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At least 307 records · Page 17Linked to original sources
PubMed1984

[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↗
PubMed1985

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↗
PubMed2000

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↗
PubMedDate not supplied

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↗
PubMed1999

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↗
PubMed1984

[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↗
PubMed2002

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↗
PubMed2002

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↗
PubMed1987

[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↗
PubMed1988

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↗
PubMed1985

Immune system dysfunction contributes to the aetiology of spontaneous hypertension.

Spontaneously hypertensive rats (SHRs) have a depressed T lymphocyte system, especially a reduced activity of the suppressor T cells, and it has been postulated that an auto-immune defect may be important in the aetiology of hypertension in these rats. In an earlier study we demonstrated that chronic immunosuppressive therapy prevents approximately 50% of the hypertension in the SHR. In the present study, an attempt was made to correct the immune imbalance by implanting thymic tissue from normotensive rats into SHRs. Weekly thymic implants from Wistar donor rats into 16-week-old SHRs produced a maximal reduction (P less than 0.05) in the tail-cuff pressure, after 4 weeks, to a level of 156 +/- 2.3 mmHg (n = 8) in thymus-implanted SHRs versus 189 +/- 2.5 mmHg (n = 6) in sham-implanted SHRs. Also, neonatal thymic implants delayed development of spontaneous hypertension and attenuated the final hypertensive state. Mean arterial pressure averaged 186 +/- 2.8 mmHg in 22-week-old, neonatally sham-implanted SHRs, while it was reduced (P less than 0.05) to 164 +/- 4.2 mmHg in the neonatally thymus-implanted SHRs at this time. The thymic implants had little effect on total T cell, helper T cell or suppressor T cell counts. However, the antihypertensive effect of the thymic implants was associated with a substantial increase in the blastogenic responsiveness of suppressor T cells from the SHRs. These results support the hypothesis that immunological dysfunction plays an important role in the aetiology of spontaneous hypertension.

Animals↗
PubMed2002

A possible relationship between bumblefoot responsive to potassium arsenite and micrococci in the blood of three birds of prey.

Pododermatitis (bumblefoot) is a major health problem of falcons world-wide because healing processes in the talons are difficult and lengthy. A peregrine (Falco peregrinus), a merlin (Falco columbarius) and a saker falcon (Falco cherrug) with bumblefoot at different stages ranging from III to V, were all found to be carriers of micrococcus-like organisms in the blood and two of them were successfully treated with 0.5% potassium arsenite in low dosage given intravenously. A number of considerations are made on the immune dysfunction aspects of bumblefoot in birds of prey and on the emerging role of arsenic-based medicaments in the treatment of animal and human immune dysfunction syndromes.

Animals↗
PubMed1992

Spontaneously hypertensive rat: lymphoid depression is age dependent and mediated via a mononuclear cell subpopulation.

Immune dysfunction has been reported in spontaneously hypertensive rats (SHR), particularly in mature animals with established hypertension. The current study examined the time course of development of immune dysfunction and defined its cellular basis in male SHR and control normotensive Wistar-Kyoto rats (WKY). Mitogen-induced proliferative responses in lymphoid cells obtained from induced proliferative responses in lymphoid cells obtained from SHR thymus and spleen before (age 4 wk) and during the development of (ages 8 and 12 wk) hypertension and in age-matched normotensive WKY were monitored. A 50% reduction in concanavalin A (Con A)-induced proliferative responses was seen in SHR thymocytes compared with those of WKY at 12 wk only, suggesting differences in immature T-cell populations. Con A-induced T-cell proliferative responses in splenocytes also differed between strains: greatest (as much as 8-fold) decreases were found in 12-wk-old SHR. Similar findings were obtained in splenocytes stimulated with lipopolysaccharide (LPS), indicating differences in B-cell function. Mononuclear cells depleted of their adherent cell population were prepared from SHR and WKY at 12+ wk of age and assayed for their proliferative responses to LPS and Con A. The remaining nonadherent mononuclear cells of SHR had proliferative responses equal to or greater than those of WKY. Further, when SHR splenic mononuclear cells were allowed to adhere to plastic, and the adherent fraction was co-cultured with either SHR G-10 nonadherent or unfractionated SHR splenic mononuclear cells, proliferative responses were suppressed by as much as 88%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed2001

Serum leptin levels are higher but are not independently associated with severity or mortality in the multiple organ dysfunction/systemic inflammatory response syndrome: a matched case control and a longitudinal study.

OBJECTIVE: Hypercatabolism and immune dysfunction are closely associated with the development of systemic inflammatory response--multiple organ dysfunction (SIRS/MODS) in critical illness. It remains unclear however, whether leptin, an adipocyte-derived hormone whose levels are influenced by several cytokines and which regulates immune function, food-intake and energy expenditure is independently related to the development of and/or severity and mortality from SIRS/MODS. DESIGN AND PATIENTS: To assess the role of leptin in SIRS/MODS we performed a matched case control and a longitudinal study (14 days) in 35 critically ill patients with SIRS/MODS and 35 matched controls. RESULTS: Baseline leptin levels were positively associated with body mass index (BMI) and TNF-alpha (P < 0.01) in patients and with IGF-1 and IL-6 levels (P < 0.05) in controls. Furthermore, leptin levels exhibited a progressive increase from the first to the last day of the study and although baseline levels were not different, peak leptin levels as well as leptin levels on the last day of the study were significantly higher in cases than in controls (P < 0.05). TNF-alpha levels, IL-6 and cortisol levels were also higher, whereas IGF-1 levels were lower in cases (P < 0.05). To assess whether leptin levels are independently associated with SIRS/MODS we performed multivariate logistic regression analysis which revealed that leptin up-regulation in cases is mediated by elevated TNF-alpha and cortisol levels. Finally, there was no independent association between leptin and survival in this group of critically ill patients. CONCLUSION: We conclude that cytokines and cortisol upregulate leptin levels, which may contribute to the development of the hypercatabolism, wasting and immune dysfunction but leptin levels are not independently associated with severity or mortality of patients with systemic inflammatory response-multiple organ dysfunction.

Adult↗
PubMed1994

Imbalance between oxidants and antioxidants in the lungs of HIV-seropositive individuals.

Following the initial infection with HIV, there is evidence of immune dysfunction despite an apparent normal clinical state. In the context that the lung is a major site affected by opportunistic infection, and that some components of the immune system are activated during early HIV infection, we hypothesized that there may be activation of alveolar macrophages (AM), a key component of the pulmonary host defense system. Compared to cells from normal individuals, AM of asymptomatic HIV-seropositive (HIV+) individuals (CDC-stage II) spontaneously released significantly more superoxide anion (O2-.) (P < 0.002). The O2-. release by AM of HIV-infected individuals was comparable to the spontaneous O2-.-release by AM of cigarette smokers (P > 0.6), a condition often associated with chronic damage of respiratory tissues. The destructive effects of oxidants are normally suppressed by antioxidant defense systems. Evaluation of the concentrations of glutathione, a major component of the pulmonary antioxidant protective screen, demonstrated that the HIV+ state is also characterized by a significant glutathione deficiency in lung epithelial lining fluid (P < 0.001) and in venous plasma (P < 0.001). This suggests that the alveolar structures of HIV+ individuals are continuously exposed to increased amounts of toxic oxygen radicals without adequate protection, i.e. the reactive oxygen metabolites may cause sufficient tissue damage culminating in interstitial lung disease. Further, since many immune functions are susceptible to injury by extracellular oxidants, the consequences of an unsuppressed oxidant burden in the lung may amplify the extent of local immunocompromise. In addition, since glutathione plays an important role in modulating lymphocyte activation and effector functions independent of its antioxidant activity, the systemic glutathione deficiency may contribute to the progressive global immune dysfunction that characterizes HIV infection.

Adult↗
PubMed1995

Evidence for a shift from a type I lymphocyte pattern with HIV disease progression. Hemophilia Growth and Development Study.

Whether a shift from a type I (cell mediated) immune profile occurs with progressive HIV-related immune dysfunction is a matter of heated debate. We analyzed data for 333 HIV antibody-positive (HIV+) and -negative (HIV-) hemophilic children/adolescents, to examine whether the relationships among immunologic parameters and vaccine-related serology supported a shift with advancing HIV infection. In stepwise logistic regression analysis of HIV+ children's data, anergy to a panel of delayed hypersensitivity skin test antigens was positively associated with serum immunoglobulin A (IgA) levels (p = 0.012) and CD8+ cell counts (p = 0.021) and negatively associated with CD4+ cell counts (p = 0.002). Modeling supported anergy as a positive correlate of log IgA level (p = 0.046) and CD4+ lymphocyte count as a negative correlate, for HIV+ participants only (p < 0.0001). For mumps, the proportion of vaccinated HIV+ participants with protective IgG antibody titers was higher among those with CD4+ lymphocyte counts < 200 cells/mm3 (p = 0.058). For HIV+ participants < 14 years of age, this same trend was seen for measles and rubella, but was not seen in any age group for bacterial vaccine antigens. The intercorrelations among skin test anergy, CD4+ lymphocyte counts, serum IgA levels, and viral vaccine antigen-related serologic titers for HIV+ participants are consistent with an association between progressive HIV-related immune dysfunction and a predominance of type II (humoral immunity) or Type 0 (mixed immunity), relative to type I, lymphocyte profiles.

Adolescent↗
PubMed1986

Association between anorectal dysplasia, human papillomavirus, and human immunodeficiency virus infection in homosexual men.

Cells from the anorectal mucosa of 61 homosexual men were examined microscopically for evidence of papillomavirus infection and dysplastic changes. There was cytological evidence of dysplasia with concomitant features of human papillomavirus (HPV) infection on at least one occasion in 24 men and of papillomavirus infection without dysplasia on at least one occasion in a further 26: dysplasia was present for over one year in 9 of 14 men who were re-examined. Dysplasia was associated with a history of anal warts, frequent receptive anal intercourse, presence of serum antibody to human immunodeficiency virus (HIV), and immune dysfunction as judged by a low CD4/CD8 ratio, but not with the lifetime number of sexual partners. The association of longlasting dysplasia with anti-HIV was independent of the association with immune dysfunction. Thus infection of anorectal mucosal cells with papillomavirus seems to be frequent among homosexual men and may predispose to dysplasia.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Kawasaki disease: a maturational defect in immune responsiveness.

Kawasaki disease (KD), an acute febrile disease in children of unknown etiology, is characterized by a vasculitis that may result in coronary artery aneurysms (CAAs). In new patients with KD, a selective and prolonged T cell unresponsiveness to activation via the T cell antigen receptor CD3 was observed, whereas proliferation to other stimuli was intact. This "split T cell anergy" delineated KD from other pediatric infections and autoimmune diseases and correlated with CAA formation (P<.001). A transient immune dysfunction was also suggested by an incomplete responsiveness to measles-mumps-rubella (MMR) vaccination in patients with KD versus controls (P<.0001; odds ratio, 15.6; 95% confidence interval, 4.8-51.1), which was overcome by revaccination(s). The reduced responsiveness to MMR in patients with KD suggests a subtle and predetermining immune dysfunction. An inherent immaturity to clear certain antigens may be an important cause that precipitates KD and the immune dysregulation during acute disease.

Antibodies, Viral↗