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At least 217 records · Page 12Linked to original sources
PubMed2003

Measles and mumps vaccination as a model to investigate the developing immune system: passive and active immunity during the first year of life.

Evaluations of neutralizing antibody responses in 6-, 9- and 12-month-old infants given measles or mumps vaccine indicated that 6-month-old infants had diminished humoral immune responses associated with passive antibody effects, but also had an intrinsic deficiency in antiviral antibody production, which was independent of passive antibody effects. In contrast, lower neutralizing antibody titers in 9-month-olds were related only to passive antibody effects. Measles and mumps-specific T-cell proliferation and interferon-gamma (IFNgamma) production were induced by vaccination at 6, 9 or 12 months, regardless of passive neutralizing antibodies or age. These observations suggest a need to refine concepts about passive antibody interference and primary vaccine failure, taking into account the sensitization of antiviral T-cells, which occurs in the presence of passive antibodies and is observed in infants who do not develop active humoral immunity. A second dose of measles vaccine given at 12-15 months enhanced antiviral T-cell responses to measles in infants who were vaccinated at 6 or 9 months, and produced higher seroconversion rates. Since T-cell immunity is elicited under the cover of passive antibodies, the youngest infants benefit from the synergistic protection mediated by maternal antibodies and their own capacity to develop sensitized antiviral T-cells, which prime for subsequent exposures to the viral antigens. Conceptually, maternal immunization approaches with vaccines that can be given to women of child-bearing age before pregnancy, or that are safe for administration during pregnancy, should enhance passive antibody protection. Rather than being detrimental to infant adaptive immune responses, maternal vaccination can be coupled effectively with vaccine regimens that elicit priming of antiviral immune responses in infants during the first year of life.

Aging↗
PubMed1998

Effect of nicotine on the immune system: possible regulation of immune responses by central and peripheral mechanisms.

Nicotine (NT) treatment impairs T-cell receptor (TCR)-mediated signaling, leading to the arrest of T cells in the G1 phase of the cell cycle and inhibition of the antibody plaque-forming cell (AFC) response to sheep red blood cells (SRBC). This paper summarizes some of the previous findings related to cigarette smoke/NT and the immune response, and presents preliminary evidence suggesting that mice chronically treated with NT (0.5 mg/day/kg body weight) have a depressed inflammatory response in the turpentine-induced abscess model of inflammation. This ability of nicotine to attenuate an inflammatory response may also be the cause of reduced mortality of chronically nicotine-treated mice from acute influenza A pneumonitis. Moreover, in LEW rats, decreased anti-SRBC AFC responses were also observed after intracerebroventricular (i.c.v.) administration of relatively small concentrations of NT (28 micrograms/day/kg body weight) which, when given peripherally, did not affect the AFC response. In vitro the addition of NT to T cells increased protein tyrosine kinase (PTK) activity and intracellular Ca2+ concentration [Ca2+]i. These results support the hypothesis that NT alters immune responses by directly interacting with T cells, as well as indirectly through brain-immune interactions.

Abscess↗
PubMed1993

Defective mucosal immunity and normal systemic immunity of Mongolian gerbils, Meriones unguiculatus, to reinfection with Strongyloides venezuelensis.

The systemic and local protective activity of Mongolian gerbils was examined after re-infection with Strongyloides venezuelensis. Mongolian gerbils were unable to expel S. venezuelensis adult worms from the intestine for over ten weeks after a primary infection. Therefore, immune animals were prepared by treating with mebendazole four weeks after a primary infection and then they were challenged by different maturation stages of the parasite; subcutaneous inoculation with the infective larvae (L3) obtained by faecal culture, oral administration of L3 obtained from the lungs of rats three days after a primary infection, or oral implantation of adult worms obtained from the intestines of rats seven days after a primary infection. The results show that, although immune animals were highly resistant against challenge infection by subcutaneous inoculation with cultured L3, they were unable to expel orally administered lung-recovered L3 nor orally implanted adult worms. Although potentiated mastocytosis was induced by challenge infections with lung-recovered L3 and adult worms, all mast cells were formalin-resistant, heparin-containing cells and never seen in the epithelial layer. In spite of the defective protective capacity at the intestinal mucosa, circulating antibody production specific to S. venezuelensis adult as well as L3 antigen was positive. Therefore, the inability of Mongolian gerbils to expel S. venezuelensis adult worms from the intestine seems to be due to the defects of effector/regulator cells, presumably mast cells, but not due to immune unresponsiveness to parasite antigen.

Animals↗
PubMed1994

Primitive vertebrate immunity: what is the evolutionary derivative of molecules that define the adaptive immune system?

The adaptive immune system is capable of responding to an infinite number of antigens with the antigen-specific receptors immunoglobulin (Ig) and the T cell receptor (TCR). Ig binds soluble antigens while TCR recognizes antigen bound in clefts of polymorphic self-encoded major histocompatibility complex (MHC) class I and class II molecules. All of these molecules are wholly or partially composed of Ig superfamily domains. TCR and Ig use V-set Ig superfamily domains, always in heterodimeric forms, in antigen recognition. Although the ways in which TCR and Ig bind antigen are fundamentally different, the structure of the heterodimeric V domains is probably identical. The antigen-binding cleft of MHC proteins has a structure unlike Ig superfamily domains, although several investigators have proposed that this cleft is evolutionarily derived from Ig domains. We believe the MHC cleft is a primitive structure, perhaps related to the peptide-binding domains of intracellular chaperone proteins. A model is proposed whereby chaperone proteins were the primordial MHC molecules, presenting peptides derived from invariant proteins residing inside cells for recognition by lymphocytes with minimally diverse receptors. Such a system may be reflected today by the epithelial immune system, apparently governed by monomorphic MHC molecules and lymphocytes with unconventional antigen-specific receptors.

Adaptation, Physiological↗
PubMed1999

Reciprocal interdependence between pineal gland and avian immune system. NEL Review.

The immune system of mammals and birds exhibits the same basic anatomical and functional organization, including dichotomy into the cellular and humoral immune response. Specificities of avian immune system may be, however, very useful for understanding numerous phylogenetic and evolutionary mysteries. Similarities and differences between mammals and birds in terms of several pineal gland functions are well known, and they seem to include the immunomodulatory activity of melatonin (MEL) as well. Embryonic pinealectomy of the chicken demonstrated functional interrelationships between the development of the pineal gland, immune system and/or neuroendocrine network, and embryonic bursectomy influenced the diurnal rhythm of the pineal gland function and abolished the effect of immunization on serum MEL level. Also immunization with a thymo-dependent antigen (SRBC) evoked some changes in the chicken nocturnal pineal NAT activity. We have found that the pineal gland and MEL control the diurnal rhythm of immunity in the chicken, but we were not able to demonstrate any immunostimulatory and anti-glucocorticoid MEL effects, regardless of the chicken's age, sex, season, and hormone dose used. The existence of functional connections between the pineal gland and the immune system in chickens was, however, confirmed in other experimental approaches. Specific and reversible binding of 2-[125I]iodoMEL to the membrane preparations from lymphoid glands was demonstrated in several avian species. In vitro MEL diminished lymphocyte proliferation stimulated by the common T-cell mitogens, while alone failed to influence the blast formation. Reciprocal functional connections between the avian immune system and the pineal gland seem to be well documented, but the mechanism(s) involved have to be elucidated.

Journal Article↗
PubMed2002

[Plasmacytoid monocytes and plasmacytoid dendritic cells. Immune system cells linking innate and acquired immunity].

Plasmacytoid monocytes (PM), originally described by pathologists as cells occurring in the interfollicular area of human lymph nodes, are emerging cells in the scenario of the immune system. PM normally circulate between peripheral blood, lymphoid organs and sites of inflammation using specific migratory pathways and signalling; PM are easily recognizable on the basis of their distinctive morphology and phenotype (CD3-, CD11c-, CD14-, CD20-, CD36+, CD56-, CD68+, CD123+, BD-CA2+). Recently it has been shown that PM produce high levels of type I interferon, thus corresponding to natural interferon-producing cells. Furthermore, PM or their precursors may differentiate in vitro towards a new subset of dendritic cells, supporting a function in antigen-dependent T cell priming. Taken together, these data suggest PM play a relevant role in the immune system, linking innate and acquired immunities. In fact, PM seem to be crucial in the pathogenesis of different immune-mediated human diseases including viral infections and autoimmune disorders, and to be involved in the immune control of some malignant neoplasms. The issue concerning the cell lineage of PM remains unresolved, but the frequent association between a tumoral expansion of PM and myelo-monocytic leukemia, together with cytogenetic identity between the two cell populations identified in rare cases, corroborates the myeloid origin of PM.

Animals↗
PubMed1997

[Is the immune system our sixth sense? Relation between the immune and neuroendocrine systems].

There is an overwhelming evidence that cytokines, peptide hormones and neurotransmitters, as well as their receptors, are present in the brain, endocrine and immune systems. The structure and pattern of synthesis of these peptides by leukocytes appear similar to those synthesized in the neuroendocrine system, although some differences exist. Once secreted, these peptide hormones may function as endogenous regulators inside of the each system and also in bidirectional communication between the immune and neuroendocrine systems. Such communication suggest an immunoregulatory role for the brain and a sensory function for the immune system which may sense stimuli that are not recognized by the central and peripheral nervous systems (noncognitive stimuli). The plasma hormone concentrations contributed by lymphocytes usually do not reach the levels required when the pituitary gland is the source, but because immune cells are mobile, they have the potential to deposit the hormone locally at the target site. Several immunoregulatory cytokines, including IL-1, IL-2, IL-6, IFN-gama and TNF are produced not only in the immune system but in the neuroendocrine system as well. They have profound effects on neuroendocrine functions especially on hypothalamic pituitary axes. Neuroendocrine influences that modulate the immune function mainly include mental and physical stress. It can reduce the resistance of organism to infectious diseases and malignancies by compromising the immune system directly or indirectly. The brain is not an immunologically privileged site and therefore may become the target of immunologic attacks resulting in neuroimmunological diseases with an autoimmune component. The impact of psychological and psychosocial factors on the immune system is studied by psychoneuroimmunology whereas neuroendocrine immunology is generally interested in the interactions between the immune and neuroendocrine systems under physiological and pathological conditions. The recognition of the identity of ligands and receptors in the immune, nervous, and endocrine systems suggest a radically altered view of the immune systems impact on other tissues and organ systems, and vice versa. This will undoubtedly change our understanding of physiology, and consequently should profoundly impact the practice of medicine. (Tab. 5, Fig. 4, Ref. 85.)

Animals↗
PubMed1993

[Immune system and hypophysis].

The immune system does not function in isolation from either nervous or endocrine system. Recent advances in biology have made it clear that there are many connections between immune system and hypothalamo-pituitary axis. Among them, relationship of cytokines to hypothalamus is of great interest. We reviewed functions of the cytokines such as interleukin, interferon and tumour necrosis factor. For example, IL-1 releases ACTH from the hypophysis being mediated by corticotropin releasing hormone in the hypothalamus. ACTH shows inhibitory effect on the immune system. Interferons, as well as interleukins bring fever and anorexia via opioid receptors in the hypothalamus. There are some evidences which show effect of IL-1 on the posterior hypophysis which secretes vasopressin and oxytocin. There are, however, many unknown mechanisms in this field. The resolution of the specific interactions between the immune system and the hypothalamo-pituitary axis is subject to further investigations.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Nutrition and the immune system of the gut.

Studies suggest that the development and expression of the regional immune system in the gastrointestinal (GI) tract is relatively independent of systemic immunity. This is reflected in significant differences in functional response of T cells and B cells and affects cytokine patterns and activation pathways when regional immunity is compared to systemic immunity. Nutrients have fundamental and regulatory influences on the immune response of the GI tract and, therefore, on host defense. In addition to the effect of nutrition during development, the local impact of different dietary and antigenic elements on the regional immune system contributes to potential diversion of the two systems throughout life. The route of exposure during antigenic contact is known to affect host immune response, whether it be a normal process, happening in the context of normal environmental encounter with nonpathogenic microbes or planned immunization, or occurring as a result of resolution of a potentially pathologic process i.e., an infectious encounter. Interactions at the local level profoundly influence systemic immune response, in part because of intrinsic differences in these systems, and also because of different requirements for optimal function. Although inflammatory processes are central to host defense in the periphery, the protective blocking action of the secretory immunoglobulin A immune response is crucial to local host defense, and, therefore, to the integrity of GI tract immune function. For these reasons, interaction with normal bacteria of the GI tract may be seen as the model of how the system has evolved and provide clues to the restoration of balance in the immunocompromised host. Reduction of normal commensal bacteria in the context of infection or after antibiotic treatment may interfere with nutrient availability and impair beneficial stimulation of GI immune response. This impairment may be associated with continued colonization with opportunistic microbes and inflammatory immune response that could lead to malabsorption and malnutrition. Study of the impact of nutrient imbalance on the function of the GI tract has profound implications for clinical medicine and may in the future lead to the rational design of preventive approaches to support immune response and host defense.

Digestive System↗
PubMed1999

Hyporesponsiveness of the systemic and mucosal humoral immune systems in chickens infected with Salmonella enterica serovar enteritidis at one day of age.

Newly hatched chicks lack immunological maturity, which could compromise their ability to respond to infection by pathogens such as Salmonella enterica serovar enteritidis (S. enteritidis; SE). A study was conducted in which chicks were infected with a sublethal dose of SE at 1 d posthatch, and the systemic and intestinal immune responses to the challenge were followed over time. Birds infected at this age experienced difficulty in clearing the infection, and 50% of the individual birds remained persistently infected until 23 wk of age. These birds exhibited only a marginal systemic and mucosal humoral immune response to the infection. No response or little response was observed 1 wk postchallenge; responses increased somewhat over time. On many of the sampling times, 50% or more of the culture-positive birds lacked a detectable plasma or intestinal response. Levels of 10(3) to 10(5) SE/g of feces could be found in the intestines of birds eliciting a good IgA response, indicating that, when these birds did respond mucosally, the IgA produced was incapable of clearing the organism once the infection was established. Birds infected during this time also experienced reduced ability to respond to vaccination. Compared with uninfected controls, depressed responsiveness to an S. enteritidis bacterin was observed in infected birds 1 and 2 wk after administration, whereas those individuals receiving an inactivated Newcastle disease vaccine (NDV) experienced a reduced response 4 and 6 wk postvaccination, indicating that the persistent infection affected the ability of the immune system to respond to homologous and heterologous antigens. These results demonstrate that exposure of chickens to SE early in life interferes with the ability of these individuals to respond humorally to the infection and to other antigenic stimuli; such effects can be observed for at least 23 wk.

Animals↗
PubMed2004

The role of asymmetry of nervous and immune systems in the formation of cellular immunity of (CBaxC57Bl/6) F1 mice.

We have previously shown the existence of functional asymmetry of the immune system and the role of brain hemispheres and different lobes of thymus in the development of humoral immune response in (CBA x C57Bl/6) F1 mice. The role of asymmetry of the nervous and immune systems in the formation of the cellular immune response [delayed-type hypersensitivity (DTH) reaction] in these mice has been studied in our work. In order to test the influence of asymmetry of the primary immune organs, thymus, on the cellular immune response, mice were thymectomized and then we studied the effect of the injection of cells from contralateral thymus lobes of right-dominant and left-dominant donors by motor asymmetry on how pronounced the DTH reaction in the back left paw was. The injection of thymocytes from right-dominant donors appeared to result in significant differences in DTH reaction between left- and right-handed mice. At the same time, our experiments failed to discover any pronounced role of thymus asymmetry in the formation of DTH reaction. In order to test the influence of asymmetry of peripheral immune organs, regional lymph nodes, on the regulation of cellular immune response, we compared the DTH reaction in left and right paws of mice. We found that the intensity of the DTH reaction to sheep red blood cells in the front paws of (CBA x C57Bl/6) F1 mice depends not only on whether the antigen is injected into the left or right paw but also on the motor asymmetry of the hemispheres. While comparing the DTH reaction in the back left and right paw of mice we showed that in both right- and left-handed mice it was much more pronounced in the left paw than in the right one. The data obtained testify to the functional asymmetry of bilateral lymph nodes located near the forming cellular immune reaction. Thus, the results obtained show that the intensity of DTH reaction in (CBA x C57Bl/6) F1 mice depends on the functional asymmetry of regional lymph nodes and motor of brain hemispheres. The thymus functional asymmetry is of slight importance in DTH reaction.

Animals↗
PubMed1997

In defense of mucosal surfaces. Regulation and manipulation of the mucosal immune system.

The mucosal immune system defends the host against pathogens, most of which invade through mucosal surfaces. Antigen sampling in the mucosal immune system in the intestine occurs constantly in specialized inductive sites known as gut associated lymphoreticular tissue or GALT. Antigen-primed cells then migrate to effector sites in the gut lamina propria and epithelium as well as to other mucosal tissues. A variety of strategies are being pursued to develop effective oral vaccines that will protect mucosal surfaces. Some approaches involve recently identified mucosal adjuvants, the best known of which is cholera toxin. One approach is illustrated in which antigen and adjuvant are incorporated in the inner water phase of a water-in-oil-in-water or multiple emulsion, thus protecting antigen and delivering it into GALT.

Adjuvants, Immunologic↗
PubMed1998

Metamorphosis and the amphibian immune system.

Studies of the ontogeny of immunity in a limited number of representative amphibians have shown that while the immune systems of the larval forms are competent to defend against potential pathogens in the temporary ponds they inhabit, they are not equivalent to the mature immune systems that develop after metamorphosis. Metamorphosis is a critical time of transition when increased concentrations of metamorphic hormones, principally thyroid hormones (TH) and corticosteroid hormones (CH), orchestrate the loss or reorganization of many tissues and organ systems, including the immune system. Immune system reorganization may serve to eliminate unnecessary lymphocytes that could be destructive if they recognized newly emerging adult-specific antigens on the adult tissues. Increased corticosteroids during metamorphosis appear to induce apoptosis of susceptible lymphocytes. This cell death can be inhibited in vitro or in vivo by the corticosteroid receptor antagonist, RU486. A coordinate increase in both TH and CH at metamorphosis may be common to all amphibians that undergo metamorphosis. Current evidence suggests that the central hypothalamic mediator that induces pituitary production of both thyroid-stimulating hormone and adrenocorticotropic hormone in larval amphibians is corticotropin-releasing hormone. Most amphibians probably survive the temporary immunosuppression associated with metamorphosis with no deleterious effects. However, it is hypothesized that if environmental stressors result in the induction of metamorphosis at a less than optimal body size and state of immune maturation, the immune system destruction would be more significant, and the amphibians could be at greater risk of infection and death.

Amphibians↗
PubMedDate not supplied

Regional dichotomy of idiotypic expression on senescent B lymphocytes in systemic and mucosal immune systems: selective changes in NPb and T15 idiotypes with aging.

The age-associated changes in the expression of NPb and T15 idiotypes on antibody-secreting B cells in the spleen and bronchial lymph nodes (BLN) of mice following peritoneal immunization with (4-hydroxy-3-nitrophenylacetyl) acetic acid (NP) and phosphorylcholine (PC) as antigens were investigated. Changes in the NPb or T15 idiotype expressions were detected by the inhibition of anti-NP or anti-PC elispot-forming cells (SFC) with monoclonal (Mab) anti-idiotypic antibodies, Mabs Ac38 and Ac146, or AB1-2, respectively. We found that Mabs Ac38 and Ac146 significantly inhibited anti-NP IgM and IgG SFC responses in the spleen from 4-month old animals in a dose-dependent manner as opposed to a lack of effect on 24-month old splenic cells. There were no significant effects on anti-NP SFC responses in the BLN from either young or old mice. Similar results were obtained using Mab AB1-2 inhibition of T15 idiotype on anti-PC SFC responses in the spleen and BLN. No age-related changes in the gamma- and kappa-light chain contents of the secreted anti-NP antibodies by B cells in the spleen and BLN were observed. The kinetics of the appearance of endogenously auto-anti-idiotype blocked, hapten augmentable (HA) anti-NP IgM SFC responses revealed significantly higher percentages of HA SFC in the spleen and BLN, 14 days after immunization for both young and old mice. The findings suggest that the age-related changes in the idiotypic expression on antigen-specific antibody repertoires in the spleen and mucosa-associated tissues may be caused by the activation of subsets of B cells with different VH gene expressions.

Aging↗
PubMed1998

The immune system can affect learning: chronic immune complex disease in a rat model.

Evidence is presented that the immune system can affect central nervous system functioning, leading to changes in learning. Immune complex disease is induced in rats and their behavior tested using a Lashley maze. Significant differences in behavior were found between the animals with high disease activity and those with low disease activity and the non-disease controls. These changes were not due to uremia and are most likely due to the immune response. There is some evidence immune complex deposits in the choroid plexus may play some role, but not the sole or major role in the behavioral changes. This provides a model by which immunologic processes can cause neuropsychiatric manifestations in autoimmune diseases like lupus, as well as showing that immune processes can affect behavioral functioning.

Animals↗
PubMed1998

Neuroendocrine and immune system interactions in stress and depression.

Based on the extensive characterization of communication pathways between the nervous system and the immune system, there has been increasing interest in the impact of the nervous system on the development and expression of disorders involving the immune system and the contribution of the immune system to psychiatric disease. A vast literature has documented the impact of various stressors on a wide array of immune partners, and the specific neuroendocrine pathways involved have been elucidated. The impact of cytokines on neuroendocrine function and behavior has also been determined, and the relevance of cytokines to the pathophysiology of depression has become an exciting new research frontier. This article provides a foundation for integrating neuroendocrine-immune interactions into the formulation of neuropsychiatric and immunologic disease.

Depression↗
PubMed2006

Use of early passage fetal intestinal epithelial cells in semi-high-throughput screening assays: an approach to identify new innate immune system adjuvants.

Innate immune system stimulants (innate adjuvants) offer complementary approaches to vaccines and antimicrobial compounds to increase host resistance to infection. The authors established fetal bovine intestinal epithelial cell (BIEC) cultures to screen natural product and synthetic compound libraries for novel mucosal adjuvants. They showed that BIECs from fetal intestine maintained an in vivo phenotype as reflected in cytokeratin expression, expression of antigens restricted to intestinal enterocytes, and induced interleukin-8 (IL-8) production. BIECs could be infected by and support replication of bovine rotavirus. A semi-high-throughput enzyme-linked immunosorbent assay-based assay that measured IL-8 production by BIECs was established and used to screen commercially available natural compounds for novel adjuvant activity. Five novel hits were identified, demonstrating the utility of the assay for selecting and screening new epithelial cell adjuvants. Although the identified compounds had not previously been shown to induce IL-8 production in epithelial cells, other known functions for 3 of the 5 were consistent with this activity. Statistical analysis of the throughput data demonstrated that the assay is adaptable to a high-throughput format for screening both synthetic and natural product derived compound libraries.

Adjuvants, Immunologic↗