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Results for “Immune dysfunction”

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At least 1,747 records · Page 97Linked to original sources
PubMed1991

The regulation of IgA B-cell differentiation.

IgA B-cell differentiation is affected by several kinds of events. One key event, IgA B-cell switch differentiation, is a process that may be controlled by tissue-specific "switch" cells or an identifiable switching cytokine or lymphokine that operates in an IgA-specific fashion. Another event, or group of events is IgA B-cell terminal differentiation in B cells already switched to IgA. Such terminal differentiation may also be regulated in an IgA-specific fashion, at least insofar as class-nonspecific lymphokines can be presented to IgA B cells in a class-specific fashion by cells bearing IgA-Fc receptors. Emerging knowledge of the regulation of IgA B cells offers many opportunities to enhance or inhibit IgA B-cell development at several levels. In coming years this will prove important, not only in devising ways of protecting against mucosal pathogens, but also in modifying immunologic diseases that have their basis in mucosal immune system dysfunction.

B-Lymphocytes↗
PubMed1990

[Changes in immunological indicators in patients with surgical endotoxemia after UV-irradiation of blood].

Changes in the values of the immune status during UV autohemotherapy were studied in 22 patients with surgical endotoxicosis of various genesis. Maximum tension of immunogenesis was found in all patients. The time course of changes in the general pool of rosette-forming and separate populations of neutrophils, as well as in the index of immunocompetent cell ratios are evidence of the high informativeness of these tests in determining the severity of the immune system dysfunctions.

Adult↗
PubMedDate not supplied

The biology and pathophysiology of complement receptors.

Activation of the complement cascade leads to the generation of multiple breakdown products which bind on to specific cellular receptors and regulate their function. In this review, we describe the biochemical and physiological features of the 7 known complement receptors. Four of them (complement receptors 1, 2, and 3 and receptors for C3a) bind cleavage fragments of the third component of the complement and three have specificity for C1q, factor H and C5a. In patients with systemic lupus erythematosus, a unique human autoimmune disorder, the numbers of CR1 on the surface of the red blood cells are decreased; in this review we discuss the implications in the pathogenesis of SLE. A number of patients have now been reported whose cells lack CR3 from their surface; this deficiency is associated with a number of immune cell dysfunctions which are discussed in detail. Finally, we discuss aberrations in the expression of complement receptors in certain human leukemic cells.

Antigen-Antibody Complex↗
PubMed1985

[Pulmonary pneumocystosis in an adult patient].

A 34-year-old male with no diseases in the past developed, after a 7-day alcoholic abuse, an acute pancreatitis and ulcerative necrotic colitis. At the autopsy, apart from the underlying disease, the pulmonary pneumocystosis was found which is considered by the authors as a complication of a severe pathology of the alimentary tract organs followed by immune system dysfunction.

Acute Disease↗
PubMed1985

In vitro T cell hyperreactivity in Obese strain (OS) chickens is due to a defect in nonspecific suppressor mechanism(s).

Spontaneous autoimmune thyroiditis of OS chickens is associated with a marked hyperreactivity of the T cell system. The purpose of the present study was to investigate the underlying regulatory mechanisms. Co-cultivation experiments between Con A-stimulated OS and NWL lymphocytes in communicating cultures revealed soluble regulatory factors to be responsible for the observed functional differences: the high proliferative response to Con A and hyperproduction of IL 2 of OS cells was found to be due to a deficiency in the conditioned medium of dialyzable inhibitory factor(s) that regulate IL 2 secretion of NWL lymphocytes. Furthermore, sera of young NWL chickens were found to profoundly inhibit the IL 2-promoted lymphoblast proliferation. This IL 2 antagonizing activity is lost with age (3 to 6 yr) and was found to be significantly diminished in OS birds throughout ontogeny, thus pointing to possible parallels between immune regulatory dysfunction in autoimmunity and in physiologic aging. Both enhanced T cell response and the defect in serum suppressor were inherited by (OS X CB)F1 animals, indicating that these two aberrations may be related to each other.

Animals↗
PubMed1985

Bovine viral diarrhea in a newborn calf.

Bovine viral diarrhea virus was believed to be the cause of ill-thrift since birth, resulting in death of a Holstein calf. Bovine viral diarrhea virus was isolated from Peyer's patches and mesenteric lymph nodes, but serum neutralizing antibodies were not detected. The lymphoid depletion and myeloid suppression seen in this case may be a factor in the immune system dysfunction described for bovine viral diarrhea. Typical ulcerative lesions within the alimentary tract were not observed.

Animals↗
PubMed1983

The viral hypothesis in parkinsonism.

The most crucial unanswered question in Parkinson's disease is its fundamental cause. Since Carlsson's original suggestion that dopamine may be a transmitter in the central nervous system involved in the control of motor function and that it may be involved in the Parkinsonian syndrome (Carlsson, 1959), and the now-classic paper by Ehringer and Hornykiewicz (1960) which definitively showed the significant reduction of dopamine concentration in the neostriatum of cases of idiopathic Parkinson and postencephalitic parkinsonism, the vast amount of work on the subject has focused on the biochemical and pharmacologic correlates of this dopaminergic system failure involving particularly the nigrostriatal pathways. The concept of a specific neurotransmitter deficiency associated with a specific neurological syndrome potentially amenable to replacement therapy, has appropriately generated a considerable degree of clinical and research interest for over 20 years, but, with few exceptions, there has been hardly any focused or concerted research effort on looking at direct causal factors or primary initiating events in this disease process. As in Alzheimer's disease, another of the degenerative diseases of the brain of unknown origin with a specific biochemical substrate, any etiologic hypothesis for Parkinson's disease--whether a virus, an age-related immune system dysfunction, a genetic factor, a "trophic" substance, or a toxin--would have to explain the selective involvement of specific transmitter-defined neuronal pathways, the non-specificity of the brain lesions that define the disease, and the clinical involvement of a sizeable segment of the aging population. Of the several plausible hypotheses mentioned earlier, which are not necessarily mutually exclusive, we would like to critically consider the possibility of a viral cause.

Alzheimer Disease↗
PubMed1993

2,3,7,8-tetrachlorodibenzo-p-dioxin increases cardiac myocyte intracellular calcium and progressively impairs ventricular contractile responses to isoproterenol and to calcium in chick embryo hearts.

Binding by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to the Ah receptor leads to transcriptional activation of several genes and a toxicity syndrome that includes tumor promotion, wasting, hormonal and immune system dysfunction, and death. Recent findings indicate that TCDD may also affect cardiac function. Here, we used the chick embryo, a TCDD-sensitive species, to further characterize the effects of TCDD on ventricular muscle contraction and on cardiac myocyte [Ca2+]i assessed with fura 2. The results show that TCDD causes an evolving sequence of contractile defects, independent of changes in diet, first impairing cAMP-modulated contraction (after 48 hr) and later (by seven days) decreasing responses to [Ca2+]o. Phenobarbital, even at high doses, failed to affect the inotropic response to isoproterenol, supporting the specificity of the ventricular contractile effects of TCDD. TCDD treatment also depressed inotropic responses to theophylline and forskolin, indicating that it has a post-beta-adrenergic receptor effect on cAMP action. In contrast to its depression of responses to beta-adrenergic stimuli and to [Ca2+]o, TCDD did not affect initial tensions of ventricular muscle stimulated at 1 Hz or the force-frequency response up to 1 Hz, indicating that TCDD-treated ventricles can respond normally at slow rates of stimulation. TCDD treatment depressed lusitropic (relaxation) responses to isoproterenol and to increasing [Ca2+]o indicating that it impairs the ability of the sarcoplasmic reticulum to sequester Ca2+. Fura 2-based measurements showed that [Ca2+]i was nearly doubled after TCDD treatment. The increase in [Ca2+]i is consistent with the decrease in the contractile response to [Ca2+]o, amelioration of the response to isoproterenol by subphysiologic concentrations of [Ca2+]o, and intermittent lack of response to electrical stimulation in high K+ observed in ventricles from TCDD-treated embryos. TCDD treatment also depressed the initial increase in [Ca2+]i by isoproterenol, consistent with the decreased contractile response to isoproterenol. The findings show that TCDD causes well defined, progressive impairment of avian ventricular responses to inotropic stimuli, providing new evidence that the heart is a target of TCDD action and that TCDD disturbs intracellular calcium processing.

Animals↗
PubMedDate not supplied

Role of humoral immunity in acute cardiac allograft dysfunction.

To elucidate the pathogenic mechanisms of acute allograft dysfunction that is not caused by acute cellular rejection, we have studied the clinical and immunopathologic characteristics of 11 heart transplant recipients who had acute allograft dysfunction in the absence of interstitial mononuclear cell infiltrates on endomyocardial biopsy samples. Six of eleven patients (54%) had a striking increase in levels of anti-HLA antibodies in close temporal proximity with the episode of acute allograft dysfunction. Cardiac allograft function improved in all patients with intensification of immunosuppression.

Adult↗
PubMed1998

Neurobehavioral properties of chemical sensitivity syndromes.

Chemical sensitivity Syndromes refers to aggregations of symptoms marked by largely subjective neurobehavioral complaints and hypothesized links to immune system dysfunction. The entities reviewed here consist of the Multiple Chemical Sensitivity Syndrome, the Sick Building Syndrome, the Chronic Fatigue Syndrome, and the Gulf War Syndrome. Except for the Chronic Fatigue Syndrome, toxic chemical exposures are accorded a significant role in their etiology. The connections are ambiguous because of the variety of chemical agents cited and, for the most part, the relatively low levels at which exposures occur. Conventional clinical signs are also typically lacking. Explanatory mechanisms include psychiatric diagnoses such as somatization, behavioral mechanisms such as conditioning and generalization, neuropharmacological mechanisms such as sensitization, and psychoneuroimmunological mechanisms such as those involving the hypothalamic-pituitary-adrenal axis. Laboratory animal experimentation and controlled clinical trials, especially with inhaled material, provide the means for exploring the proffered explanations.

Fatigue Syndrome, Chronic↗
PubMedDate not supplied

Alterations in the lymphocytic and mononuclear phagocytic systems of turkey poults associated with exposure to poult enteritis and mortality syndrome.

In vivo and in vitro mononuclear phagocytic system functions, expression of lymphocyte subset cell surface markers in the thymus and bursa of Fabricius, and lymphocyte subset dynamics during the course of poult enteritis and mortality syndrome (PEMS) were examined. PEMS is an acute, transmissible, infectious intestinal disease accompanied by high mortality and morbidity. The etiology of this multifactorial disease remains to be elucidated; however, turkey coronavirus was initially assumed to be one of the primary agents involved. Further investigation demonstrated that turkey coronavirus was not always detectable in poults exhibiting PEMS symptoms, and, thus, PEMS poults began to be identified as positive or negative for turkey coronavirus. In each trial, uninfected hatchmate controls were compared with turkey poults that were contact exposed to PEMS poults at 7 days of age. Following intravenous inoculation, control poults cleared Escherichia coli from their circulation by 60 min, whereas viable E. coli were still present in the circulation of PEMS poults at 60 min postinoculation. Inflammatory response measured by Sephadex-elicited abdominal exudate cell recruitment and the adherence potential of abdominal exudate cells was not significantly different between uninfected and PEMS poults. The percentage of glass-adherent abdominal exudate macrophages was higher in PEMS poults. However, the ability of these macrophages to phagocytize sheep red blood cells and the average number of sheep red blood cells per phagocytic macrophage were both lower compared with uninfected controls. CD4+ expression in thymic tissue of PEMS poults at 9 days postinfection was significantly lower. The CD4+:CD8+ lymphocyte ratio in peripheral blood leukocytes from coronavirus-negative PEMS poults was lower than that from both uninfected and coronavirus-positive PEMS poults at 14 days postinfection. In the spleen, the CD4+:CD8+ lymphocyte ratio was higher in coronavirus-positive PEMS poults as compared with the other treatments. In conclusion, immune system dysfunction in PEMS is associated with impaired mononuclear phagocytic system function and alterations in lymphocyte populations.

Animals↗
PubMed2006

CNS immune privilege: hiding in plain sight.

Central nervous system (CNS) immune privilege is an experimentally defined phenomenon. Tissues that are rapidly rejected by the immune system when grafted in sites, such as the skin, show prolonged survival when grafted into the CNS. Initially, CNS immune privilege was construed as CNS isolation from the immune system by the blood-brain barrier (BBB), the lack of draining lymphatics, and the apparent immunoincompetence of microglia, the resident CNS macrophage. CNS autoimmunity and neurodegeneration were presumed automatic consequences of immune cell encounter with CNS antigens. Recent data have dramatically altered this viewpoint by revealing that the CNS is neither isolated nor passive in its interactions with the immune system. Peripheral immune cells can cross the intact BBB, CNS neurons and glia actively regulate macrophage and lymphocyte responses, and microglia are immunocompetent but differ from other macrophage/dendritic cells in their ability to direct neuroprotective lymphocyte responses. This newer view of CNS immune privilege is opening the door for therapies designed to harness autoreactive lymphocyte responses and also implies (i) that CNS autoimmune diseases (i.e. multiple sclerosis) may result as much from neuronal and/or glial dysfunction as from immune system dysfunctions and (ii) that the severe neuronal and glial dysfunction associated with neurodegenerative disorders (i.e. Alzheimer's disease) likely alters CNS-specific regulation of lymphocyte responses affecting the utility of immune-based therapies (i.e. vaccines).

Animals↗
PubMed2005

Immune suppression in cancer: effects on immune cells, mechanisms and future therapeutic intervention.

Evidence indicates that the healthy immune system is necessary for control of malignant disease and that immune suppression associated with cancer contributes to its progression. Tumors have developed strategies to successfully evade the host immune system, and various molecular and cellular mechanisms responsible for tumor evasion have been identified. Certain of these mechanisms target immune anti-tumor effector cells. Dysfunction and apoptosis of these cells in the tumor-bearing host creates an immune imbalance that cannot be corrected by immunotherapies aimed only at activation of anti-tumor immune responses. Reversal of existing immune dysfunction(s) and normalization of lymphocyte homeostasis in patients with cancer needs to be a part of future cancer immunotherapy. Therapeutic strategies are being designed to correct the immune imbalance, deliver adequate in vivo stimulation, transfer effector T cells capable of in vivo expansion and provide protection for the immune effector cells re-populating the host. Survival of these cells and long-term memory development in patients with malignancy are necessary for improving clinical benefits of cancer immunotherapies.

Humans↗
PubMed1983

Delayed phytohemagglutinin-stimulated production of adenosine triphosphate by aged human lymphocytes: possible relation to mitochondrial dysfunction.

The decreased immune response associated with aging may, in part, reflect intrinsic age-related biochemical alterations in lymphocytes from older animals. We measured levels of lymphocyte adenosine triphosphate (ATP) and continuous [3H]thymidine incorporation in phytohemagglutinin-stimulated lymphocytes from young and old humans, and the effects thereon of inhibitors of mitochondrial oxidative phosphorylation and protein synthesis. No difference was found in adenine nucleotide content between young and old subjects. After 24 hours of culture there was a decrease in ATP, with recovery and 2--3-fold increase at 48 hours in young cells after phytohemagglutinin stimulation. We observed a clearcut delay in older lymphocytes of the increase in ATP and [3H]thymidine incorporation following phytohemagglutinin stimulation. We found no evidence for decreased viability or diminished number of responding units in aged cultures. The evidence suggests that mitochondrial dysfunction may play a role in the immunodeficiency of aging.

Adenine Nucleotides↗
PubMed2006

Immune suppression prevents renal damage and dysfunction and reduces arterial pressure in salt-sensitive hypertension.

The goal of this study was to test the hypothesis that renal infiltration of immune cells in Dahl S rats on increased dietary sodium intake contributes to the progression of renal damage, decreases in renal hemodynamics, and development of hypertension. We specifically studied whether anti-immune therapy, using mycophenolate mofetil (MMF), could help prevent increases in renal NF-kappaB activation, renal infiltration of monocytes/macrophages, renal damage, decreases in glomerular filtration rate (GFR) and renal plasma flow, and increases in arterial pressure. Seventy-four 7-to 8-wk-old Dahl S, Rapp strain rats were maintained on an 8% Na, 8% Na + MMF (20 mg.kg(-1).day(-1)), 0.3% Na, or 0.3% Na + MMF diet for 5 wk. Arterial and venous catheters were implanted at day 21. By day 35, renal NF-kappaB in 8% Na rats was 47% higher than in 0.3% Na rats and renal NF-kappaB was 41% lower in 8% Na + MMF rats compared with the 8% Na group. MMF treatment significantly decreased renal monocyte/macrophage infiltration and renal damage and increased GFR and renal plasma flow. In high-NA Dahl S rats mean arterial pressure increased to 182 +/- 5 mmHg, and MMF reduced this arterial pressure to 124 +/- 3 mmHg. In summary, in Dahl S rats on high sodium intake, treatment with MMF decreases renal NF-kappaB and renal monocyte/macrophage infiltration and improves renal function, lessens renal injury, and decreases arterial pressure. This suggests that renal infiltration of immune cells is associated with increased arterial pressure and renal damage and decreasing GFR and renal plasma flow in Dahl salt-sensitive hypertension.

Animals↗
PubMedDate not supplied

[Development of of non-immunising, paraspecific vaccine from attenuated pox viruses: a new type of vaccine].

The various research periods leading to the development of paraspecific vaccines are described. Paraspecific vaccines are new, pyrogen-free, non-toxic preparations that contain non-immunising antigens and can be used to generate endogenic protective, non-antigen specific mechanisms in the sense of paramunization in humans and animals. They consist of highly attenuated and inactivated (0.05% beta-propiolactone) virus strains of various poxvirus genera. They activate the T helper cells and cellular elements of the paraspecific (innate) immune system and initiate the associated production and release of cytokines (cytokine cascade) with the goal of eliminating dysfunctions of the immune systems, rapidly enhancing the individual's non-pathogen- and non-antigen-specific defences and exerting a regulatory effect on the interplay between the immune, hormone, nervous and vascular systems (signal-transduction mediators). They can be used systemically (intramuscularly) and locally (mucous membranes, skin). Immunization with paraspecific vaccines does not lead to postvaccinal complications and can be carried out as often as necessary, even for a number of years. They are compatible with conventional medicines and conventional specific vaccines. Closely linked protein complexes in the envelopes of the virus particles are responsible for their efficacy some of those envelope protein complexes possess the properties of weak super antigens. Paraspecific vaccines have proved effective in combating viral infections, in particular herpes and hepatitis B and C infections, and chronic inflammatory diseases, and also as adjuvant therapy for tumours, for curing stress-related disturbances and dysfunctions of the immune system.

Animals↗
PubMed2003

Development of a non-immunising, paraspecific vaccine from attenuated pox viruses: a new type of vaccine.

The various research periods leading to the development of paraspecific vaccines are described. Paraspecific vaccines are new, pyrogen-free, non-toxic preparations that contain non-immunising antigens and can be used to generate endogenic protective, non-antigen specific mechanisms in the sense of paramunization in humans and animals. They consist of highly attenuated and inactivated (0.05% Betapropiolactone) virus strains of various poxvirus genera. They activate the T helper cells and cellular elements of the paraspecific (innate) immune system and initiate the associated production and release of cytokines (cytokine cascade) with the goal of eliminating dysfunctions of the immune systems, rapidly enhancing the individual's non-pathogen- and non-antigen-specific defences and exerting a regulatory effect on the interplay between the immune, hormone, nervous and vascular systems (signal-transduction mediators). They can be used systemically (intramuscularly) and locally (mucous membranes, skin). Immunization with paraspecific vaccines does not lead to postvaccinal complications and can be carried out as often as necessary, even for a number of years. They are compatible with conventional medicines and conventional specific vaccines. Closely linked protein complexes in the envelopes of the virus particles are responsible for their efficacy, some of those envelope protein complexes possess the properties of weak super antigens. Paraspecific vaccines have proved effective in combating viral infections, in particular herpes and hepatitis B and C infections, and chronic inflammatory diseases, and also as adjuvant therapy for tumours, for curing stress-related disturbances and dysfunctions of the immune system.

Animals↗