immune cell apoptosis in rodent glioma models and confer long-lasting antiglioma immunity in vivo.

CD70 (CD27 ligand) promotes the expansion of primed lymphocytes by enhancing cell survival. Surprisingly, we previously observed that CD70 aberrantly expressed on human glioma cells promoted immune cell apoptosis and inhibited alloreactive lysis. Here we report that ectopic expression of CD70 in mouse glioma cells enhances apoptosis of T, B and NK cells in coculture, but nevertheless promotes glioma cell lysis by NK cells in vitro. In nude mice, CD70 expression in SMA-560 gliomas delays the glioma growth upon subcutaneous (s.c.) or intracerebral (i.c.) inoculation, suggesting a role for CD70/CD27-dependent NK cell activity in tumor surveillance. In syngeneic immunocompetent VM/Dk mice, CD70 allows the rejection of s.c. and i.c. implanted SMA-560 tumors. The tumorigenicity of CD70-expressing glioma cells is abrogated when TGF-beta signaling is blocked. Moreover, mice surviving the s.c. CD70 glioma challenge subsequently also reject wild-type glioma cells administered i.c. Similarly, CD70-expressing GL-261 gliomas are rejected in syngeneic C57BL/6 mice, while glioma growth is restored in C57BL/6 CD27(-/-) mice, suggesting that the CD70/CD27 interaction recruits a tumor-specific T-cell repertoire and induces tumor-specific memory. Altogether, these observations indicate that the net effect of aberrant CD70 expression in gliomas is immune stimulatory rather than immune paralytic and encourage its application in tumor immunotherapy.

Animals↗

PubMedDate not supplied

Immune reactivity to mite allergens in nonatopic subjects: immune deviation or immune ignorance.

Most subjects without IgE to Dermatophagoides pteronyssinus do not have IgG to Der p 1 or Der p 2 (as measured by RIA). However, by immunoblot or ELISA, IgG reactivity (mostly IgG1) to mite components is easily detectable. This discrepancy is caused largely by immune reactivity to mite components with a high molecular weight under native conditions (possibly mite gut flora cross-reactive with human gut flora) and partially by the presence of IgG with low affinity for fluid-phase antigen. We conclude that the pattern of IgG antibody in subjects without IgE to mites does not support the notion of immune deviation, but rather indicates a lack of a mite-induced high-affinity immune response.

Animals↗

PubMed1991

Inhibition of platelet GPIIb/IIIa binding to fibrinogen by serum factors: studies of circulating immune complexes and platelet antibodies in patients with hemophilia, immune thrombocytopenic purpura, human immunodeficiency virus-related immune thrombocytopenic purpura, and systemic lupus erythematosus.

We have studied the conditions of in vitro binding of platelet glycoprotein IIb/IIIa (GPIIb/IIIa) to fibrinogen and applied the results to identify and measure the serum inhibitors to the binding. For the enzyme-linked immunosorbent assay, platelet extract was delivered to a fibrinogen-coated microtiter plate that was incubated for 2 hours, followed by incubation with anti-GPIIb/IIIa monoclonal antibody for another 2 hours. The plate was then incubated with peroxidase-conjugated anti-mouse IgG for color development. The binding was shown to be calcium-dependent. The binding was partially blocked by treating the coated fibrinogen with anti-fibrinogen antibody. Reduction or dissociation of GPIIb/IIIa resulted in the total loss of its ability to bind to fibrinogen. Platelet extracts of patients with hemophilia showed decreased binding (25% and 14%, compared with control platelet extract), and an extract from a patient with Glanzmann's thrombasthenia showed no binding. With the enzyme-linked immunosorbent assay we have measured serum inhibitors to GPIIb/IIIa binding to fibrinogen in 35 hemophilia A, 17 immune thrombocytopenic purpura, 22 human immunodeficiency virus-related immune thrombocytopenic purpura, and 29 systemic lupus erythematosus serum samples. In those patients with inhibition by serum, polyethylene glycol precipitation of circulating immune complexes (CICs) decreased the inhibition by the supernatants, and all the resolubilized CIC precipitates demonstrated inhibition, which indicates that CICs play a major role in the inhibition of GPIIb/IIIa binding to fibrinogen. This, then, provides evidence of CIC-mediated impaired GPIIb/IIIa binding to fibrinogen in hemophilia A, HIV-ITP, and SLE.

Antibodies↗

PubMed1983

Antigen size and charge in immune complex glomerulonephritis. II. Passive induction of immune deposits with dextran-anti-dextran immune complexes.

Utilizing dextrans of restricted sizes (10,000, 70,000, 500,000 daltons), modified with regard to charge (neutral, polycationic, polyanionic) and an anti-dextran murine IgA myeloma, W3129, the authors have examined a model that may be used in the study of the combined effect of size and charge on renal deposition of immune complexes. Polycationic DEAE dextran complexes, using the 10,000 dalton antigen, showed a mesangiocapillary pattern of deposition. The other antigens showed focal to diffuse mesangial localization of varying degree. This indicates the potential usefulness of this system in examining the factors important in glomerular immune injury. The relevance to other observations, importance of polysaccharide antigens, and role in circulating versus in situ or "planted" immune complex models are considered.

Animals↗

PubMed1981

Immunity to influenza in ferrets. XIV: Comparative immunity following infection or immunization with live or inactivated vaccine.

Immunization by live influenza virus induced a greater protective effect against subsequent challenge by the homologous virus than by the corresponding killed virus vaccine. Furthermore, tracheas excised from 11-day and 28-day influenza-virus-infected ferrets were more resistant to reinfection than tracheas excised from ferrets immunized by killed influenza vaccine, despite equivalent serum antibody titres at these times. Histological examination of trachea sections taken from vaccinated and virus-infected animals showed an increased cellular inflammatory infiltrate in the latter at Days 11 and 28 after immunization. The amount of IgG detected in these sections, measured by a fluorescent antibody technique, correlated with the extent of cellular infiltration, the fluorescence being both intra- and extracellular for sections from virus-infected animals, but only extracellular in sections from Day-28 vaccinated animals. In contrast there was little or no cellular infiltration into lung tissues, the levels of IgG detected being comparable to those in sections taken from control animals. These results provide further evidence that live influenza vaccines induce local antibody in the upper respiratory tract of ferrets, in contrast to killed influenza vaccines, and that this local induction may play a significant role in the greater protective efficacy of live influenza vaccines.

Animals↗

PubMed1989

Aging and immunity to tuberculosis: prolonged survival of old mice infected with Mycobacterium tuberculosis by adoptive immunization with memory-immune T lymphocytes.

This study shows that memory immune T lymphocytes, harvested from young (3-month-old) mice infected intravenously with Mycobacterium tuberculosis and then exposed to protracted chemotherapy with isoniazid, are capable of adoptively protecting old (24 month) mice from a subsequent fatal challenge infection. Survival of such adoptively protected animals was prolonged, but did not extend beyond the mean survival time of uninfected old control mice. During this time the passively transferred memory T cell population retained their functional capacity to protect against subsequent tuberculosis infection. These data indicate, therefore, that reconstitution of decayed cell-mediated antimicrobial immunity in old mice in vivo with memory T cells is technically feasible, although the life span of the animal is not extended over that of control animals. They indicate, moreover, that the memory T cells remain functional in what some reports have considered a suppressive environment and show further that the macrophages with which the infused T cells interact in the aged host remain functionally able to express acquired resistance.

Aging↗

PubMed1996

Brugia pahangi in cats: the passive transfer of anti-microfilarial immunity from immune to non-immune cats.

Serum from cats (Felis catus) that were repeatedly infected with Brugia pahangi and had become amicrofilaraemic (mf-ve) was injected intravenously into microfilaraemic (mf+ve) cats. If more than 1 microliter of immune serum per 1000 mf was injected, microfilarial counts fell dramatically within minutes and, in some cats, mf completely disappeared. In most cases mf reappeared 21-44 days later. However, in two experiments mf never reappeared and circulating antigen (indicative of the presence of living adults) could not be detected. At autopsy no adult worms were found, but in one cat 6 mf/ml were detected by filtration of cardiac blood. Passive transfer of single Ig isotypes showed that IgG is the immunoglobulin responsible for the mf killing effect of immune serum, and that IgG1 is probably the most active isotype. Mf killing and destruction, occurred in the lungs in an antibody dependent cell mediated reaction involving neutrophils, eosinophils and mononuclear cells. Three of the 20 recipient cats died from what appeared to be anaphylactic shock while under anaesthesia probably due to the sudden release of inflammatory mediators in the lung.

Animals↗

PubMed2006

Why can't the immune system control HIV-1? Defining HIV-1-specific CD4+ T cell immunity in order to develop strategies to enhance viral immunity.

Globally, at least 60 million people have been infected with the human immunodeficiency virus type 1 (HIV-1), the majority of whom will develop the acquired immunodeficiency syndrome (AIDS) leading to tremendous morbidity and the mortality. Understanding the immunopathogenesis of AIDS and the immune correlates of viral protection are necessary to develop effective vaccines and immunotherapies. A major focus of our laboratory has been to understand the CD4+ T cell immune response directed against HIV- 1, and to determine mechanisms of T cell dysfunction that lead to viral escape. In addition, we are interested in evaluating the TNF-TNFR family members as potential molecular adjuvants that could be incorporated into vaccines which could be used to further boost T cell immunogenicity in healthy or HIV-1-infected individuals, as many of these molecules have been shown to replace the functions of CD4+ T cell help.

AIDS Vaccines↗

PubMed1969

Cells involved in the immune response. VI. The immune response to red blood cells in irradiated rabbits after administration of normal, primed, or immune allogeneic rabbit bone marrow cells.

Irradiated rabbits given allogeneic bone marrow cells from normal adult donors responded to an injection of sheep red blood cells by forming circulating antibodies. Their spleen cells were also capable of forming many plaques using the hemolysis in gel technique, and were also capable of undergoing blastogenesis and mitosis and of incorporating tritiated thymidine upon exposure to the specific antigen in vitro. However, irradiated rabbits injected with allogeneic bone marrow obtained from rabbits injected with sheep red blood cells 24 hr prior to sacrifice (primed donors) were incapable of mounting an immune response after stimulation with sheep red cells. This loss of reactivity by the bone marrow from primed donors is specific for the antigen injected, since the immune response of the irradiated recipients to a non-cross-reacting antigen, the horse red blood cell, is unimpaired. Treatment of the bone marrow donors with high-titered specific antiserum to sheep red cells for 24 hr prior to sacrifice did not result in any diminished ability of their bone marrow cells to transfer antibody-forming capacity to sheep red blood cells. The significance of these results, with respect to the origin of the antigen-reactive and antibody-forming cells in the rabbit, is discussed.

Animals↗

PubMed1984

Studies on immunity in hybridoma-bearing mice. A. Immune response to antigens. I. Role of subcutaneously injected IgE-producing hybridoma on antibody production of different isotypes against immunizing antigens.

When immunized with ovalbumin (OVA), mice bearing subcutaneously injected anti-dinitrophenyl (DNP) IgE-secreting hybridoma cells do not produce anti-OVA IgE antibodies as long as anti-DNP IgE is present in abundance in their sera. As soon as the titer of anti-DNP IgE antibody falls, anti-OVA IgE antibody appears. This inhibition of production of anti-OVA IgE is attributed to Fc epsilon-bearing T cells which have a suppressive action of limited duration. Other isotypes of anti-OVA antibodies are produced in similar amounts as in controls which were immunized with OVA but not injected with hybridoma cells.

Animals↗

PubMedDate not supplied

Humoral immunity and composition of immune complexes in patients with rheumatoid arthritis, with special reference to IgE-containing immune complexes.

IgE-containing circulating immune complexes (IgE-CIC) were determined with a 2.5% PEG-precipitation assay in 98 patients with classical or definite rheumatoid arthritis (RA). Of the 45 IgE-CIC positive sera, only 4 had elevated total serum IgE. IgE-CIC positive patients had more active disease than patients without IgE-CIC, as determined by their more swollen joints and higher Ritchie indices (p less than 0.04 and 0.02, respectively). Apart from IgE, other immunoglobulin isotypes, rheumatoid factor (RF) of the IgG-, IgA- and IgM-classes, C3 and antinuclear antibodies could be demonstrated in the IgE-containing PEG-precipitates. IgE-RF could not be demonstrated in serum or in IgE-CIC. Anti-IgE of the IgM-class (IgMaIgE) were frequently found (28/45 patients) in the IgE-positive PEG-precipitates. All 14 patients positive for IgGaIgE in the IgE-CIC were also positive for IgMaIgE in the CIC. As in the serum, there was a good correlation in the CIC between the level of IgGaIgE and the level of IgMaIgE (r = 0.64). The correlation between the respective levels of IgGaIgE and IgMaIgE in serum and in CIC was high (r = 0.93 and 0.79, respectively). On the other hand, only 1 patient was positive for IgAaIgE in the IgE-CIC. We conclude that IgE and aIgE of the IgM- and IgG-classes are frequently present in the immune complex form in RA and that they are correlated with the clinical activity of arthritis.

Adult↗

PubMed1979

Purification of soluble immune complexes from serum using polymethylmetacrylate beads coated with conglutinin or C1q. Application to the analysis of the components of in vitro formed immune complexes and of immune complexes occurring in vivo during leishmaniasis.

A procedure for the isolation of immune complexes from human sera has been developed. Two steps are involved: (1) lipid-free serum is precipitated by polyethylene glycol; (2) the solubilized precipitate is absorbed on a column of polymethylmethacrylate beads coated with conglutinin (K) or C1q; the column is washed, the complexes are then eluted, using 0.02 M EDTA (for K column) or 0.5 M NaCl (for C1q column). This procedure permitted the purification and the characterization of soluble 125I-BSA-anti-BSA, 125 I-tetanus toxoid-anti-tetanus toxoid, and 125-I-HBsAg-anti-HBsAg complexes made in vitro in the presence of fresh human serum. The isolated complexes were shown to contain antigen, antibody, C1q, C1r, C1s and C3. When normal human serum was submitted to such a procedure, no detectable amount of protein was present in the final eluted fraction. Immune complexes formed in vivo were also purified by conglutinin column from the serum of a patient with disseminated leishmaniasis. The isolated material was found to contain IgM, IgG, C1q, C1r, C1s, C3c and C3d. The purified complexes dissociated at acid pH were found to contain anti-IgG and anti-leishmania antibodies.

Adult↗

PubMed1986

Effects of anti-schistosomal chemotherapy on immune responses, protection and immunity. III. An effective regimen of praziquantel does not alter immune capabilities of normal mice.

Praziquantel is a broad spectrum anti-helminthic drug active against a variety of parasitic trematodes and cestodes. This report studies the effects of a schistosomacidal regimen of praziquantel on the generation of the cell-mediated and humoral response capabilities of normal, uninfected mice. Three doses of 100 mg praziquantel/kg body weight at 4-hr intervals cured several strains of mice with Schistosoma mansoni infections of several intensities. When this curative regimen was applied to normal, uninfected mice it did not alter peripheral blood leukocyte counts, circulating eosinophil numbers or splenic weights. Neither did this regimen alter the development of responsiveness to sheep erythrocytes (SRBC) as measured by dermal delayed-type hypersensitivity (DTH) or the number of splenic plaque forming cells. Furthermore, DTH and serum antibody responses to a soluble antigen (bovine serum albumin) were also comparable in treated and untreated mice. It appears that an anti-schistosomacidal regimen of praziquantel does not alter normal murine cellular or humoral immune responses.

Animals↗

PubMed2005

A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States: recommendations of the Advisory Committee on Immunization Practices (ACIP) part 1: immunization of infants, children, and adolescents.

This report is the first of a two-part statement from the Advisory Committee on Immunization Practices (ACIP) that updates the strategy to eliminate hepatitis B virus (HBV) transmission in the United States. The report provides updated recommendations to improve prevention of perinatal and early childhood HBV transmission, including implementation of universal infant vaccination beginning at birth, and to increase vaccine coverage among previously unvaccinated children and adolescents. Strategies to enhance implementation of the recommendations include 1) establishing standing orders for administration of hepatitis B vaccination beginning at birth; 2) instituting delivery hospital policies and procedures and case management programs to improve identification of and administration of immunoprophylaxis to infants born to mothers who are hepatitis B surface antigen (HBsAg) positive and to mothers with unknown HBsAg status at the time of delivery; and 3) implementing vaccination record reviews for all children aged 11-12 years and children and adolescents aged <19 years who were born in countries with intermediate and high levels of HBV endemicity, adopting hepatitis B vaccine requirements for school entry, and integrating hepatitis B vaccination services into settings that serve adolescents. The second part of the ACIP statement, which will include updated recommendations and strategies to increase hepatitis B vaccination of adults, will be published separately.

Adolescent↗

PubMed1991

Vaccination with the major secretory protein of Legionella induces humoral and cell-mediated immune responses and protective immunity across different serogroups of Legionella pneumophila and different species of Legionella.

In a previous study, we demonstrated that immunization of guinea pigs with the major secretory protein (MSP) of Legionella pneumophila, serogroup 1 induced humoral and cell-mediated immune responses to MSP and protective immunity against lethal aerosol challenge with this serogroup of L. pneumophila. Although serogroup 1 L. pneumophila cause most cases of Legionnaires' disease, other serogroups of L. pneumophila and species of Legionella cause many cases. In this study, we have examined if immunization with MSP induces humoral and cell-mediated immune responses and protective immunity across different serogroups of L. pneumophila and species of Legionella. By immunoblot analysis, MSP from L. pneumophila serogroup 1 (Lp1 MSP), L. pneumophila serogroup 6 (Lp6 MSP), and Legionella bozemanii (Lb MSP) shared common epitopes recognized by guinea pig anti-Lp1 MSP antiserum. These MSP molecules, however, were not identical as they had different apparent m.w. Immunization of guinea pigs with MSP induced strong cell-mediated immune responses across the different serogroups and species, as indicated by splenic lymphocyte proliferation and cutaneous delayed-type hypersensitivity in response to both homologous and heterologous MSP. Immunization with MSP induced strong protective immunity across two serogroups of L. pneumophila; overall, 9 survived aerosol challenge with L. pneumophila serogroup 1 compared to 0 of 12 (0%) sham-immunized control animals (p = 3 x 10(-4), Cochran-Mantel-Haenzel chi 2 statistic for pooled data). Immunization with MSP also induced protective immunity across species of Legionella but protection was species-specific. Whereas immunization with Lb MSP induced protective immunity against L. pneumophila, neither immunization with Lp1 MSP nor immunization with Lb MSP induced protective immunity against L. bozemanii, which produces MSP. Not surprisingly, immunization with MSP did not induce protective immunity against MSP-negative Legionella micdadei. In the case of both L. bozemanii and L. micdadei, immunization with a sublethal dose did confer protective immunity to aerosol challenge indicating that these species do contain immunoprotective components. This study demonstrates that immunization with MSP induces humoral and cell-mediated immune responses across different serogroups of L. pneumophila and species of Legionella, but that the capacity of MSP immunization to induce protective immunity is species-specific. Nevertheless, an MSP vaccine has the potential to induce protective immunity against the great majority of cases of Legionnaires' disease.

Aerosols↗

PubMed1981

Levamisole and bovine immunity: in vitro and in vivo effects on immune responses to herpesvirus immunization.

Levamisole was shown to enhance in vitro blastogenic responses of bovine lymphocytes to nonspecific mitogens (phytohemagglutinin and pokeweed mitogen) as well as to infectious bovine rhinotracheitis virus and purified protein derivative. Greatest enhancement was observed at suboptimal concentrations of viral antigen. In addition to enhancing lymphocyte reactivity levamisole also affected macrophage activity as determined by increased Fc receptor activity and [3H]glucosamine incorporation. Levamisole (5-50 micrograms/mL) enhanced type II immune (or gamma) interferon production by macrophage-lymphocyte cultures. Administration of levamisole and attenuated infectious bovine rhinotracheitis vaccine virus in vivo did not elevate cellular or humoral responses.

Animals↗

PubMed1976

The immune response in cirrhotic rats. Antigen distribution, humoral immunity, cell-mediated immunity and splenic suppressor cell activity.

The immunological disturbances occurring as a result of liver disease have been studied in an animal model of cirrhosis. The mononuclear phagocytic cells of the normal liver phagocytose large amounts of antigen irrespective of whether that antigen is injected directly into the portal or into the systemic circulations. The liver therefore acts as a filter 'in series' and 'in parallel' with the spleen and reduces the immunogenicity of antigens entering the organism by either of these routes. In rats with hepatic cirrhosis, there is a reduction in the capacity of the liver to phagocytose the flagellar antigen of Salmonella adelaide. This results in increased stimulation of splenic lymphoid tissue and in an increased antibody response to this thymus-independent antigen. The increased antigenic stimulus to the spleen may also be responsible for the increased suppressor-cell activity which has been demonstrated in these rats, and may be the mechanism of the diminished cell-mediated immune response both in this animal model of cirrhosis and in the human disease state. These studies suggest that many of the immunological disturbances associated with chronic liver disease may be the result of maldistribution of antigen occurring because of impaired hepatic phagocytic capacity.

Animals↗

PubMed1984

Transfer rate of transplacental immunity to tetanus from non-immunized and immunized mothers.

Tetanus antitoxin was quantitatively measured in 912 pregnant women by indirect hemagglutination test. The mothers who received no dose, one dose and two doses of tetanus toxoid were 64.6%, 10.1% and 25.3% respectively. The percentage of mothers with protective antibodies in the groups receiving none, one, and two doses of tetanus toxoid were 95.4, 100 and 100. The level of protective antibody in the newborn and the magnitude of transfer rate of passive immunity to tetanus depended directly upon the level of tetanus antitoxin in maternal serum. Mothers who had tetanus antitoxin of 1.28 IU/ml or more could transfer protection to almost all of the newborns (97%-100%) irrespective of doses of tetanus toxoid administration. However, mothers who had received two doses of tetanus toxoid during pregnancy not only confer good protection but also transfer a high tetanus antitoxin levels to their newborns.

Adult↗