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At least 343 records · Page 19Linked to original sources
PubMed2003

'Order from disorder sprung': recognition and regulation in the immune system.

Milton's epic poem Paradise lost supplies a colourful metaphor for the immune system and its responses to pathogens. With the role of Satan played by pathogens seeking to destroy the paradise of human health, GOD intervenes and imposes order out of chaos. In this context, GOD means 'generation of diversity': the capacity of the innate and specific immune responses to recognize and eliminate a universe of pathogens. Thus, the immune system can be thought of as an entity that self-assembles the elements required to combat bodily invasion and injury. In so doing, it brings to bear the power of specific recognition: the ability to distinguish self from non-self, and the threatening from the benign. This ability to define and protect self is evolutionarily very old. Self-recognition and biochemical and barrier defences can be detected in primitive organisms, and elements of these mechanisms are built upon in an orderly way to establish the mammalian immune system. Innate immune responses depend on the use of a limited number of germline-encoded receptors to recognize conserved molecular patterns that occur on the surfaces of a broad range of pathogens. The B and T lymphocytes of the specific immune response use complex gene-rearrangement machinery to generate a diversity of antigen receptors capable of recognizing any pathogen in the universe. Binding to receptors on both innate and specific immune-system cells triggers intricate intracellular signalling pathways that lead to new gene transcription and effector-cell activation. And yet, regulation is imposed on these responses so that Paradise is not lost to the turning of the immune system onto self-tissues, the spectre of autoimmunity. Lymphocyte activation requires multiple signals and intercellular interactions. Mechanisms exist to establish tolerance to self by the selection and elimination of cells recognizing self-antigens. Immune system cell populations are reduced by programmed cell death once the pathogen threat is resolved. Once Paradise has been regained, memory cells remain in the body to sharply reduce the impact of a second exposure to a pathogen. Vaccination programs take advantage of this capacity of the human immune system for immunological memory, sparing millions the suffering associated with disease scourges. Thus does the order of the immune response spring from the disorder of pathogen attacks, and thus is Paradise preserved.

Adaptation, Physiological↗
PubMed1996

The immune system in ultraviolet carcinogenesis.

The immune system plays an important role in ultraviolet (UV) carcinogenesis by contributing to host resistance against skin cancer development. UV radiation, however, circumvents immune surveillance against skin cancers by modulating the immune response in a way that favors tumor development. Studies addressing the cellular mechanisms by which UV radiation modifies immune function are summarized. These studies demonstrate that UV irradiation of the skin produces both local, nonspecific immune suppression that inhibits immune effector functions within irradiated skin, as well as systemic, specific immune suppression against antigens introduced at a critical time after exposure to UV radiation. Evidence is presented suggesting that the production of cytokines by epidermal cells in response to UV-induced DNA damage is an important component of UV-induced specific immune suppression.

Animals↗
PubMedDate not supplied

[Morphofunctional characteristics of human immune system in surgical stress].

Morphofunctional aspects of the immune system (spleen, Peyer's patches, peripheral blood) were studied in patients with essential hypertension, rheumatic lesions of the heart and rheumatic patients after surgery. Surgical intervention caused considerable immunodepression. The entire system of coordinated functioning of immune organs got impaired. Immunodepressive restructuring of lymphoid organs affects all the structural units. Changes of the vascular-stromal complex are accompanied by changes in the most sensitive and complex mechanisms of the immune system such as vascular endothelium and population of progenitor cells. Metabolic basis transport and synthesis in the endothelium are perversed. In the progenitor cells proliferative activity of lymphocytes was sharply decreased while there was an increase in the function of suppressor T-lymphocytes. It is concluded that desynchronization of enzyme functioning in the vascular component of both the spleen and lymphoid system of the intestine can be regarded as a sign of disintegration of the entire system of immune organs during stress caused by a surgical intervention.

Female↗
PubMedDate not supplied

Alpha2-macroglobulin: an evolutionarily conserved arm of the innate immune system.

All animals and plants have immune systems that protect them from the diversity of pathogens that would otherwise threaten their survival. The different components of the immune system may inactivate the pathogens themselves or promote the inactivation and clearance of toxic products produced by the pathogens. An important category of virulence factors of bacterial and prokaryotic pathogens are the proteases, which act to facilitate the invasion of the pathogens and to promote their destructive growth in the host organism. The present review concentrates on the comparative biology of an evolutionarily conserved arm of the immune system, the protein, alpha2-macroglobulin. alpha2-Macroglobulin is an abundant protein of the plasma of vertebrates and members of several invertebrate phyla and functions as a broad-spectrum protease-binding protein. Protease-conjugated alpha2-macroglobulin is selectively bound by cells contacting the body fluids and alpha2-macroglobulin and its protease cargo are then internalized and degraded in secondary lysosomes of those cells. In addition to this function as an agent for protease clearance, alpha2-macroglobulin binds a variety of other ligands, including several peptide growth factors and modulates the activity of a lectin-dependent cytolytic pathway in arthropods.

Amino Acid Sequence↗
PubMed2000

Cellular and humoral immune system in schizophrenia: a conceptual re-evaluation.

Immune alterations in schizophrenia have been described for decades. However, modern immunological methods and new insights into the highly developed and functionally differentiated immune system allow an integrative view of both the older and also more recent findings of immunological abnormalities in schizophrenia. The conceptual advances in immunology require the re-evaluation of elder immunological findings in schizophrenia. In this overview, recent advances in immunological research regarding the differentiation between T-Helper-1 and T-Helper-2 cells and between the so-called specific and unspecific arms of the immune system are discussed. The unspecific "innate" immune system shows signs of an over-activation in unmedicated schizophrenic patients, as increased monocytes and gamma delta-cells point to. Increased levels of Interleukin-6 (IL-6) and the activation of the IL-6 system in schizophrenia might be the result of the activation of monocytes/macrophages, too. In contrast, several parameters of the specific cellular immune system are blunted, e.g. the decreased T-helper-1 (TH-1) related immune parameters in schizophrenic patients, both in vitro and in vivo. It seems that a TH-1-TH-2 imbalance with a shift to the TH-2 system is associated with schizophrenia. During therapy with antipsychotics, the specific TH-1 related immune answer becomes activated, but the B-cell system and the antibody production become activated too.

Antibody Formation↗
PubMed2004

Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system.

Vitamin D is an important immune system regulator. The active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], has been shown to inhibit the development of autoimmune diseases, including inflammatory bowel disease (IBD). Paradoxically, other immune system-mediated diseases (experimental asthma) and immunity to infectious organisms were unaffected by 1,25(OH)2D3 treatment. There are similar paradoxical effects of vitamin D deficiency on various immune system functions. Vitamin D and vitamin D receptor (VDR) deficiency resulted in accelerated IBD. Experimental asthma was unaffected by 1,25(OH)2D3 treatment and was less severe among VDR-deficient mice. Vitamin D is a selective regulator of the immune system, and the outcome of 1,25(OH)2D3 treatment, vitamin D deficiency, or VDR deficiency depends on the nature of the immune response (eg, infectious disease, asthma, or autoimmune disease). An additional factor that determines the effect of vitamin D status on immune function is dietary calcium. Dietary calcium has independent effects on IBD severity. Vitamin D-deficient mice on low-calcium diets developed the most severe IBD, and 1,25(OH)2D3 treatment of mice on low-calcium diets improved IBD symptoms. However, the best results for IBD were observed when the calcium concentration was high and 1,25(OH)2D3 was administered. Both the type of immune response and the calcium status of the host determine the effects of vitamin D status and 1,25(OH)2D3 on immunity.

Animals↗
PubMed2005

The peptide molecular links between the central nervous and the immune systems.

The central nervous system (CNS) and the immune system were for many years considered as two autonomous systems. Now, the reciprocal connections between them are generally recognized and very well documented. The links are realized mainly by various immuno- and neuropeptides. In the review the influence of the following immunopeptides on CNS is presented: tuftsin, thymulin, thymopoietin and thymopentin, thymosins, and thymic humoral factor. On the other side, the activity in the immune system of such neuropeptides as substance P, neurotensin, some neurokinins, enkephalins, and endorphins is discussed.

Animals↗
PubMed2005

A DNA vaccine coding for gB and gD of pseudorabies virus (suid herpes type 1) primes the immune system in the presence of maternal immunity more efficiently than conventional vaccines.

DNA vaccines are capable of priming the immune system of neonates in the presence of maternal antibodies. However, it is still not clear whether the extent of priming and protection against challenge infections induced by a DNA vaccine in maternally immune newborns is better than that induced by conventional vaccines. To study this, we used the pseudorabies virus (PRV) infection model in the natural host, the pig. We compared the efficacy of a DNA vaccine with the efficacy of a conventional modified live vaccine (MLV) and an inactivated vaccine (IV) in maternally immune newborn piglets. We measured the priming of the immune response and the degree of protection against challenge infection for all vaccine types. We vaccinated piglets with or without maternal immunity twice, at the age of 5 and 9 weeks, and we assessed protection by challenge infection with virulent PRV at the age of 15 weeks. Vaccination with DNA or conventional vaccines induced both humoral and cell-mediated immune responses in maternally immune animals. DNA vaccination seemed not to suffer from suppression by maternal immunity and resulted in similar or stronger immune responses in maternally immune piglets as compared in naïve piglets. In contrast, vaccination with conventional vaccines resulted in weaker immune responses in maternally immune piglets than in naïve piglets. Moreover, DNA vaccination provided better protection against challenge infection in maternally immune piglets than in naive piglets, whereas vaccination with conventional vaccines did not.

Animals↗
PubMed1997

Rapid evolution of immunoglobulin superfamily C2 domains expressed in immune system cells.

To test the hypothesis that proteins expressed in cells of the vertebrate immune system evolve unusually rapidly, 107 orthologous immunoglobulin C2 domains were compared between human and murine rodent. The analysis showed that the rate of nonsynonymous (amino-acid-altering) nucleotide substitution in these domains was correlated with factors associated with protein structure and with breadth of tissue expression, as well as with the rate of synonymous substitution. However, when such factors were controlled for statistically, there remained a strong positive association between expression in the immune system and nonsynonymous rate, with the highest rates being seen in genes expressed in the immune system only. Certain immune system genes are known to be subject to positive selection favoring diversity at the amino acid level; most of these genes encode receptors that interact directly with foreign antigens. The observed acceleration of the rate of nonsynonymous evolution in C2 domains of immune system proteins may be explained by either (1) reduced constraint at the amino acid level on molecules interacting with immune system receptors that are themselves evolving rapidly due to positive diversifying selection or (2) positive selection favoring amino acid changes correlated with changes in the immune system receptors.

Animals↗
PubMed2003

Intestinal exposure to a parasite antigen in utero depresses cellular and cytokine responses of the mucosal immune system.

The response of the mucosal immune system of 4-6-week old lambs to viable Trichostrongylus colubriformis larvae was compared in two groups of animals, one exposed to T. colubriformis antigen and the other to saline while in utero. Exposure to larval antigen two-thirds of the way through gestation resulted in significant reduction in the frequency of jejunal goblet cells and of ileal eosinophils, CD 1b(+) antigen-presenting cells and CD4(+), CD5(+) and CD8(+) cells. However, it resulted in a significant increase in the jejunal CD8(+) response to postnatal challenge. The expression of the cytokines TNF-alpha and IL-1 beta in the ileum, and of jejunal NSE, was significantly reduced by in utero exposure, whereas those of jejunal TNF-alpha and ileal TGF-beta were increased. The observed changes in cellular and cytokine responses to challenge with viable larvae, in those lambs previously exposed in utero, indicated that the intestinal mucosal immune system remains susceptible to down-regulation until considerably later in foetal development than is the case for other components of the immune system.

Administration, Oral↗
PubMed1999

The immune system in the elderly: III. Innate immunity.

The capability to cope with infectious agents and cancer cells resides not only in adaptive immune responses against specific antigens, mediated by T and B lymphocytes clonally distributed, but also in natural immune reactions. These innate defence mechanisms include chemotaxis, phagocytosis, natural cytotoxicity, cell interactions, and soluble mediators or cytokines. However, specific and natural immune mechanisms are always closely linked and interconnected, providing the primary defense against pathogens. The Authors discuss the main changes observed with advancing age in granulocytes and natural killer (NK) cell activity, in the expression and function of adhesion molecules, and in the pattern of cytokine production. Since phagocytic function is the primary mechanism through which the immune system eliminates most extracellular pathogenic microorganisms, analysis of this function is of clinical importance. Neutrophils from aged subjects often exhibit a diminished phagocytic capacity, as well as a depressed respiratory burst, notwithstanding an activated state. The activity of NK cells during aging has been studied extensively and different results have been reported. The most consistent data indicate an increase in cells with high NK activity with advancing age. Cells from healthy centenarians can efficiently kill target cells. This finding seems to suggest that innate immunity and in particular NK cell activity, is not heavily deteriorated with age. Conversely, a low NK activity is a predictor of impending morbidity. Immunosenescence is associated with increased expression of several cell adhesion molecules (CAM) resulting in an augmented capacity to adhere. Finally, also the cytokine network, responsible for differentiation, proliferation, and survival of lymphoid cells, undergoes complex changes with age. The main findings are a Th1 to Th2 cytokine production shift and an increased production of proinflammatory cytokines, which could explain many aspects of age-associated pathological events, such as atherosclerosis and osteoporosis.

Aged↗
PubMedDate not supplied

[The features of the brain immune system in brain neoplasms].

Examining responses of the local immune system of the brain in neurocancer patients suggests that the immune system is involved in the neuroimmune interaction of both physiological and pathological conditions in the central nervous system (CNS). The setting off the local immune system of the brain is of functional nature, similar to functional analogy with the local system of the mucosae. By functional analogy, the aggregate of immune responses in the nervous tissue and cerebrospinal fluid should be called local and the system that includes these responses should named the local immune system of the brain. Due to the fact that nervous, endocrine, and immune regulatory pathways intersect in the CNS (hypothalamus), it is expedient to call this aggregate of defensive factors and mechanisms in CNS more broadly--the neuroimmune system.

Albumins↗
PubMed2005

On modelling the immune system as a complex system.

We argued that immune system is an adaptive complex system. It is shown that it has emergent properties. Its network structure is of the small world network type. The network is of the threshold type, which helps in avoiding autoimmunity. It has the property that every antigen (e.g. virus or bacteria) is typically attacked by more than one effector. This stabilizes the equilibrium state. Modelling complex systems is discussed. Cellular automata (CA)-type models are successful, but there are much less analytic results about CA than about other less successful models e.g. partial differential equations (PDE). A compromise is proposed.

Immune System↗
PubMed2002

Enhanced cytomegalovirus infection of developing brain independent of the adaptive immune system.

Cytomegalovirus (CMV) has been suggested as the most prevalent infectious agent causing neurological dysfunction in the developing brain; in contrast, CMV infections are rare in the adult brain. One explanation generally given for the developmental susceptibility to the virus is that the developing immune system is too immature to protect the central nervous system from viral infection, but as the immune system develops it can protect the brain. We suggest an alternate view: that developing brain cells are inherently more susceptible to CMV infection, independent of the immune system. We used a recombinant mouse CMV that leads to green fluorescent protein expression in infected cells. Control experiments demonstrated a high correlation between the number of cells detected with the viral GFP reporter gene and with immunocytochemical detection of the virus. After intracerebral inoculation, the number of CMV-infected cells in neonatal brains was many times greater than in mature control or mature immunodepressed SCID mice, and the mortality rate of neonates was substantially greater than SCID or control adults. Parallel experiments with live brain slices inoculated in vitro, done in the absence of the systemic immune system, generated similar data, with immature hippocampus, hypothalamus, cortex, striatum, and cerebellum showing substantially greater numbers of infected cells (100-fold) than found in adult slices in these same regions. Interestingly, in the cerebellar cortex, CMV-infected cells were more prevalent in the postmitotic Purkinje cell layer than in the mitotic granule cell layer, suggesting a selective infection of some cell types not dependent on cell division. Together, these data support the view that CMV has an intrinsic preference for infection of developing brain cells, independent, but not mutually exclusive, of the developmental status of the systemic immune system in controlling CMV infection.

Aging↗
PubMed2000

Modulation of the fish immune system by hormones.

Immune-neuroendocrine interactions in fish, as in mammals, have become a focus of considerable interest, with the modulation of immune responses by hormones receiving particular attention. Cortisol, growth hormone (GH), prolactin (PRL), reproductive hormones, melanin-concentrating hormone (MCH) and proopiomelanocortin (POMC)-derived peptides have all been shown to influence immune functions in a number of fish species. This review summarises the known effects of these hormones on the fish immune system, as well as the often complex interactions between different hormones. The possible implications for fish health, with respect to aquaculture and the changes in immunocompetence that take place during different stages in the fish life cycle are also discussed.

Animals↗
PubMed2002

Memorizing innate instructions requires a sufficiently specific adaptive immune system.

During its primary encounter with a pathogen, the immune system has to decide which type of immune response is most appropriate. Based on signals from the innate immune system and the immunological context in which the pathogen is presented, responding lymphocytes will adopt a particular phenotype, e.g. secrete a particular profile of cytokines. Once stimulated, lymphocytes store the appropriate type of response by differentiating from a naive to a memory phenotype. This allows the appropriate type of immune reaction to be regenerated upon re-stimulation of those memory clones. We developed a computer simulation model in which cross-reacting effector/memory clones contribute to the immunological context of pathogens. If a pathogen is recognized by both naive clones and pre-existing effector/memory clones, the naive lymphocytes adopt the effector mechanism of the memory clone. The adaptive immune system thereby stores immunological decisions and somatically learns to induce the right type of immune response to pathogens sharing epitopes. The influence of effector/memory lymphocytes may be detrimental when they cross-react to new pathogens that require a different kind of immune response. Here, we show that the immune system needs to be sufficiently specific to avoid such mistakes and to profit from the information that is stored in effector/memory lymphocytes. Repertoire diversity is required to reconcile this specificity with reactivity against many pathogens.

Aged↗