Immune status in a primary smallpox vaccinee who failed to develop an immunization site reaction.
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Adult↗
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Results for “immune development”
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Cattle protected from onchocerciasis by ivermectin are highly susceptible to infection after drug withdrawal.
Ivermectin administration is now the major tool in the control of human onchocerciasis (caused by Onchocerca volvulus) based on its suppression of microfilariae and hence the prevention of disease. However, in Africa, transmission is not eliminated and treated populations continue to be exposed to infective larval (L(3)) challenge, albeit at reduced levels. We have investigated whether protective immunity might develop under such conditions using the analogous host-parasite system Onchocerca ochengi in cattle, based on our previous findings in cattle exposed to challenge, that in vivo ivermectin attenuates the development of adult infections and that irradiation-attenuated L(3) induce significant protection. In a two-phase prospective study over 4 years, groups of cattle were exposed to severe natural challenge. In the first phase, 38/40 animals treated either with ivermectin or with moxidectin at either monthly or 3-monthly intervals had not developed detectable infections after 22 months of exposure whereas, in a non-treated control group (n = 14) nodule prevalence was 78.6% and the geometric mean (range) nodule load was 4.8 (0-33). In the second phase, all drug treatments were withdrawn, a new control group (n = 8) introduced, and exposure continued at the same site. After 24 months, all groups had developed patent infections, with geometric mean (range) nodule loads of 17.4 (4-99), 38.4 (10-111), 50.7 (26-86), 14.3 (0-69) and 14.7 (0-55) for the control, monthly-ivermectin, 3-monthly ivermectin, monthly moxidectin and 3-monthly moxidectin groups, respectively. There was no evidence of protection-indeed the 3-monthly ivermectin group was significantly (P < 0.05) hyper-susceptible. In addition, microfilarial densities and the rate of increase in microfilarial load were significantly higher (P < 0.05) in the ivermectin-treated groups than in control animals. These results have important implications for ivermectin-based control of human onchocerciasis and suggest that humans exposed to ongoing transmission in endemic areas whilst receiving ivermectin are unlikely to develop immunity and will be highly susceptible should drug distribution cease.
Animals↗
Regulatory T cell adjustment of quorum growth thresholds and the control of local immune responses.
The consequences of regulatory T cell (Treg) inhibition of interleukine 2 secretion is examined by mathematical modelling. We demonstrate that cytokine dependent growth exhibits a quorum T cell population threshold that determines if immune responses develop on activation. Secretion inhibition manipulates the growth dynamics and effectively increases the quorum threshold, i.e. to develop immune responses a higher number of T cells need to be activated. Thus Treg induced secretion inhibition can provide a mechanism for tissue specific regulation of the balance between suppression (control) and immune responses, a balance that can be varied at the local tissue level through the regulation of the local active Treg population size. However, nonspecific inhibition is prone to escape of initially controlled autoimmune T cells through cross reactivity to pathogens and bystander proliferation on unrelated immune responses.
Animals↗
Insights into lymphocyte development from X-linked immune deficiencies.
The genetic immune deficiencies have drawn the attention of physicians and immunologists for more than 40 years. The selectivity of these deficiencies brings into focus the contribution of the response of each arm of the immune system to specific pathogens. Recently, the genes underlying four X-linked defects in immune development in humans have been identified by either positional cloning or candidate-gene cloning techniques. Remarkably, these genetic defects reveal a microcosm of lymphocyte developmental controls involving cell-cell interactions, combinatorial cell surface receptor specificity and lineage-specific signal transduction.
Amino Acid Sequence↗
Mice immunized with DNA encoding a modified Pseudomonas aeruginosa exotoxin A develop protective immunity against exotoxin intoxication.
A recombinant plasmid, which contains the Pseudomonas aeruginosa exotoxin A (PE) gene with a C-terminal deletion, was inserted into expression vector pSecTag Xpress. The expression of this bacterial exotoxin in an animal cell was first demonstrated in 3T3 cell by transient transfection and western blot assay. Recombinant plasmid DNA was then injected intramuscularly to BALB/c mice, anti-PE specific antibodies were found in all animals vaccinated with plasmid containing the PE gene and with 'detoxicated' recombinant PE protein. Mice vaccinated with DNA were protected from the intoxication of lethal dosage of P. aeruginosa exotoxin A. Our results indicated that mice vaccinated with DNA encoding the PE gene could express PE protein in vivo, induced specific immune response, and provided sufficient protective immunity that safeguarded mice from the injection of lethal dosage of PE toxin.
ADP Ribose Transferases↗
Assessment of immune function development in mice irradiated in utero with 2450-MHz microwaves.
Groups of time-bred pregnant mice were irradiated with 2450-MHz microwaves at an incident power density of 28 mW/cm2 for 100 min daily from day 6 to day 18 of pregnancy. The average specific absorption rate (SAR) was 16.5 W/kg. Two experiments were performed under these conditions. At 3 and 6 weeks of age the mice were assessed for development of the primary immune response to sheep erythrocytes, in vitro mitogen-stimulated lymphocyte proliferation, and natural killer (NK) cell activity. No consistent significant difference in the primary immune response, in the mitogen response, or in the NK cell activity was observed between irradiated and sham-irradiated mice.
Animals↗
Chemokines as therapeutic targets in renal disease.
Increased understanding of the fundamental importance of the role of chemokines and their receptors in inflammation, together with the demonstration of their involvement in human and experimental inflammatory renal disease, make these molecules potential therapeutic targets. A number of recent studies using genetically deficient mice and chemokine receptor antagonists in animal models have demonstrated that chemokine inhibition can attenuate experimental renal injury. Because there is simultaneous expression of multiple chemokines and receptors in disease, strategies that are aimed at antagonizing multiple chemokines receptor interactions are likely to be more effective than therapies that target a single chemokine. It is also now recognized that chemokines are involved in normal immune development and immune regulation. These observations, together with the results of studies that have demonstrated deleterious effects of chemokine receptor antagonism in experimental renal disease, highlight the need for thorough understanding of the role of individual chemokines in the pathogenesis of different types of renal disease before optimal therapeutic interventions may be achieved.
AIDS-Associated Nephropathy↗
Analysis of inhibitory epitopes in the Plasmodium falciparum rhoptry protein RAP-1 including identification of a second inhibitory epitope.
Immune responses to Plasmodium falciparum rhoptry-associated protein 1 (RAP-1), RAP-2, and RAP-3 appear to contribute to protection against infection by this human malarial parasite. This conclusion is suggested by results of monkey immunization trials and of cell culture studies showing antibody-dependent inhibition of erythrocyte invasion. In the present study, splenectomized owl monkeys were infected with P. falciparum in order to monitor anti-RAP-1 antibody production as antiparasite immunity developed. The monkeys responded to a primary infection with the production of antibodies to a fragment of RAP-1 containing amino acids 1 to 294 (RAP-1(1-294)). After drug cure and reinfection, the monkeys had a prolonged prepatent period, indicating they had already developed partial immunity to the parasite. Sera from these animals showed major increases in anti-RAP-1(1-294) antibodies. In contrast, only low levels of antibodies to inhibitory B-cell epitope 1 (iB-1), an inhibitory epitope in RAP-1(1-294) with the sequence N200TLTPLEELYPT211, was observed after the initial parasite infection, and the anti-iB-1 antibodies were not readily boosted upon reinfection. These results suggest that iB-1 is an immunogenic but not immunodominant epitope and that anti-iB-1 antibodies do not substantially contribute to early stages of naturally acquired immunity in the owl monkey model. To identify additional epitopes bound by inhibitory antibodies, mouse monoclonal antibodies were produced with a recombinant fusion protein containing RAP-1(1-294). Monoclonal antibody 1D6 inhibited parasite invasion of erythrocytes in vitro. 1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2. iB-2, like iB-1, is found near the amino terminus of p67, a RAP-1 processing product thought to be involved in merozoite invasion of erythrocytes. Since anti-iB-1 antibodies were not readily produced during parasite infection, it may be desirable to direct antibody responses to particular epitopes in RAP-1, such as iB-1 and iB-2.
Amino Acid Sequence↗
Alteration of gene expression in human cells treated with the agricultural chemical diazinon: possible interaction in fetal development.
Agricultural chemicals frequently alter human health or development, typically because they have endocrine agonist or antagonist activities and alter hormone-regulation of gene expression. The insecticide, diazinon, was evaluated for gene expression disrupting activity using MCF-7 cells, an estrogen-dependent human cell line, to examine the capacity of the insecticide to disrupt gene expression essential for morphological development, immune system development or function, and/or central nervous system development and function. MCF-7 cells were treated with 30, 50 or 67 ppm diazinon, and gene expression was measured in treated cells compared to expression in untreated or estrogen-treated cells. DNA microarray analysis of diazinon-treated cells showed significant up- or down-regulation of a large number of genes compared to untreated cells. Of the 600 human genes on the Phase 1 chip utilized for these studies, two specific genes--calreticulin and TGF-beta3--were selected for corroboration using quantitative real time PCR (qrtPCR). qrtPCR, completed to assess gene expression levels for calreticulin and TGFbeta3, confirmed results showing significant up-regulation of these two genes obtained from the microarray data. These studies were designed to provide baseline data on the gene expression-altering capacity of a specific chemical, diazinon, and allow a partial assessment of the potentially deleterious effects associated with exposure of human cells to this chemical. Currently, it is not known whether results from cells in vitro can be extrapolated to human health consequences of chemical exposure.
Agrochemicals↗
[Experimental imutiol stimulation of the primary immunological response to tetanus anatoxin].
The data on the influence of imuthiol on humoral and cell-mediated immunity developing after immunization against tetanus are presented. Experiments were made on 166 guinea pigs with the use of imuthiol in doses of 25 and 125 mg/kg and tetanus toxoid in doses of 1.5 and 6.0 BU/kg. The dynamic observation of the animals lasted 30 days. The data of the passive hemagglutination test and the neutralization test indicated that imuthiol had considerable influence on the formation of humoral immunity. The results of skin reactions with tetanin, in vitro cell reactions, as well as resistance tests, showed that imuthiol exerted influence on delayed hypersensitivity, the mechanisms of cell-mediated resistance and survival after challenge. The data on the influence of imuthiol could be registered even at early stages after immunization, the immunostimulating action of the preparation reaching its maximum with tetanus toxoid used in a dose of 6.0 BU/kg and imuthiol, in a dose of 125 mg/kg.
Animals↗
Control of coccidiosis in turkeys with diclazuril and monensin: effects upon performance and development of immunity to Eimeria species.
The effects of diclazuril and monensin, when included in the feed of turkeys from 0 to 10 wk, upon performance and development of immunity to Eimeria species was investigated. Birds were initially inoculated with a low dose of oocysts of three species of Eimeria at 3, 5, 7, and 9 days of age in order to simulate a natural infection. Weight gain and feed intake from 0 to 6 wk of age was significantly greater in medicated birds compared with those that received no anticoccidial medication. Weight gain and feed intake from 6 to 10 wk was greater in birds that received diclazuril than in unmedicated birds. No differences in performance were evident after drug withdrawal from 10 to 16 wk. Immunity to Eimeria species developed by 10 wk in birds that received no anticoccidial medication but did not develop in those given diclazuril or monensin.
Animal Feed↗
Innate recognition systems in insect immunity and development: new approaches in Drosophila.
Phagocytosis is important in immune defense and development in vertebrates and invertebrates. It leads to swift ingestion of microorganisms and dying cells by phagocytes. How particles are recognized is not well understood. Studies in insects, and Drosophila in particular, argue that these are powerful model systems to dissect this process.
Animals↗
[Development of the immune system].
The development of immune defense mechanisms begins early during fetal life but is not yet completed at birth. The earliest hematopoietic stem cells, which give rise to the lymphocytic and myelomonocytic cell lines, appear between the fourth and eight weeks postconception. T cells, responsible for cellular immune defense mechanisms, are first detectable at 12 weeks and seem to acquire their functional capabilities at the 16th week. B lymphocytes, responsible for humoral immunity, can be identified in the fetal liver at eight weeks and are functional at the 12-th-13th week, with the ability to produce specific IgM antibodies. Thus, in theory, fetuses of more than 16 weeks can produce a full immune response. Neonates still have incomplete development of a number of mechanisms involved in nonspecific immunity (natural killer, polynuclear and macrophage chemo-attraction, complement system).
B-Lymphocytes↗
Unexpected association between induction of immunity to the universal tumor antigen CYP1B1 and response to next therapy.
PURPOSE: The carcinogen activator cytochrome P450 1B1 (CYP1B1) is expressed on almost all human tumors with rare expression on normal tissues. Anti-CYP1B1-specific T cells kill CYP1B1-expressing tumors, providing the rationale to examine CYP1B1 as a target for immunotherapy. EXPERIMENTAL DESIGN: ZYC300, a plasmid DNA of CYP1B1 encapsulated in biodegradable poly-DL-lactide-coglycolide microparticles, was used in a phase I clinical trial to treat 17 patients with advanced stage, progressive cancer. ZYC300 was administered i.m. at a fixed dose of 400 microg every other week for up to 12 doses. RESULTS: Thirteen patients received six vaccinations and five received all 12 doses. No significant adverse events were observed. Six patients developed immunity to CYP1B1, three of whom developed disease stabilization. All but 1 of 11 patients who did not develop immunity to CYP1B1 progressed and did not respond to salvage therapy. Five patients who developed immunity to CYP1B1 required salvage therapy for progressive metastatic disease and showed marked response to their next treatment regimen, most of which lasted longer than 1 year. CONCLUSIONS: The association between immunity to CYP1B1 and response to next salvage therapy was not expected. Because six of the seven patients who had clinical benefit regardless of the nature of salvage therapy had developed immunity to CYP1B1, it seems highly unlikely that this occurred by chance alone. Regardless of the mechanism(s) that induced tumor regression, these findings force us to rethink how the generation of antitumor immunity might be integrated into the treatment of cancer.
Aged↗
[Effect of bee pollen on development of immune organ of animal].
OBJECTIVE: To study on the effect of been pollen on development of immune organ of animal. METHOD: A total of 144 one day-old broilers were randomly divided into 2 groups, in which each group included 72 chickens. The control group was fed on the basal diet for 42 days, and that of experiment group supplemented 1.5% bee pollen. Six chickens in each group were selected and slaughtered at 7, 14, 21, 28, 35, 42 days respectively, and the thymuses, cloacal bursa and spleens were obtained, weighted, fixed in Bouin liquid and made into paraffin section. RESULT: Compared with control group, the weight and the relative weight of thymuses, cloacal bursa and spleens of experiment group increased significantly (P < 0.05) or extremely significantly (P < 0.01). In experiment group, the cortex of thymic lobule, bursa nodule and Periarterial Lymphatic Sheaths thicken obviously; the volume of bursa nodule, splenic nodule and ellipsoid augmented, and the germinal center of splenic nodule were obvious; the thymic corpuscle increased; the plica of cloacal bursa developed well and the degenerating of it retarded. CONCLUSION: The diet supplemented bee pollen could boost the early development of thymus and cloacal bursa, retard the degenerating of cloacal bursa and promote the immune response of spleen.
Animal Nutritional Physiological Phenomena↗
Reconstitution of the B cell repertoire after bone marrow transplantation does not recapitulate human fetal development.
Immune reconstitution during bone marrow transplantation has been proposed to produce a fetal-type immune system. This characteristic may contribute to the relative immunodeficiency that occurs in the early post-transplant period. This review reappraises recent studies of immunoglobulin heavy chain genes produced by the recovering immune system. Comparison of these genes to those that are generated by fetal and adult B cells, demonstrates that there is no evidence to support the conclusion that adult lymphocytes in the graft reverse to a fetal stage of differentiation. In terms of lymphocyte diversity, the inadequacy of the recovering immune system is more likely to be explained by a combination of other factors - such as the delayed occurrence of somatic hypermutation and class switching, and clonal dominance.
Adult↗
Influence of the genetic background and parasite load of mice on the immune response developed against nymphs of Ixodes ricinus.
The immune response of BALB/c (H-2d), DBA (H-2d), C57BL/6 (H-2b), C3H (H-2k), CBA (H-2k), SJL (H-2s), and FVB (H-2q) mice infested once with 15 nymphs of Ixodes ricinus is polarized toward Th2 as suggested by cytokines produced by lymph node cells stimulated with concanavalin A. The parasite load does not influence the polarization of the immune response as observed in BALB/c mice, which developed a Th2 response when infested with 5 or 45 nymphs. As assessed by attachment and weights of engorged nymphs, no resistance was acquired by BALB/c, C57BL/6, or C3H mice undergoing three successive infestations. However, these mice produced a gradual increase in IgE.
Animals↗
Recapitulation of normal and abnormal BB rat immune system development in scid mouse/rat lymphohemopoietic chimeras.
Mice homozygous for the mutation "severe combined immune deficiency" (C.B17-scid/scid) lack functional T and B lymphocytes and readily accept tumor xenografts. Partial lymphohemopoietic scid/human and mouse/rat chimeras have been described, but complete chimerization with thymic engraftment and generation of donor-origin thymocytes has not been achieved. We now report that low-dose irradiation permits the engraftment of BB rat fetal liver stem cells in scid recipients. We observed that BB rat fetal liver cells injected into irradiated scid mice establish a rat hemopoietic system in the scid mouse bone marrow and populate the scid mouse thymus. These stem cells generated rat-origin thymocytes that migrated to the scid mouse spleen, a peripheral lymphoid organ. Finally, we found that xenogeneic chimeras created using fetal liver cells from the abnormal (lymphopenic, diabetes prone) subline of BB rats recapitulated both the quantitative and phenotypic abnormalities of the donor rat. Xenogeneic lymphohemopoietic chimeras established in scid mice may provide a powerful new tool in the study of immune system development and autoimmunity.
Animals↗