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At least 1,531 records · Page 85Linked to original sources
PubMed2005

A novel DNA adjuvant, N3, enhances mucosal and systemic immune responses induced by HIV-1 DNA and peptide immunizations.

AIMS: The study was designed to evaluate a novel cationic lipid DNA adjuvant (N3) and its function for HIV-1gp160/rev DNA plasmid delivered intranasally. The primary N3/HIV-DNA plasmid immunizations were boosted intranasally with a gp41 peptide in a anionic L3 adjuvant. This novel prime-boost strategy of mucosal immunization provided a broad HIV-1 envelope specific immunity, and recognition of viruses of subtypes A, B and C. CONCLUSIONS: Intranasal N3-adjuvanted gp160/rev DNA prime followed by one L3-peptide boosting immunization, induced broadly neutralizing antibodies against HIV-1 in the mucosa and systemically. The needle-free intranasal prime-boost strategy using two different adjuvant formulations reduced significantly the dose of DNA needed.

Animals↗
PubMed2005

Immunization with DNA vaccines encoding different mycobacterial antigens elicits a Th1 type immune response in lambs and protects against Mycobacterium avium subspecies paratuberculosis infection.

Paratuberculosis, or Johne's disease, is a disease of domestic and wild ruminants that culminate with a chronic enteritis caused by Mycobacterium avium subsp. paratuberculosis. The aim of this work was to evaluate the type of immune response, Th1 or Th2, induced by DNA vaccinations in lambs of Sarda breed. Twenty-five lambs, serum negative for M. paratuberculosis, were selected at birth from equally serum negative mothers. The lambs were inoculated at 5 months of age with three different mycobacterial antigens cloned into a mammalian expression vector as fusion protein with the enhanced green fluorescent protein (pEGFP-N1). The animals were divided in five groups containing each five lambs. Each group was vaccinated as following (A: physiological solution; B: Gudair; C: p-85A-Mav; D: p-85A-BCG; E: p-Hsp65). Immune response was evaluated by measuring the expression of INF-gamma (Th1 type response) and IL-10 (Th2 type response) by real-time PCR. Gene expression was estimated by comparing the results with that of beta-actin. INF-gamma expression level was increased in lambs vaccinated with plasmids codifying mycobacterial antigens, in particular with p-Hsp65, in comparison with the controls suggesting stimulation of a Th1 immune response similar to that supported by natural infection of M. paratuberculosis. Moreover, animals were infected orally with live M. paratuberculosis. Three months after vaccination and again INF-gamma and IL-10 expression was evaluated in order to verify in vivo the protection level of the vaccines. Plasmids p-85A-BCG and p-Hsp65 seem to elicit a stronger protective immune response against M. paratuberculosis by evaluating the expression level of INF-gamma and evaluating the presence of M. paratuberculosis and animal cell organ damage post-mortem.

Animals↗
PubMed2006

Humoral immune responses by prime-boost heterologous route immunizations with CTB-MPR(649-684), a mucosal subunit HIV/AIDS vaccine candidate.

CTB-MPR(649-684) is a translational fusion protein consisting of the cholera toxin B subunit and a 36-residue peptide, MPR(649-684), corresponding to the conserved membrane proximal ectodomain of gp41. CTB-MPR(649-684) was previously shown to induce HIV-1 transcytosis-blocking antibodies in mice. In this report, we describe an effective immunization regimen for this novel anti HIV-1 vaccine-candidate. Bacterially-produced CTB-MPR(649-684) was intranasally and/or intraperitoneally administered to investigate several prime-boost heterologous route immunization regimens. Mucosal priming with the adjuvant cholera toxin elicited significant levels of vaginal IgA and serum IgG specific to MPR(649-684). Systemic boosting after mucosal priming enhanced the levels of serum and mucosal antibodies. Systemic priming induced a strong serum anti-MPR(649-684) IgG response, which was efficiently recalled and augmented by either systemic or mucosal boosting. However, this regimen was less effective in inducing secretory anti-MPR(649-684) IgA. The serum anti-MPR(649-684) IgG subtype profile revealed that both IgG1 and IgG2a were induced in all the immunization regimens, and that mucosal co-administration of cholera toxin shifted the bias to the latter subtype. We concluded that, of the various immunization regimens examined here, mucosal priming with adjuvant followed by systemic boosting exhibited the best response in respect to either systemic or mucosal anti-MPR(649-684) antibodies. Most importantly, mucosal antibodies elicited by this regimen significantly inhibited HIV-1 transcytosis in a human tight epithelium model.

AIDS Vaccines↗
PubMed1993

Contribution of serum inhibitory factors and immune cellular defects to the depressed cell-mediated immunity in patients with head and neck cancer.

The immune system of patients with head and neck cancer is frequently depressed. Serum inhibitory factors and immune cell dysfunction are known contributors to this depression, but their relative roles are unclear. We have examined these factors to determine whether a common pathway is involved. Is the defect an unresponding "switched-off cell" or is it a remedial defect responsive to the removal of serum inhibitory factors and/or to lymphokine restoration? Immune tests were performed in 66 patients with high-stage head and neck cancer. Serum inhibitory factors were measured by incubation of heat-inactivated serum (10%) with phytohemagglutinin (PHA)-stimulated lymphocytes or natural killer (NK) cells using the K562 assay. Lymphokine-activated killer (LAK) cell cytotoxicity was measured (in the presence/absence of serum) using chromium 51-labeled Raji tumor cells cultured 5 days with interleukin-2 (IL-2) (100 or 1,000 U/mL) and/or interferon-alpha (INF-alpha) (100 U/mL). IL-2 receptors, CD25 or p55 (low affinity) and p75 (high affinity), were measured by flow cytometry through fluorescence-activated cell sorter analysis. Serum inhibitory factors were detected in more than 50% of the patients. Head and neck cancer sera significantly inhibiting the normal lymphocyte response to PHA (11 of 22 patients), as well as significantly inhibiting the NK response of normal lymphocytes and the functional expression of the IL-2 receptor. LAK cell function at low-dose IL-2 was depressed in 45% of the patients (9 of 20) and was restored by increased IL-2 (1,000 U/mL) or a combination of IL-2 and INF-alpha. Twenty-five percent of the patients were unresponsive to maximum lymphokine stimulation. Half of the patients had depressed expression of the low-affinity IL-2 receptor (CD25). The cause of immune depression in patients with head and neck cancer is multifactorial and is related to serum inhibitory factors, as well as to inherent cellular defects. Based on these data, we would suggest a therapeutic approach in selected patients that includes the removal of serum inhibitory factors by plasmapheresis and restoration of cellular defects by combined IL-2 with or without INF-alpha.

Adult↗
PubMed2002

Passive immunization with convalescent serum, or oral immunization with formalin-killed organisms, does not protect mice against gastrointestinal challenge with Listeria monocytogenes.

Listeria monocytogenes is an important foodborne pathogen in both humans and animals. In addition, murine listeriosis is a widely used model for studying the molecular pathogenesis of an intracellular pathogen, and the regulation of protective cellular immunity. Little attention has been paid to protective immunity against L. monocytogenes in the gastrointestinal tract, where a secretory immune response might prevent attachment of the bacteria to the intestinal epithelium. In this study we found that neither opsonization of L. monocytogenes with immune serum, nor repeated oral administration of killed L. monocytogenes, protected mice against gastrointestinal challenge with L. monocytogenes.

Administration, Oral↗
PubMed1999

Systemic and mucosal immune responses of pigs to parenteral immunization with a pepsin-digested Serpulina hyodysenteriae bacterin.

Serpulina hyodysenteriae infection of pigs, swine dysentery, causes a mucohemorrhagic diarrhoea resulting in significant economic losses to swine producers. The pathogenesis of this disease is poorly understood. Regardless, commercial vaccines have been developed and are in use. Thus, the present study was designed to examine cellular immune responses induced by parenteral S. hyodysenteriae vaccination. Significant antigen-specific interferon-gamma (IFN-gamma) and blastogenic responses were detected from peripheral blood lymphocytes isolated from vaccinated pigs. However, poor IFN-gamma responses were detected from colonic lymph node lymphocytes from these same pigs despite significant antigen-specific blastogenic responses. In addition, peripheral blood IFN-gamma responses were diminished by either in vitro depletion of CD4 expressing cells or by in vitro treatment with porcine IL-10. Colonic lymph node IFN-gamma responses were not inhibited by treatment with porcine IL-10. Vaccination also resulted in increased percentages of both mucosal and peripheral blood CD8 single positive cells with concurrent decreases in percentages of CD4 single positive cells as compared to percentages of these same populations from non-vaccinated pigs. In conclusion, these studies show that parenteral S. hyodysenteriae vaccination results in cellular immune responses detectable both peripherally (systemic immunity) as well as at the site of infection (mucosal immunity). However, it appears that regulatory mechanisms affecting IFN-gamma production in response to S. hyodysenteriae antigen differ between peripheral and colonic compartments.

Animals↗
PubMed2000

Immunization with DNA, adenovirus or both in biodegradable alginate microspheres: effect of route of inoculation on immune response.

To determine the potential for biodegradable alginate microspheres to be used as a delivery vehicle for DNA based vaccines, we constructed a plasmid, pMNe-gal-SV40, containing the bacterial beta-galactosidase (LacZ) gene under the control of the murine cytomegalovirus (MCMV) immediate-early promoter and the simian virus 40 (SV40) polyadenylation signal. The effect of the route of administration and co-administration of adenovirus on systemic and mucosal immune responses were investigated. Mice were inoculated orally, intranasally (i.n.), intramuscularly (i.m.), subcutaneously (s.c.) or intraperitoneally (i.p.) on days 0, 14 and 28 with microspheres containing plasmid DNA, bovine adenovirus type 3 (BAd3) or plasmid DNA + BAd3. Systemic routes of immunization (i.m., s.c. and i.p.) resulted in higher LacZ- or BAd3-specific IgG ELISA titers compared to those obtained by mucosal routes of inoculation (oral and i.n.). Mucosal immunization led to slightly higher titers of LacZ- or BAd3-specific IgA at mucosal sites compared to those obtained by the various systemic routes. All the routes of immunization induced LacZ-specific lymphoproliferation. Co-administration of BAd3 enhanced the LacZ-specific IgG response irrespective of the route of administration.

3T3 Cells↗
PubMed2000

Immune responses to pertussis antigens eight years after booster immunization with acellular vaccines in adults.

Pertussis-specific antibody and cell-mediated immune (CMI) responses were studied in adults 8 years after booster immunization with either a bicomponent (pertussis toxin and filamentous hemagglutinin) or a monocomponent (pertactin) acellular vaccine and in age-matched healthy controls. The levels of vaccine-induced antibodies were also compared between the serum samples collected before, 1 month, 4 years, and 8 years after immunization. Over the follow-up period, geometric mean values (GMV) of antibodies to the vaccine antigens decreased in both groups of vaccinees. However, the 8-year postimmunization GMV were 3-20 times higher than preimmunization GMV (all P values <0.01). Moreover, both antibody and CMI responses to the vaccine antigens were significantly higher in the vaccinees than in the controls (all P<0.01 for antibody; all P<0.001 for CMI responses). The results show that antibody and CMI responses induced by acellular pertussis vaccines can persist for up to 8 years after booster immunization of adults primed with whole-cell vaccine.

Adhesins, Bacterial↗
PubMed2002

Mechanisms of immune privilege for tumor cells by regulatory cytokines produced by innate and acquired immune cells.

In murine tumors, innate immunity act as a trigger for the development of acquired immunity. The innate immune cells, natural killer (NK) and natural T (NKT) cells, generate the acquired immune cells, cytotoxic T lymphocytes (CTLs) and T helper (Th) 1 cells, by releasing interferon (IFN)-gamma. Regulatory T cells co-infiltrate with these tumoricidal effectors. In the innate phase, T cell receptor (TCR) gammadelta-bearing T (gammadelta T) and TCRalphabeta intermediate T cells are the regulators that suppress NK and NKT cells by elaborating interleukin (IL)-4, IL-10 and transforming growth factor (TGF)-beta. The acquired phase has Th3/T regulatory 1-like cells that inhibit CTLs and Th1 cells by TGF-beta. Thus, cytokines from regulatory T cells exert profound effects on tumor growth.

Animals↗
PubMed2001

Protective immune response against cutaneous leishmaniasis by prime/booster immunization regimens with vaccinia virus recombinants expressing Leishmania infantum p36/LACK and IL-12 in combination with purified p36.

In susceptible mice Leishmania infection triggers a CD4(+) Th2 response that has been correlated with evasion of the host immune system. To develop approaches that might trigger a Th1 response leading to protection against Leishmania we generated vaccinia virus recombinants (VVr) expressing the relevant p36/LACK protein of Leishmania infantum (VVp36) or co-expressing p36/LACK and interleukin-12 (VVp36IL12). Susceptible BALB/c mice were immunized with the VVr in various prime/booster protocols that included purified p36/LACK protein, followed 3 weeks later by a challenge with live L. major promastigotes. The course of the infection was monitored by measuring lesion development, parasite load and immunological parameters (IFN-gamma and IL-10 secretion by in vitro-stimulated lymphocytes, and specific IgG isotypes), before and after challenge. We found protocols of prime/booster immunization (VVp36/VVp36; VVp36IL12/p36; p36/VVp36IL12) that elicited different levels of protection in infected animals. The protocol of priming with purified p36 followed by a booster with VVp36IL12 induced 52% reduction in lesion size and a two-log unit reduction in parasite load. This partial protection correlated with activation of a specific Th1 type of immune response. These protocols could be of interest in the prophylaxis against Leishmania spp. and other parasitic diseases.

Animals↗
PubMed2003

Vaccinia virus pathogenicity in atopic dermatitis is caused by allergen-induced immune response that prevents the antiviral cellular and humoral immunity.

Atopic dermatitis (AD) serves as a contraindication for the immunization of AD patients with a live vaccinia virus (VV) vaccine. The antiallergen IgE interacts with the Fc receptors (FcepsilonRI) on dendritic cell (DC) membranes and with allergen molecules. The immunological events that lead to AD disease, the activation of the T-helper 2 (Th2) immune response, the synthesis of the cytokines IL-4, IL-5, IL-13, and the inhibition of the T-helper 1 (Th1) damage the capacity of the host to develop anti-VV cytotoxic cells (CTLs). In the presence of Th2-derived cytokine IL-4 in the AD skin and the synthesis of VV proteins that interfere recruitment of DCs by host cytokines, the VV can cause a generalized infection. Conceptually, new VV recombinants may be needed for human immunization. Such VV recombinants should lack the genes that interfere with the host immune system and express a mutated human IL-4 cytokine gene that will prevent negative regulatory mechanisms. Such improved VV recombinants may be used to express genes from pathogenic viruses.

Allergens↗
PubMed2002

The innate immune response to tumors and its role in the induction of T-cell immunity.

Recent genetic studies have resurrected the concept that the adaptive and innate immune systems play roles in tumor surveillance. Natural killer (NK) cells recognize many tumor cells but not normal self cells, and they are thought to aid in the elimination of nascent tumors. Two main strategies are employed by NK cells to recognize tumor targets. Many tumor cells down-regulate class I major histocompatibility complex (MHC) molecules, thus releasing the NK cell from the inhibition provided by class I MHC-specific inhibitory receptors ('missing self recognition'). More recently, it has become clear that a stimulatory receptor expressed by NK cells, T cells and macrophages (NKG2D) recognizes ligands (MHC class I chain related [MIC], H6O, retinoic acid early inducible [Rae1] and UL16 binding proteins [ULBP]) that are up-regulated on tumor cells and virally infected cells but are not expressed well by normal cells. Ectopic expression of these ligands on tumor cells leads to the potent rejection of the tumors in vivo. Importantly, mice that previously rejected the ligand+ tumor cells develop T-cell immunity to the parental (ligand-) tumor cells. The recognition of induced-self ligands as a strategy to recognize abnormal self sets a precedent for a new immune recognition strategy of the innate immune system.

Animals↗
PubMed1973

Effect of active immunization with irradiated tumour cells on specific serum inhibitors of cell-mediated immunity in patients with disseminated cancer.

The sera from patients with advanced cancer were tested for their specific inhibitory effects on the cytotoxicity of autologous lymphocytes on tumour cells in a microculture assay. By adding a standard volume of the sera to suspensions of well-washed lymphocytes the inhibitory effect was quantitated by comparison with the effect of normal allogeneic serum. Significant levels of inhibitory activity were detected in 7 patients (one massive primary melanoma, 4 with disseminated melanoma, one with metastatic hypernephroma and one with a recurrent leiomyosarcoma). The patient with a massive primary melanoma was treated by extensive surgical excision. This procedure was associated with the rapid and complete disappearance of the serum inhibitory effect. In the other cases surgical intervention was minimal and the serum inhibitor was unaffected. All 6 of these patients were then immunized with irradiated autologous tumour cells and the serum inhibitory activity assayed. In 5 cases the serum inhibitor rapidly became undetectable after a single immunization. The one patient who failed to respond in this manner had very extensive disease and died within 2 weeks of the study. Repeated monthly immunization in the case of recurrent leiomyosarcoma was associated with the maintenance of the serum inhibitory activity at very low levels and with good clinical progress. The response to a single immunization is transient, the inhibitor becoming detectable again at 14-21 days. The possible role of circulating antigen in this serum inhibitory activity is discussed, as is the potential value of assaying the sera of cancer patients for serum inhibitory activity, as a means of monitoring the effects of treatment.

Adenocarcinoma↗
PubMed1980

Tubulointerstitial immune complex nephritis in rats immunized with Tamm-Horsfall protein.

Rats immunized with Tamm-Horsfall protein (TH) developed autoantibodies to TH and tubulointerstitial nephritis with granular deposits of IgG, C3, and TH at the base of tubular cells of the thick ascending limb of Henle's loop and selective infiltration of leukocytes around this distal nephron segment. Selective IgG deposition at the base of cells in the tubular segment containing TH and the direct relationships of the amount of immune deposits and the severity of histologic lesions to serum levels of anti-TH antibodies suggest a pathogenetic role for the autoantibodies to TH. The immune deposits in this model of tubulointerstitial nephritis appear to be the consequence of in situ formation of immune complexes. This mechanism involves the diffusion of circulating antibodies to TH across tubular basement membranes and their combination with TH molecules associated with tubular cell surface membranes.

Animals↗
PubMed2006

DNA damage: a trigger of innate immunity but a requirement for adaptive immune homeostasis.

Chromosome breakage is frequently associated with viral infection and cellular transformation, but it is also required for two processes that are crucial for the development and function of adaptive immunity: V(D)J recombination and class-switch recombination. The cellular responses that result from this type of DNA damage, which are mostly activated by the protein kinase ataxia-telangiectasia mutated (ATM), lead to cell-cycle arrest at several checkpoints and efficient DNA repair. This Review focuses on the important roles of these DNA-damage responses in the activation of innate immunity and the targeting of the innate immune response to infected or transformed cells, as well as in the development and function of adaptive immunity.

Animals↗
PubMed1970

Cells involved in cell-mediated and transplantation immunity. II. A consideration of the functional identity of the cells involved in both humoral and cell-mediated immunity: a phylogenetic approach.

The literature concerned with the types of cells that participate in the humoral and cell-mediated immune response has been reviewed. It is postulated that the initial cells that are involved in mediating both types of immunity are functionally identical in that both are antigen-reactive cells. In the case of the humoral immune response, the interaction of the antigen-reactive cells with the antigen leads to the release or transfer of "information" to the antibody-forming cell, resulting in the synthesis and secretion of antibody molecules. In the case of cell-mediated immunity, it is considered that the primitive antigen-reactive cell itself transforms into the sensitized cell which infiltrates the site of antigen administration.

Antibodies↗
PubMed1968

Cells involved in the immune response. IV. The response of normal and immune rabbit bone marrow and lymphoid tissue lymphocytes to antigens in vitro.

Cell suspensions of immune rabbit lymph nodes and spleen were capable of undergoing blastogenesis and mitosis and of incorporating tritiated thymidine when maintained in culture with the specific antigen in vitro. They did not respond to other, non-cross-reacting antigens. The blastogenic response obtained with immune lymph node cells could be correlated with the antibody synthesizing capacity of fragment cultures prepared from the same lymph nodes. Cell suspensions of immune bone marrow responded to non-cross-reacting antigens only whereas cell suspensions of immune thymus, sacculus rotundus, and appendix did not respond when exposed to any of the antigens tested. On the other hand, neither fragments nor cell suspensions prepared from lymph nodes, spleen, and thymus of normal, unimmunized rabbits responded with antibody formation and blastogenesis when exposed to any of the antigens. However, normal bone marrow cells responded with marked blastogenesis and tritiated thymidine uptake. The specificity of this in vitro bone marrow response was demonstrated by the fact that the injection of a protein antigen in vivo resulted in the loss of reactivity by the marrow cell to that particular antigen but not to the other, non-cross-reacting antigens. Furthermore, bone marrow cells of tolerant rabbits failed to respond to the specific antigen in vitro. It was also demonstrated that normal bone marrow cells incubated with antigen are capable of forming antibody which could be detected by the fluorescent antibody technique. This response of the bone marrow cells has been localized to the lymphocyte-rich fraction of the bone marrow. It is concluded that the bone marrow lymphocyte, by virtue of its capacity to react with blastogenesis and mitosis and with antibody formation upon initial exposure to the antigen, a capacity not possessed by lymphocytes of the other lymphoid organs, has a preeminent role in the sequence of cellular events culminating in antibody formation.

Animals↗
PubMed1971

Specific immune response genes of the guinea pig. I. Dominant genetic control of immune responsiveness to copolymers of L-glutamic acid and L-alanine and L-glutamic acid and L-tyrosine.

The immunogenicity of three random copolymers of amino acids with L-glutamic acid and L-alanine (GA), L-glutamic acid and L-tyrosine (GT), or L-glutamic acid, L-alanine, and L-tyrosine (GAT), administered in complete Freund's adjuvant, was studied in several inbred and random-bred guinea pig strains. The animals were tested for delayed sensitivity and their sera were assayed for the presence of antibody directed against the immunizing polymer. All of the guinea pigs developing delayed hypersensitivity also had significant antibody levels in their sera. Inbred strain 2 guinea pigs responded to immunization with GA, but failed to form detectable responses to GT. Inbred strain 13 animals, on the other hand, responded to GT, but not to GA. The (2 x 13)F(1) hybrids responded to both GA and GT with both delayed hypersensitivity and circulating antibody. Thus, the ability of these inbred guinea pigs to respond immunologically to GA or GT is controlled by distinct autosomal dominant genes. A variable percentage of random-bred guinea pigs, depending on their source as well as their strain, responded to immunization with GA and with GT. All guinea pigs, both inbred and random bred, responded to immunization with GAT. The ability to respond immunologically to GAT, therefore, does not seem to be under simple genetic control. However, the levels of anti-GAT antibody found in the sera of animals lacking the ability to respond to GA were much lower than those detected in GA responder animals.

Alanine↗