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PubMed2000

The immune system and schizophrenia. An integrative view.

Immune alterations in schizophrenia have been described for decades. Modern immunological methods and new insights into the highly developed and functionally differentiated immune system allow an integrative view of both the older and the recent findings of immunological abnormalities in schizophrenia. Both the unspecific and the specific arms of the immune system seem to be involved in the dysfunction of the immune system in schizophrenia. The unspecific, "innate" immune system shows signs of overactivation in unmedicated schizophrenic patients, as indicated by increased monocytes and gamma delta-cells. 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. On the other hand, several parameters of the specific cellular immune system are blunted, such as, for example, 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 antipsychotic therapy with neuroleptics, the specific TH-1-related immune answer becomes activated, but in addition the B cell system and antibody production increase.

Humans↗
PubMed2002

Basal metabolic rate and the evolution of the adaptive immune system.

Vertebrates have evolved an adaptive immune system in addition to the ancestral innate immune system. It is often assumed that a trade-off between costs and benefits of defence governs the evolution of immunological defence, but the costs and benefits specific to the adaptive immune system are poorly known. We used genetically engineered mice lacking lymphocytes (i.e. mice without adaptive, but with innate, immunity) as a model of the ancestral state in the evolution of the vertebrate immune system. To investigate if the magnitude of adaptive defence is constrained by the energetic costs of producing lymphocytes etc., we compared the basal metabolic rate of normal and lymphocyte-deficient mice. We found that lymphocyte-deficient mice had a higher basal metabolic rate than normal mice with both innate and adaptive immune defence. This suggests that the evolution of the adaptive immune system has not been constrained by energetic costs. Rather, it should have been favoured by the energy savings associated with a combination of innate and adaptive immune defence.

Adaptation, Physiological↗
PubMed1999

The immune system in the elderly: I. Specific humoral immunity.

Profound and complex changes in the immune response occur during the aging process. Immunosenescence is reflected by a sum of disregulations of the immune system and its interaction with other systems. Many of the changes would appear to implicate age-related deficiencies of the immune responses. The term immunosenescence designates therefore a sort of deterioration of the immune function which is believed to manifest itself in the increased susceptibility to cancer, autoimmune disease, and infectious disease. Evidence has been accumulating from several studies which suggest an association between immune function and individual longevity. However, there are observations, especially in very old healthy people, that several immune functions are unexpectedly well preserved and substantially comparable to those observed in young subjects. These findings raise the question of whether the alterations that can be observed in the immune parameters of the elderly are a cause or a result of underlying disease processes. Moreover, studies on centenarians revealed a remodeling of the immune system rather than a deterioration, suggesting that the changes observed during immunosenescence do not correspond to immunodeficiency. The underlying mechanisms of these events are however still unclear. The purpose of the present review is to assess the status of research on the immunobiology of aging. In this first section, we focus attention on the B cell biology of aging. In clinical practice, the changes in humoral immune responsiveness and antibody-mediated defense mechanisms could greatly influence the incidence and outcome of bacterial infections and autoimmune diseases as well as the response to vaccines.

Aged↗
PubMed1989

Effects of antibiotics on the mammalian immune system.

Studies on the immune effects of antibiotics are in their infancy. Most currently available data fit into the anecdotal category--there are no standard assays for determination of immune inhibition or enhancement. Most studies were performed in vitro; minimal correlation is made between the mode of action and the intracellular penetration of the test antibiotics, and mechanisms of noted effects are largely unexamined and unexplained. Thus, the observations are frequently contradictory and difficult to interpret. Nevertheless, it has become apparent that certain antibiotics do have potent immunomodulating actions. The clinical impact of such immunomodulation is unknown, since few studies have been performed in patients receiving antibiotics and virtually no studies have examined the effect of antibiotics on the immune system of those at highest risk for sustaining an adverse effect, the immunocompromised patient. Well-planned studies on antimicrobial action, adapting the rapidly expanding knowledge of the immune system currently being generated and utilizing the advances in technology for scrutiny of immune affectors, are badly needed. With a better understanding of the effects of such agents on host cells as well as target cells, it is conceivable that in the future antibiotic therapy will consist of regimens that provide not only optimal anti-infective therapy but also optimal immunomodulating support.

Animals↗
PubMed1994

Sympathetic nervous system modulation of the immune system. III. Alterations in T and B cell proliferation and differentiation in vitro following chemical sympathectomy.

Functional changes in lymph node (LN) and spleen lymphocytes were examined following sympathetic denervation of adult mice with 6-hydroxydopamine (6-OHDA). Sympathectomy reduced in vitro proliferation to concanavalin A (ConA) by LN cells and decreased LN Thy-1+ and CD4+ T cells. At the same time, ConA-induced interferon-gamma (IFN-gamma) production was increased, but interleukin-2 (IL-2) production was not altered. After sympathectomy, lipopolysaccharide (LPS)-stimulated proliferation of LN B cells was enhanced, in parallel with an increase in the proportion of sIgM+ cells. LPS-induced polyclonal IgM secretion was decreased, whereas polyclonal IgG secretion was dramatically enhanced. In the spleen, ConA and LPS responsiveness was reduced after sympathectomy, as was IL-2 and IFN-gamma production. The decreased proliferation was not associated with changes in splenic T and B cell populations. The uptake blocker desipramine prevented the 6-OHDA-induced changes in spleen and LN, indicating that these alterations were dependent upon neuronal destruction. These results provide evidence for heterogeneity of sympathetic nervous system regulation of T and B lymphocyte function and for organ-specific influences on immune function.

Animals↗
PubMedDate not supplied

The effects of sex hormones on the immune system in pregnancy.

The immune system is affected by sex steroids. Immunoglobulin synthesis, T-cell subsets, and a variety of cytokines are targets for sex steroids. Hormonal variations are found in patients with rheumatic diseases. These variations include the hydroxylation of estrone and the oxidation of testosterone, both of which are altered in rheumatic disease. These changes are magnified in the pregnant state. More estrogen metabolites of the C-16 variety can bind to cells (lymphocytes and erythrocytes) and his reaction is accelerated in pregnancy. The role of the catechol estrogens is discussed. These compounds may be important to some of the vasospastic symptoms seen during pregnancy in patients; moreover, oxidation of testosterone to weak androgens is found in women with systemic lupus erythematosus (SLE). Overall, interesting observations and conclusions will evolve from a better understanding of sex hormone metabolism and its effects on the immune system in pregnancy.

Female↗
PubMed2004

Evolution of the innate immune system: the worm perspective.

Simple model organisms that are amenable to comprehensive experimental analysis can be used to elucidate the molecular genetic architecture of complex traits. They can thereby enhance our understanding of these traits in other organisms, including humans. Here, we describe the use of the nematode Caenorhabditis elegans as a tractable model system to study innate immunity. We detail our current understanding of the worm's immune system, which seems to be characterized by four main signaling cascades: a p38 mitogen-activated protein kinase, a transforming growth factor-beta-like, a programed cell death, and an insulin-like receptor pathway. Many details, especially regarding pathogen recognition and immune effectors, are only poorly characterized and clearly warrant further investigation. We additionally speculate on the evolution of the C. elegans immune system, taking into special consideration the relationship between immunity, stress responses and digestion, the diversification of the different parts of the immune system in response to multiple and/or coevolving pathogens, and the trade-off between immunity and host life history traits. Using C. elegans to address these different facets of host-pathogen interactions provides a fresh perspective on our understanding of the structure and complexity of innate immune systems in animals and plants.

Amino Acid Sequence↗
PubMed1986

Estradiol-induced alteration in the immune system. II. Suppression of cellular immunity in the rat is not the result of direct estrogenic action.

Estradiol has been reported to suppress numerous cellular immune response. What is not known is how estradiol exerts this effect. In vivo administration of estradiol to male rats caused time-related immunomodulatory effects leading to enhancement of lymphocyte transformation while suppressing a mixed lymphocyte reaction (MLR) response. The suppression of the MLR response was not due to alterations in the ratio of helper and suppressor T cells, nor was it due to alterations in either cell viability or the number of cells in culture. Lymphocytes cultured in vitro with estradiol, however, fail to show any alteration in the responsiveness in either MLR or lymphocyte transformation assays. The suppressive effects of estradiol cannot be transferred from a primary MLR culture to a second MLR culture using the supernatants from the primary MLR culture. Lymphocytes from animals given estradiol in vivo show no alteration in the production of interleukin 2: added in vitro to primary MLR cultures, Interleukin 2 failed to restore full responsiveness to lymphocytes from animals treated in vivo with estradiol. These results suggest that estradiol acts indirectly to cause an alteration in the responsiveness of the regulatory cells of the cellular immune system.

Animals↗
PubMed2004

Divergent roles for C-type lectins expressed by cells of the innate immune system.

In recent years there has been increasing interest in the diversity and function of carbohydrates present on a range of endogenous mammalian glycoproteins and pathogen surfaces. It is clear that carbohydrate structures are not merely structural components of the molecules which bear them but are, in many instances, a source of information to be decoded by biological systems including the immune system. Macrophages and other antigen presenting cells express a variety of pattern recognition molecules which allow discrimination between self and non-self ligands and are well known for their ability to recognise and internalise foreign antigens. The role of carbohydrates as molecular determinants of self/non-self has been recognised for many years and a family of proteins known as the C-type lectins are implicated as the main players in carbohydrate recognition within the immune system. More recently, C-type lectin receptors which bind ligands other than carbohydrates have been identified, and there are additional receptors which bind both carbohydrate and non-carbohydrate ligands. In this review article we seek to shed light on the varied roles of this family of receptors, particularly those receptors expressed by antigen presenting cells and those with known ligands. We also review more recent data on several members of this family.

Animals↗
PubMed1988

"Classical" neuroendocrine peptide hormones produced by cells of the immune system.

Cells of the immune system are shown to produce peptide hormones whose production was once thought to be restricted to neuroendocrine tissue. Interestingly, in some cases, very specific stimuli elicit the production of one species of neuropeptide hormone. In other instances, it appears that some peptide hormones are constitutively produced. In either situation, the various immunocyte-derived hormones have biological activity in endocrinological assays. In the present report, a review of the various neuroendocrine hormones produced by cells of the immune system is discussed.

Animals↗
PubMed2001

CD1d and natural T cells: how their properties jump-start the immune system.

Cellular and humoral immune mechanisms recruited to defend the host from infectious agents depend upon the early immune events triggered by antigen. The cytokine milieu within which the immune response matures is the most important of many factors that govern the nature of the immune response. Natural T cells, whose function is controlled by CD1d molecules, are an early source of cytokines that can bestow type 1 or type 2 differentiative potential upon helper T lymphocytes. This review attempts to illuminate the glycolipid antigen presentation properties of CD1d, how CD1d controls the function of natural T cells and how CD1d and natural T cells interact to jump start the immune system. CD1d is postulated to function as a sensor, sensing alterations in cellular lipid content by virtue of its affinity for such ligands. The presentation of a neo-self glycolipid, presumably by infectious assault of antigen-presenting cells, activates natural T cells, which promptly release pro-inflammatory and anti-inflammatory cytokines and jump-start the immune system.

Animals↗
PubMed2002

The immune system: a target for functional foods?

The immune system acts to protect the host from infectious agents that exist in the environment (bacteria, viruses, fungi, parasites) and from other noxious insults. The immune system is constantly active, acting to discriminate 'non-self' from 'self'. The immune system has two functional divisions: the innate and the acquired. Both components involve various blood-borne factors (complement, antibodies, cytokines) and cells. A number of methodologies exist to assess aspects of immune function; many of these rely upon studying cells in culture ex vivo. There are large inter-individual variations in many immune functions even among the healthy. Genetics, age, gender, smoking habits, habitual levels of exercise, alcohol consumption, diet, stage in the female menstrual cycle, stress, history of infections and vaccinations, and early life experiences are likely to be important contributors to the observed variation. While it is clear that individuals with immune responses significantly below 'normal' are more susceptible to infectious agents and exhibit increased infectious morbidity and mortality, it is not clear how the variation in immune function among healthy individuals relates to variation in susceptibility to infection. Nutrient status is an important factor contributing to immune competence: undernutrition impairs the immune system, suppressing immune functions that are fundamental to host protection. Undernutrition leading to impairment of immune function can be due to insufficient intake of energy and macronutrients and/or due to deficiencies in specific micronutrients. Often these occur in combination. Nutrients that have been demonstrated (in either animal or human studies) to be required for the immune system to function efficiently include essential amino acids, the essential fatty acid linoleic acid, vitamin A, folic acid, vitamin B6, vitamin B12, vitamin C, vitamin E, Zn, Cu, Fe and Se. Practically all forms of immunity may be affected by deficiencies in one or more of these nutrients. Animal and human studies have demonstrated that adding the deficient nutrient back to the diet can restore immune function and resistance to infection. Among the nutrients studied most in this regard are vitamin E and Zn. Increasing intakes of some nutrients above habitual and recommended levels can enhance some aspects of immune function. However, excess amounts of some nutrients also impair immune function. There is increasing evidence that probiotic bacteria improve host immune function. The effect of enhancing immune function on host resistance to infection in healthy individuals is not clear.

Animals↗
PubMed2001

Symposium on 'dietary influences on mucosal immunity'. How dietary antigens access the mucosal immune system.

The intestinal epithelium is a selective barrier where incompletely-digested food antigens are transmitted to the immune system. Food antigens are often the starting point of intestinal diseases such as food allergy or coeliac disease. The intestinal epithelial cells (IEC) take up and process food antigens mainly by fluid-phase transcytosis involving two functional pathways, one minor direct pathway without degradation and another major lysosomal degradative pathway. Among the peptidic metabolites generated during transepithelial transport of luminal antigens, some have a molecular mass compatible with a binding to restriction (major histocompatibility complex; MHC) molecules; the latter can be up regulated on enterocytes, especially in inflammatory conditions. Indeed, interferon-gamma not only increases the paracellular absorption of antigens, but also their transcytosis across epithelial cells. It has been reported that enterocytes may even directly present peptidic epitopes to underlying T-cells. As a new potential way of transmitting peptidic information to the local or systemic immune system, the secretion by IEC of antigen-presenting vesicles called exosomes and bearing MHC-peptide complexes has recently been proposed. Many other factors such as nutritional or environmental factors can also influence the properties of the epithelial barrier and the outcome of the immune response to lumen antigens.

Animals↗
PubMed1992

Antigen processing in the mucosal immune system.

The mucosal immune system is concerned with host defense along the moist surfaces of the body which have contact with the external environment. These sites contain specialized lymphoid structures which contain precursors for IgA-synthesizing B lymphocytes and immunoregulatory T lymphocytes which will determine whether oral tolerance or a strong immune response develops against antigens administered orally. The key step to antigen processing in the gastrointestinal tract involves its initial uptake from the gut lumen by specialized follicle associated epithelium called 'M' cells. M cells originate from adjacent crypt epithelium and are interspersed between the absorptive epithelial cells in the follicle-associated epithelium. M cells cells have short, irregular microvilli, are closely associated with lymphocytes, do not have a prominent terminal web, and have only weak alkaline phosphatase activity but strong nonspecific esterase activity. M cells do not express surface MHC class II (HLA-DR) antigens. These cells take up macromolecules, viruses, bacteria and protozoa within 30 minutes from the initial presentation of the antigen to the intestinal lumen. After the initial uptake of antigen by M cells, the antigens are transported into the follicular areas to be processed by dendritic cells and brought into close contact with the antigen-specific precursors for IgA secreting plasma cells. The final result of M cell processing is the production of a vigorous secretory IgA response and local cell-mediated immunity with suppression of a systemic IgG, IgE and delayed-type hypersensitivity to orally-administered antigens.

Animals↗