[Specific immune biological dysfunction as a pathological factor in idiosyncratic allergy].
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Humans↗
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Results for “immune dysfunction”
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A twin and family study of the association between immune system dysfunction and dyslexia using blood serum immunoassay and survey data.
We conducted a study of the association between developmental reading disability (DRD) and immune disorders (ID) using both survey and immunoassay data in two separate samples of families. One sample was made up of twins and their parents and was ascertained through a population-based sampling scheme. The other sample was a set of extended pedigrees selected for apparent autosomal dominant transmission of DRD. We failed to find an association between DRD and ID in either sample, regardless of the method used to assess immune system function. Even though our twin sample provided evidence that both DRD and immune conditions were significantly heritable, there was no evidence for a genetic correlation between ID and DRD nor was there any clear indication that a special subgroup of individuals may be comorbid for these conditions because of genetic reasons. How these negative findings can be reconciled with the developmental hypothesis of Geschwind, Behan, Galaburda, and colleagues, and how they may relate to the gene locus influencing DRD that has been recently located in the HLA region of the short arm of chromosome 6 is discussed.
Adolescent↗
Environmental chemical-induced modification of cell-mediated immune responses.
It is therefore proposed that: 1) environmental chemicals can have specific mechanisms of toxicity and can influence antibody-mediated immunity while having no detectable effect on cell-mediated immunity, 2) immune dysfunction is related to exposure time to a chemical and the tissue concentration of that chemical, 3) recovery of immune function may occur even though chemical exposure continues, and 4) a single assay of immune function may not be appropriate to detect chemical induced immune dysfunction.
Animals↗
IL-10 mediation of activation-induced TH1 cell apoptosis and lymphoid dysfunction in polymicrobial sepsis.
Recent studies suggest that increased activation-induced lymphocyte apoptosis (AICD) is detected in mouse splenocytes during polymicrobial sepsis which may contribute to lymphocyte immune dysfunction [i.e., decreased interleukin (IL-)2 and interferon-gamma (IFN-gamma) production] leading to the associated morbidity seen in those animals. Thus, we wanted to examine the hypothesis that immune suppressive agents, such as IL-4, IL-10 or prostaglandin E2(PGE2), known to be elevated in septic animals, also contribute to this increase in AICD. Here we demonstrate that the inclusion of monoclonal antibody (mAb) to IL-10, but not anti-IL-4 or ibuprofen (IBU), blunted this sepsis induced increase in splenocyte AICD. Additionally, septic mice deficient in the IL-10 gene product (-/-) showed neither an increase in AICD nor a loss of IL-2/IFN-gamma release capacity. Interestingly, mAb to IL-10 did not altered the extent of AICD in a Th2-cell line, but exogenous IL-10 did potentiate Th1-like cell line AICD. This was consistent with the finding that the increased AICD seen in septic mouse splenocytes was restricted largely to the CD4+ cells producing IL-2 (Th1-cells) and that mAb to IL-10 treatment suppressed this change. Furthermore, IL-10 appears to mediate its AICD effect by upregulation of the Fas receptor and Fas receptor signaling protein components, but not by altered expression of Bcl/Bax/Bad family members, in septic mouse splenocytes. To the extent that these processes contribute in a pathological fashion to the animal's capacity to survive sepsis we have previously observed that in vivo post-treatment of mice with mAb IL-10 markedly attenuated septic mortality. Collectively, these data indicate that in the septic mouse the Th2 cytokine IL-10 not only serves to actively induce Th1 lymphocyte immune dysfunction but also plays a role in their apoptotic depletion. These processes in turn appear to contribute to the animal's inability to ward off lethal septic challenge.
Animals↗
Two novel mutations in exon 11 of the PAH gene (V1163del TG and P362T) associated with classic phenylketonuira and mild phenylketonuria. Mutations in brief no. 143. Online.
PKU is one of the commonest genetic disease in man, affecting 1/10,000 individuals. It presents a wide phenotypical spectrum, from classic PKU to moderate Hyperpheylalaninemia depending on the residual enzymatic activity. Two novel mutations 1163/1164delTG and P362T in exon 11 have been detected during the mutational screening of the PAH gene in 84 families. 1163/1164delTC can be confused with V388M if the mutational screening is performed with BsaAI restriction enzyme, this mutation in heterozigosis presents a moderate phenotype. P362T mutation in heterozigosis with V388M shows a classical PKU phenotype. We report here two new mutations in exon 11 of the PAH gene (GenBank U49897), V1163delTG and P362T (using cDNA sequence), detected during the analysis of 57 PKU and 36 HPA patients belonging to 84 unrelated families detected under a neonatal screening program performed in Catalonia.
DNA Mutational Analysis↗
[The lymphadenopathy syndrome. Immunologic studies of young homosexual men with and without lymphadenopathy].
Investigations on 147 young homosexual men living in Berlin (West) revealed lymphadenopathy in 61.2% (90 pat.). This finding was prominent in 43.4% of all cases. Evaluation of total T-, T-helper und T-suppressor lymphocytes by means of immunofluorescence with monoclonal antibodies showed an unchanged total number of T-lymphocytes; in contrast, the T-helper subpopulation was decreased and the T-suppressor subpopulation was increased in the peripheral blood, in comparison to a control group of heterosexual men. Therefore, a significantly reduced Th/Ts-ratio was supposed. These changes were more pronounced in the group with marked lymphadenopathy. Our investigations prove a high prevalence of lymphadenopathy and immune dysfunction among young homosexual men in Germany. Both are correlates of one syndrome characterized by persisting unexplained lymphadenopathy, immune dysfunction, and general clinical symptoms (including loss of weight, fever, diarrhoea, etc.). This so called lymphadenopathy syndrome (LAS) with the above mentioned clinical symptoms and reduction of the Th/Ts-ratio may represent a prodrome of AIDS. A long-term and careful follow-up of these patients is therefore necessary.
Adolescent↗
Assessment of the diabetogenic drugs alloxan and streptozotocin as models for the study of immune defects in diabetic mice.
The efficacy of the diabetogenic drugs streptozotocin and alloxan were evaluated as models for the study of immune defects associated with diabetes. Streptozotocin- or alloxan-treated mice, with a stable hyperglycaemia of 25-33 mmol/l plasma glucose, were severely impaired in their ability to mount antibody forming, mitogenic, or delayed-type hypersensitivity responses in vivo. Treatment of alloxan-diabetic mice with insulin in vivo completely reversed all immune defects, while insulin treatment of streptozotocin-diabetic mice restored immune function to only 70-80% of normal levels. Results obtained by viability measurements and in vitro biological assays of lymphoid function, including proliferation in response to T- and B-cell mitogens, the production of interleukin-2 by T cells, and the production of interleukin-1 by macrophages indicated that direct exposure to alloxan for 48 h (at concentrations less than or equal to 14 mmol/l) had no adverse effects on lymphoid activity, while exposure to streptozotocin was routinely toxic at concentrations greater than or equal to 1 mmol/l. Both alloxan and streptozotocin exhibited strong toxicity in vitro for isolated pancreatic islet cells. Finally, lymphocytes from streptozotocin-diabetic mice, or cells incubated in vitro with streptozotocin, contained numerous chromosomal abnormalities indicative of DNA strand breakage. Such abnormalities were absent in alloxan-diabetic mice and in cells incubated with alloxan in vitro. These results indicate that immune dysfunction associated with streptozotocin is attributable to direct and irreversible impairment of lymphoid cell function and viability. In contrast, immune dysfunction associated with alloxan-diabetes appears to be a consequence of the diabetic state.(ABSTRACT TRUNCATED AT 250 WORDS)
Alloxan↗
Locoregional immunotherapy in cancer patients: review of clinical studies.
Many patients with invasive cancer have a compromised immune system. This immune dysfunction does appear to start at the site of the tumor. Locoregional immunotherapy is given to stimulate the immune system in order to kill tumor cells either indirectly via a specific or a non-specific way or directly via cell transfer therapy. Advantages to give this immunotherapy locoregionally in stead of systemically are a higher concentration of the immunomodulator at the site of the tumor, to attract or activate effector cells, and diminished toxicity. In this review we have summarised the clinical studies using loco-regional immunotherapy in patients with cancer. Only phase I and II studies were performed. Clinical responses were seen. No single locoregional treatment has become a standard therapy. Relatively few investigations were performed to estimate the influence on the locally effector mechanisms or immune dysfunction. In future clinical trials it is essential to get a better insight in these mechanisms.
Adoptive Transfer↗
Delayed autograft loss in HIV-positive patients: two cases.
Two cases that show delayed autograft loss secondary to late polymicrobial infection in patients whose test results are positive for the human immunodeficiency virus (HIV-positive patients) are presented. Mechanisms of immune dysfunction in HIV-positive patients are reviewed, and speculation on the possible contribution of polymorphonuclear or other immune dysfunction to the graft failure in these patients is presented. Questions are raised regarding the prognostic importance of HIV positivity in patients with burns and the need for special surgical considerations in these patients. The issue of transmissibility of HIV in the burn unit setting is addressed, and infection control is discussed.
Adult↗
Immunomodulating properties of MDMA alone and in combination with alcohol: a pilot study.
Cell-mediated immune response after the administration of MDMA alone and in combination with alcohol was evaluated in a randomized, double-blind, double-dummy, cross-over pilot clinical trial conducted in four healthy MDMA consumers who received single oral doses of 75 mg MDMA (n = 2) or 100 mg MDMA (n = 2), alcohol (0.8 mg/kg), MDMA and alcohol, or placebo. Acute MDMA treatment produced a time-dependent immune dysfunction associated with MDMA plasma concentrations. Although total leukocyte count remained unchanged, there was a decrease in the CD4 T/CD8 T-cell ratio as well as in the percentage of mature T lymphocytes, probably because of a decrease in both the percentage and absolute number of T helper cells. The decrease in CD4 T-cell counts and in the functional responsiveness of lymphocytes to mitogenic stimulation was dose-dependent. The correlation between MDMA pharmacokinetics and the profile of MDMA-induced immune dysfunction suggests that alteration of the immune system may be mediated by the central nervous system. Alcohol consumption produced a decrease in T helper cells, B lymphocytes, and PHA-induced lymphocyte proliferation. Combined MDMA and alcohol produced the greatest suppressive effect on CD4 T-cell count and PHA-stimulated lymphoproliferation. Immune function was partially restored at 24 hours. These results provide the first evidence that recreational use of MDMA alone or in combination with alcohol alters the immunological status.
Adjuvants, Immunologic↗
[Cellular immunology tests applied to the diagnosis of immune system dysfunctions].
In clinical immunology, improved standardisation and simplification have made skin and laboratory tests more amenable both to routine use and more rigorous interpretation. An individual's immune status can be assessed by the in vivo investigation of delayed hypersensitivity to widely distributed antigens or by techniques such as the mitogen test ot lymphoblast transformation, lymphocyte population and sub-population (e.g. T4, T8...) counts. A more delicate test of phagocytosis is provided by the chemoluminescence test. Investigation of allergic states (immediate hypersensitivity) relies on skin tests and also on laboratory techniques such as the basophil degranulation test.
Blood Bactericidal Activity↗
The Th2-restricted immune response to xenogeneic small intestinal submucosa does not influence systemic protective immunity to viral and bacterial pathogens.
Implantation of mice with xenogeneic extracellular matrix (ECM) not only results in tissue remodeling but also elicits a strong Th2 immune response. It is possible that the Th2 cytokines induced by ECM act systemically and result in immune suppression to unrelated antigens. In this case, the recipient would be predisposed to immune dysfunction and have increased susceptibility to various pathogens. The purpose of this study was to determine if ECM implantation does, in fact, influence the immune response to other antigens. Four models were examined to determine the effects of ECM implantation on systemic immunity. In the first model, mice were subcutaneously implanted with porcine small intestinal submucosa (SIS) and immunized with a T-dependent subunit vaccine against influenza virus. The antibody response and protection against lethal infection were then measured. The second model consisted of similar experiments performed using a T-independent polysaccharide vaccine against S. pneumoniae. In the third model, mice were implanted and the cell-mediated response to dinitrofluorobenzene (DNFB) challenge was determined. The fourth model involved examining the influence of SIS implantation on rejection of xenogeneic skin grafts. We found that antibody levels of mice vaccinated against influenza virus or S. pneumoniae were not affected by SIS implantation and these mice did not exhibit increased or decreased susceptibility to either infectious agent. Similarly, mice implanted with ECM showed no cell-mediated immune dysfunction upon challenge with DNFB or xenogeneic skin grafts. The results of this study demonstrate that the Th2-restricted response induced by xenogeneic ECM implantation does not cause generalized immune suppression. Therefore, SIS implantation does not increase susceptibility to viral or bacterial pathogenic agents.
Animals↗
Principles of immunology.
The immune system, composed of innate and acquired immunity, allows an organism to fight off foreign pathogens. Healthy immunity accomplishes four essential principles: (1) ability to detect and fight off infection; (2) ability to recognize a host's own cells as "self," thereby protecting them from attack; (3) a memory from previous foreign infections; and (4) ability to limit the response after the pathogen has been removed. In an unaltered state, the intricate network of immunologic organs and cells creates an environment for proper host defense. Without adequate execution of immunologic mechanisms, a host is rendered defenseless against pathogens. Conversely, an unchecked immune response can be self-destructive. As a result of either of these untoward sequelae, immune dysfunction can elicit disease states in the host. The goal of this review is to elucidate the characteristics of a healthy immune system, focusing on the principles of immunity and the cells that participate in host protection. We also briefly discuss the clinical ramifications of immune dysfunction.
Journal Article↗
Gender affects macrophage cytokine and prostaglandin E2 production and PGE2 receptor expression after trauma.
BACKGROUND: Gender influences morbidity and mortality after injury. Hormonal differences are important; however, the role of prostaglandins as mediators in immune dysfunction relating to gender differences after trauma is unclear. We hypothesized that gender-dependent differences in PGE(2) receptor expression and signaling may be involved in immune-related differences. This study determined prostaglandin receptor subtype (EP1-EP4) expression following injury and determined whether gender differences influence EP receptor expression. MATERIALS AND METHODS: BALB/c male and female mice (estrus and pro-estrus) (n = 6 per group) were subjected to femur fracture and 40% hemorrhage (trauma) or sham injury (anesthesia). Seven days later, the splenic macrophages were harvested and stimulated with lipopolysaccharide (Escherichia coli serotype O55:B5). After 6 h mRNA samples were collected for EP receptor mRNA expression and at 24 h supernatants were collected for PGE(2), TNF-alpha, and IL-6 production. RESULTS: The expression of EP2-4 receptors was higher in female pro-estrus mice compared with male mice. EP1 receptor expression was higher in males than pro-estrus females. There was decreased expression of all four receptors after trauma in female estrus compared with control estrus mice. Macrophage PGE(2), TNF-alpha, and IL-6 production was significantly increased in injured female mice compared with female controls but there were no differences in injured male mice compared with male controls. PGE(2) and TNF-alpha production by traumatized male mice were significantly less than that produced by traumatized pro-estrus females. CONCLUSIONS: These data suggest gender-related differences in response to traumatic injury and that alterations in specific EP receptor subtypes may be involved in immune dysfunction after injury. Studies to evaluate targeted modulation of these receptor subtypes may provide further insights to gender-specific differences in the immune response after injury.
Animals↗
Are regulatory T-cells linked with aging?
There is increasing evidence for an active and 'dominant' tolerance mediated by regulatory T-cells. Out of these CD4+ 'naturally occurring' regulatory T-cells (TREGs) are currently the main research focus in this field. TREGs exert their suppressive function in vitro in a contact-dependent manner and preferentially express high levels of CD25 and the forkhead and winged-helix family transcription factor forkhead box P3 (FOXP3). Age-related increment of the prevalences of CD4+ CD25(hi) TREGs were described controversially, and whether such changes explain immune dysfunction in the elderly is still unclear. During aging thymic TREG output may decrease with significant loss of thymic capacity to generate new T-cells, and TREG homeostasis has been shown to be sustained by alternative pathways like peripheral generation of TREGs. An imbalance of TREG homeostasis would then predispose to immune dysfunction in aged individuals explaining their higher risk of immune-mediated diseases, cancer or infections.
Aging↗
Dietary nucleotides prevent decrease in cellular immunity in ground-based microgravity analog.
Microgravity and stress of spaceflights result in immune dysfunction. The role of nutrition, especially nucleotide supplementation, has become an area of intensive research and significant interest in immunomodulation for maintenance of cellular immune responses. The studies presented here evaluate the plausibility of administering nucleotides to obviate immune dysfunction in an Earth-based in vivo analog of microgravity as studied in anti-orthostatic tail suspension (AOS) of mice. Mice were divided into three housing groups: group, isolation, and AOS. Mice were fed either control chow diet (CD), or RNA-, adenine-, or uracil-supplemented CD for the 1-wk duration of the experiments. In AOS mice, supplemental nucleotides significantly increased in vivo lymph node proliferation and ex vivo lymphoproliferation response to alloantigen and mitogens, respectively, and interleukin-2 and interferon-gamma production. A lower corticosterone level was observed in uracil-supplemented CD compared with CD. These results suggest that exogenous nucleotide supplementation, especially uracil, of normal diet is beneficial in the maintenance and restoration of the immune response during the microgravity analog conditions.
Animals↗
[Anomalies of cellular immunity in Graves' disease treated by synthetic antithyroid drugs: effects on prognosis].
The involvement of humoral immunity mechanism in etiology of Graves' disease was observed for the first time in 1956. Twenty years later cellular auto-immune dysfunction was also described. To day, there is evidence for suppressor T cell deficiency and decrease in T suppressor lymphocytes in Graves' disease and cell mediated immunity might be one of the most important point in the pathogenesis of Graves disease. For the future, cellular auto-immune dysfunction might be used to predict the evolution of the disease and to choice the best therapeutic scheme.
Antithyroid Agents↗
Serological response in patients with chronic asymptomatic human immunodeficiency virus infection.
To examine a possible relationship between decreased immune function and serological parameters, such as human immunodeficiency virus (HIV) antigenaemia and the quality and quantity of whole virus antibodies and antibodies against the major core protein p24, we investigated 160 healthy HIV infected individuals (CDC classification II and III). According to the number of T-helper lymphocytes (CD4 cells) these were divided into two groups (CD4 cell counts above or below 500/microliter), which according to the lymphocyte transformation response to pokeweed mitogen (response above or below 20% of control value) were further subdivided into two groups. Both the presence of HIV antigen (p = 0.022) and the absence of p24 antibodies (p = 0.001) correlated to a decreased CD4 cell count. Lack of p24 antibodies was more frequent than was the presence of HIV antigen among persons with decreased CD4 cell count and decreased response to pokeweed mitogen, indicating that absence of p24 antibodies may be an earlier marker of immune dysfunction than the presence of HIV antigen. In persons with p24 antibodies present, a low such titer was associated with a decrease of both immune parameters. Presence of HIV antigen and absence of p24 antibodies thus seems to correlate with the severity of immune dysfunction in healthy HIV infected individuals.
Acquired Immunodeficiency Syndrome↗