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PubMed1997

Variable expression of WASP in B cell lines of Wiskott-Aldrich syndrome patients.

The Wiskott-Aldrich syndrome (WAS) arises from defects of the X-chromosome gene WASP. Severe platelet defects, thrombocytopenia with small platelets, are a hallmark of the disease, but clinical immunodeficiency based in lymphocyte dysfunction varies from negligible to life threatening among WAS patients. To address the connection between WASP mutations and clinical outcomes, we generated and characterized a panel of patient B cell lines. Three cell lines from patients with exon 2 missense mutations and mild immune dysfunction were found to express substantial levels of WASP mRNA and protein. On the other hand, 8 of 10 cell lines from patients with moderate or severe immune dysfunction lack detectable WASP protein. The findings suggest that the clinical variability of the WAS can partially be explained by the level of WASP protein in the patient's cells.

Adolescent↗
PubMedDate not supplied

Neuroimmunomodulation in cancer patients: correlations between melatonin and beta-endorphin blood levels and T helper/suppressor ratio.

The pineal gland and opioid peptides play roles in the neuroendocrine control of immunity. Both neuroendocrine and immune dysfunctions have been observed in cancer but the importance of the altered secretion of neurohormones in the immunoincompetence of cancer patients has never been investigated. This study concomitantly evaluated neuroendocrine and immune functions in 40 patients with early or advanced neoplastic disease. In each patient, melatonin and beta-endorphin blood levels and lymphocyte subtypes were determined on venous blood samples collected during the morning. Metastatic patients had lower melatonin levels and a lower T4/T8 ratio than patients without metastases but no significant correlation was found between melatonin and the T4/T8 ratio. beta-endorphin levels appeared to be normal in all patients. These results suggest that melatonin and beta-endorphin secretion have no role in determining immune dysfunctions in cancer.

Adult↗
PubMed1985

The Vancouver Lymphadenopathy-AIDS Study: 4. Effects of exposure factors, cofactors and HTLV-III seropositivity on number of helper T cells.

Results of testing for antibody to human T-lymphotropic virus (HTLV-III) and absolute numbers of helper T cells in 219 participants in the Vancouver Lymphadenopathy-AIDS (acquired immune deficiency syndrome) Study were analysed. The mean absolute helper T-cell counts in the 141 HTLV-III seronegative and the 78 seropositive men were 897/mL and 659/mL respectively (p less than 0.001). Established AIDS risk factors such as elevated lifetime number of male sexual partners and frequent receptive anal intercourse did not appear to have any significant effect on number of helper T cells that was independent of HTLV-III antibody status. Seropositive men with less than 100, 100 to 500 or more than 500 male sexual partners in their lifetime had mean absolute helper T-cell counts of 667/mL, 651/mL and 662/mL respectively. Most other risk factors, as well, did not appear to exert any effect on absolute number of helper T cells that was independent of the effect of HTLV-III antibody status. However, independent effects of a history of mononucleosis or hepatitis and of cigarette smoking were noted. The data support the hypothesis that no immune dysfunction beyond that due to the initial infection alone arises from repeated exposure to HTLV-III. Most risk factors appear to act as exposure factors, exerting their effect on the immune system merely by increasing the probability of contact with the agent. The independent effects of a history of mononucleosis or hepatitis suggest that viral agents may be cofactors in the production of immune dysfunction.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[Relations between the phagocytic activity of monocytes and the lateralization of brain injuries].

According to the authors' opinion, the different character of alterations in phagocytic activity of monocytes in primary derangement of the dominant and subdominant hemispheres results from the different functional significance of the hemispheres. The most pronounced neurogenous immune dysfunction occurs because of an injury to the dominant hemisphere. The two mechanisms of alterations in phagocytic activity of monocytes are of importance during the posttraumatic period in severe brain contusions: the central one related to neurogenous immune dysfunction and secondary one related to infectious complications.

Adolescent↗
PubMed2002

Cell-mediated immune response in MDMA users after repeated dose administration: studies in controlled versus noncontrolled settings.

Acute administration of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") produces time-dependent immune dysfunction in humans. Recreational use of MDMA generally includes repeated drug consumption, often in association with other drugs, such as alcohol and cannabis. In the laboratory setting, repeated MDMA administration to healthy MDMA consumers produced a time-dependent immune dysfunction similar to that observed with the ingestion of a single dose, and the first of the two administrations paralleled the time-course of MDMA-induced cortisol stimulation kinetics and MDMA plasma concentrations. A significant decrease in CD4 T-helper cells with simultaneous increase in natural killer (NK) cell and a decrease in functional responsiveness of lymphocytes to mitogenic stimulation was observed. Response to the second dose was either long-lasting compared with the first dose or disproportionate and did not show any parallelism with cortisol and MDMA plasma concentrations. This circumstance extended the critical period during which immunocompetence is highly impaired as a result of MDMA use. Accumulation of MDMA in the body of a poor metabolizer induced higher immunomodulatory effects with statistically significant differences in NK cell function compared with extensive metabolizers. When basal values of lymphocyte subsets were examined in a population of recreational MDMA users participating in different clinical trials, alterations in several immunological parameters were observed. The absolute number of lymphocytes, in particular T lymphocytes and CD4 T-helper cell subsets, showed a trend toward reduced values, although cell counts were within normal limits. By contrast, NK cells in MDMA consumers were reduced to one-third of those from healthy persons. A statistically significant decrease in affected immune parameters was recorded during a 2-year observation period in a subgroup of recreational MDMA users. These permanent alterations in immunologic homeostasis may result in impairment of general health and subsequent increased susceptibility to infection and immune-related disorders.

Amphetamine-Related Disorders↗
PubMed2000

Cocaine injection and coxsackievirus B3 infection increase heart disease during murine AIDS.

Coxsackievirus initiates myocarditis especially in the immunologically deficient or immature. To test whether Coxsackievirus B3 (CVB3) induced pronounced cardiomyopathy during severe immune dysfunction of murine AIDS, female C57BL/6 mice were infected with LP-BM5 retrovirus and superinfected with CVB3. Some were also injected daily with cocaine hydrochloride in 0.9% saline solution (30 mg/kg) intraperitoneally, because cocaine also suppresses cellular immune response. Heart tissue was analyzed histopathologically. Mice experiencing concurrent retrovirus and Coxsackievirus infection had a high degree of cardiac lesions consistent with myopathy compared with findings in uninfected animals (p <.05). Cocaine injection during murine retrovirus infection greatly exacerbated the pathogenesis of Coxsackievirus infection. C57BL/6 mice, essentially resistant to Coxsackievirus-induced cardiomyopathy, became susceptible during the immune dysfunction in murine AIDS. This suggests that retrovirus infection causes conditions favoring Coxsackie-induced cardiac lesions. Interleukin (IL)-2 and IL-4 expression by splenocytes from the dually infected retrovirus and Coxsackievirus group showed no significant differences when the animals were also cocaine treated. However tumor necrosis factor TNF-alpha production was significantly decreased in dually infected retrovirus + Coxsackievirus mice treated with cocaine, compared with findings in various controls (p <.05).

Animals↗
PubMed2000

Disseminated infection with Phialemonium obovatum in a German shepherd dog.

A 4-year-old spayed female German Shepherd Dog was evaluated because of left forelimb lameness. A fungal granuloma on the distal portion of the radius was determined to be the cause of the lameness; the infecting organism was identified as Phialemonium obovatum. Despite aggressive treatment with amphotericin B, itraconazole, and ketoconazole and curettage of the local area, the dog developed systemic disease and was euthanatized 5 months after initial evaluation. Immune dysfunction may have played a role in development of disseminated disease, because although serum concentrations of total IgG, IgA, and IgM were within or greater than reference ranges, results of lymphocyte proliferation assays were abnormal, which indicated cellular immune dysfunction. Infection with Phialemonium obovatum should be considered as a differential diagnosis when branching fungal organisms are detected during histologic, cytologic, or microbiologic evaluation of tissue specimens.

Animals↗
PubMed1999

Human leptin deficiency caused by a missense mutation: multiple endocrine defects, decreased sympathetic tone, and immune system dysfunction indicate new targets for leptin action, greater central than peripheral resistance to the effects of leptin, and spontaneous correction of leptin-mediated defects.

We have previously demonstrated that genetically based leptin deficiency due to a missense leptin gene mutation in a highly consanguineous extended Turkish pedigree is associated with morbid obesity and hypogonadism. We have now performed detailed assessments of endocrine, sympathetic, and immune function. We have also identified a new adult female homozygous patient in this extended family who is severely obese and amenorrheic. In this family all wild-type and heterozgous individuals have normal body weight. Seven obese members of this family, whom we presume to have been leptin deficient, died during childhood. There are several findings that indicate potentially novel targets for leptin action in humans. Four homozygous patients (1 adult male, 2 adult females, and 1 child) have sympathetic system dysfunction, whereas all heterozygous subjects have normal sympathetic system function. Despite sympathetic system dysfunction and postural hypotension, 1 of 3 homozygous adult patients has impaired renin-aldosterone function. The patients also exhibit alterations in GH and PTH-calcium function, and 1 of them has decreased bone mineral density. Despite their obesity, these patients do not have risk factors for cardiovascular disease, such as hypertension, impairments in lipid metabolism, or hyperleptinemia [corrected]. These data support the hypothesis that the obese may have central, but not peripheral, resistance to the effects of leptin and that hyperleptinemia [corrected] may mediate the cardiovascular morbidity of the obese who are not leptin deficient. Furthermore, these data indicate that there may be several new targets for leptin action in human physiology. Such new targets may lead to novel pharmacological strategies for the use of leptin agonists and antagonists in the treatment of human disease. All 19 normal weight individuals in this family are alive, whereas 7 of 11 obese individuals died in childhood after infections. The odds ratio for mortality in the context of this obesity phenotype is 25.4, indicating that this mutation severely impairs key biological functions during childhood, negatively impacting on survival. We found that only the obese child in this family had thyroid function abnormalities. The oldest homozygous female patient started to menstruate, albeit with a luteal phase defect, 7 months ago, after a delay of over 20 yr, whereas the younger adult subjects are still hypogonadic. Thus, we conclude that due to their long life span, humans who survive the negative effects of leptin deficiency during childhood can, in contrast to ob/ob mice, over decades compensate some of the effects of leptin deficiency on immunity and endocrine function through mechanisms that remain to be elucidated.

Adult↗
PubMed2002

Selenium supplementation decreases coxsackievirus heart disease during murine AIDS.

Coxsackievirus B3 (CVB3) induces myocarditis, especially in the immunodeficient or immature. To investigate whether CVB3 induced pronounced cardiomyopathy during the severe immune dysfunction of murine acquired immunodeficiency syndrome (AIDS), female C57BL/6 mice were infected with LP-BM5 retrovirus and then coinfected with CVB3. C57BL/6 mice, essentially resistant to CVB3-induced cardiomyopathy, became susceptible to this cardiomyopathy because of the immune dysfunction caused by murine AIDS. This susceptibility suggests that retrovirus infection causes conditions favoring the CVB3 induction of cardiac lesions. Mice were fed a diet supplemented with selenium (Se) at nine times the recommended daily dose for mice (0.933 mg/ kg of diet). Heart tissues were analyzed histopathologically 12 d after CVB3 challenge. Mice experiencing concurrent retrovirus and CVB3 infection had a high degree of cardiac lesions that were consistent with myopathy compared to that in uninfected mice (p < 0.05). Se supplementation during murine retrovirus infection significantly diminished the pathogenesis caused by concurrent CVB3 infection in mice that had murine AIDS. There was a significant increase in the survival of dually retrovirus and CVB3-infected mice that were fed Se, compared to that of identically treated mice that were not fed Se. Hepatic lipid peroxides were significantly diminished in the Se-supplemented mice as compared to those in immunodeficient mice without supplementation (p <F 0.1). Increased oxidation occurred in mice that had murine AIDS, which was also shown by reduced tissue vitamin E. Therefore, the reduction of retrovirally induced oxidation and inflammation by Se produced conditions that improved the survival of mice during CVB3 infection.

Animals↗
PubMed1989

[Study of the relation of the typology of nephrotic syndrome and red cell C3b receptor, T cell function].

This paper reports the determined results of rosette rates of red cell C3b receptor and active rosette (Ea) rates of T lymphocyte in 39 cases of nephrotic syndrome. Typology of nephrotic syndrome according to TCM differentiation symptoms, all the 39 cases were divided into three types: (1) 13 cases of deficiency of Qi of the Spleen with stagnancy of dampness; (2) 9 cases of deficiency of Yang of the Spleen and Kidney; (3) 17 cases of deficiency of Yin of the Liver and Kidney. The results showed that the red cell C3b receptor rosette rate and Ea rosette rate in 39 cases of nephrotic syndrome were significantly lower than those in the control. The difference between the two groups was very obvious (P less than 0.001) among the three types. The rosette rates of both in the deficiency of Qi of the Spleen and deficiency of Yang of the Spleen and Kidney were markedly decreased than those in the control (P less than 0.001). Whereas, the red cell C3b receptor rosette rate was lower than that in the control (P less than 0.01), and T cell Ea rosette rate showed no statistical difference (P greater than 0.05) in the deficiency of Yin of the Liver and Kidney. There was a close relationship between the immune dysfunction of red cell and the pathogenesis in nephrotic syndrome. There was markedly relationship between the pathogenesis of deficiency of Yang of the Spleen and Kidney and deficiency of Qi of Spleen with stagnancy of dampness and T cell immune dysfunction. While the Ea level in deficiency of Yin of the Liver and Kidney was closely correlated with the control. Probably this type was nephrotic nephrosis which had been treated with TCM-WM.

Adolescent↗
PubMed1984

Immunologic abnormalities and their significance in sinus histiocytosis with massive lymphadenopathy.

In a computerized case registry, containing 220 cases of sinus histiocytosis with massive lymphadenopathy (SHML), 23 patients were identified with clinical or routine laboratory findings suggestive or diagnostic of immune dysfunction. We divided the abnormalities into hematologic autoantibodies (nine patients), glomerulonephritis (three patients), Wiskott-Aldrich syndrome (two patients), joint disease (nine patients), unusual infections (three patients), and miscellaneous (six patients). Nine of the patients had more than one finding prompting inclusion in this study. In five patients, at least one abnormality preceded the onset of SHML. A major difference between this subgroup of 23 patients and the remaining registry population was the mortality rate. Ten of the 23 patients have died, and in many cases the cause of death could be linked to the immunologic abnormality. This study establishes an association between SHML and clinically significant immune dysfunction and provides further evidence that this frequently multisystemic disease may be one manifestation of disordered immunity.

Adolescent↗
PubMed2001

Apoptosis of leukocytes: basic concepts and implications in uremia.

Circulating blood leukocytes have short life expectancies and end their lives by committing programmed cell death or apoptosis. Apoptosis is an active form of cell death that is initiated by a number of stimuli and is intricately regulated. Apoptosis in both excessive and reduced amounts has pathological implications. Evidence suggests that apoptosis may play a role in the pathophysiology of immune dysfunction in uremia. Indeed, accelerated programmed cell death has been observed in lymphocytes, monocytes, and polymorphonuclear leukocytes among patients with chronic renal failure. This may be due in part to the retention of uremic toxins. The aim of this article is to review the evidence for accelerated leukocyte apoptosis, key regulatory apoptotic pathways, and the possible role of this highly organized process in the pathogenesis of immune dysfunction in uremia.

Apoptosis↗
PubMedDate not supplied

Is vitamin E supplementation a useful agent in AIDS therapy?

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a retrovirus infection, representing the end point in a progressive sequence of immunosuppressive changes. The literature is briefly summarized as to immunological, nutritional and other pathological modifications caused by AIDS, and properties of immunoenhancing, anti-oxidant and undernutrition-restoration of vitamin E supplementation. All these abnormalities in AIDS are similar to those that are stimulated or restored by intake of high doses of vitamin E. The drawbacks of pharmacological therapy like zidovudine (AZT), e.g. deleterious toxic side effects, inability to improve the immune dysfunctions and undernutrition initiated by the retrovirus infection, and finding of AZT-resistant HIV strains, necessitate new strategies for the clinical trials of novel therapies to treat AIDS with the existing medical therapies. Low toxicity nutritional agents with immunoenhancing and antioxidant activities like vitamin E may help to normalize retrovirus-induced immune dysfunctions, undernutrition and other pathological symptoms, thereby retarding the progression of the disease to AIDS. To address this vitamin E therapeutic role in HIV-positive individuals, This paper presents a review of vitamin E-related therapeutic roles in animals and humans, thereby showing why vitamin E supplementation could be used as a useful therapeutic agent in human AIDS therapy. Since there is a paucity of information available regarding the nutritional therapy in AIDS individuals, our purpose is to provide evidence from animal models or humans of the potential therapeutic role of vitamin E supplementation in the treatment of AIDS individuals.

Acquired Immunodeficiency Syndrome↗
PubMed2000

Immune depression in polymicrobial sepsis: the role of necrotic (injured) tissue and endotoxin.

OBJECTIVE: Recent studies suggest immune dysfunction seen after the onset of polymicrobial sepsis, as produced by cecal ligation and puncture (CLP), is not caused by endotoxin (ETX) alone, but may be caused by the combined effect of the necrotic tissue (cecal ligation, [CL]) and other microbial components. Thus, the objective of this study was to assess the ability of necrotic tissue, in the presence or absence of low-dose endotoxin, to induce changes in the capacity of immune cells to produce proinflammatory or anti-inflammatory cytokines approximating those seen in CLP. DESIGN: Experimental, prospective study. SETTING: A hospital laboratory in the Center for Surgical Research. SUBJECTS: Male C3H/HeN mice. INTERVENTIONS: Mice were subjected to a CL and saline infusion (CL/Sal), CL in combination with low-dose ETX infusion (CL/ETX) (0.025 mg ETX/25 g body weight/24 hrs by a peritoneally implanted osmotic mini-pump), ETX infusion alone, saline infusion alone (Sal), CLP, or sham-CLP (Sham). Splenocytes, splenic macrophage and peritoneal macrophage were harvested from these animals 24 hrs (late) after being subjected to the above protocols. Splenocyte and macrophage inducible cytokine release was assessed by ELISA/bioassay. Survival over a 7-day period was also examined in additional groups. MEASUREMENTS AND MAIN RESULTS: Our results indicate a marked decrease in splenic interleukin (IL)-2. In addition, peritoneal or splenic macrophage IL-6 productive capacity was depressed in cells from animals subjected to CL/ETX or CLP. Alternatively, CL, in the presence or absence of ETX, induced a marked change in macrophage cytokine release capacity comparable to that seen in CLP, ie, decreased IL-12 release and increased IL-10 secretion. To the extent these cellular alterations contribute to an increase in mortality rate, we observed in subsequent survival studies that neither CL alone nor ETX produced mortality. However, the combination of CL/ETX markedly increased 7-day mortality rate (approximately 33%), although not to the same extent as CLP (80%). CONCLUSIONS: These results collectively suggest that the response to devitalized tissue produced by cecal ligation may predispose the host to the induction of a suppressive macrophage phenotype. The subsequent exposure of these animals to microbial agents induces immune dysfunction, as well as mortality seen after such a polymicrobial septic challenge.

Animals↗
PubMed1988

Zinc in growth and development and spectrum of human zinc deficiency.

Growth retardation is seen in experimental animals as a result of severe dietary restriction of several essential trace elements. However, in humans, the effect of zinc deficiency is most pronounced. Growth failure and hypogonadism in males, related to a deficiency of zinc, have been recognized in many developing countries. A mild deficiency of zinc, affecting growth and development in children and adolescents, has been reported from developed countries as well. Zinc deficiency in humans may manifest as severe, moderate, or mild. The manifestations of severe zinc deficiency include bullous pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections due to cell-mediated immune dysfunctions, hypogonadism in males, neurosensory disorders, and problems with healing of ulcers. This condition can be fatal. A moderate level of zinc deficiency has been reported in a variety of conditions. Clinical manifestations include growth retardation and male hypogonadism in adolescence, rough skin, poor appetite, mental lethargy, delayed wound healing, cell-mediated immune dysfunctions, and abnormal neurosensory changes. A mild level of zinc deficiency may manifest with decreased serum testosterone level and oligospermia in males, decreased lean body mass, hyper-ammonemia, neurosensory changes, anergy, decreased serum thymulin activity, and decreased IL-2 activity. Although the clinical aspects of severe and moderate levels of zinc deficiency are well known, the recognition of mild levels of zinc deficiency has been difficult. Currently plasmas zinc appears to be the most widely used parameter for assessment of human zinc status, and it is known to be decreased in cases of severe and moderate deficiency of zinc.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Macrophage-tropic HIV-1 variants: initiators of infection and AIDS pathogenesis?

The importance of macrophage-tropic HIV-1 variants in AIDS pathogenesis becomes increasingly clear. Macrophage-tropic HIV-1 variants initiate infection, predominate in the asymptomatic phase, and persist throughout infection, even after the emergence of preferential T cell-tropic HIV-1 variants. HIV-1 infection of macrophages may contribute to the overall immune dysfunction observed in AIDS pathogenesis. Here, our knowledge of the biological variability of HIV-1, and specifically macrophage-tropic HIV-1 variants, is reviewed. Moreover, hypotheses about the mechanism of selection for macrophage-tropic variants in transmission, the mechanism by which these variants selectively persist in the asymptomatic phase, and how they may contribute to the general immune dysfunction are presented.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Simultaneous development of Crohn's disease and myelodysplastic syndrome progressing to acute myelocytic leukemia in a patient with a normal karyotype.

A 28-year-old man developed Crohn's disease and myelodysplastic syndrome concurrently. Chromosomal analysis of the bone marrow revealed a normal male karyotype. Subsequently, the myelodysplastic syndrome progressed to acute myelocytic leukemia. Several causes, including the medical treatment for Crohn's disease, chromosomal abnormalities, and a common underlying immune dysfunction, have been proposed as pathogenetic factors in the association with Crohn's disease of hematologic malignancies. This case suggests that neither medical treatment for Crohn's disease nor chromosomal abnormalities are inevitable causes of the development of hematologic malignancies associated with Crohn's disease. At present, the cause of the association remains unclear, although the idea of a common immune dysfunction is attractive.

Adult↗
PubMed1990

Effect of graft-versus-host disease on anti-tumor immunity.

BCL1, a spontaneous B cell leukemia of BALB/c origin, is rejected by C.B-20 (Ighb, H-40b) but not BALB/c (Igha, H-40a) mice. Adoptive transfer of C.B-20 anti-BCL1 effector cells specific for the minor histocompatibility Ag H-40a protects irradiated C.B-20 but not BALB/c recipients. Because C.B-20 donor cells could potentially generate graft-vs-host disease (GVHD) in BALB/c recipients, we investigated the possibility that GVHD prevents the anti-tumor effect. GVHD was induced in (C.B-20 X B10.D2)F1 [H-2d, H-40b X H-2d,H-40b] recipients after injection of B10.D2-primed C.B-20 donor cells. GVHD was indicated by the histologic appearance of tissue sections from C.B-20----F1 livers, target organs of GVHD, which showed a marked mononuclear cell infiltrate around the portal tracts and central veins. In addition, splenic lymphocytes from these mice had altered CD4/CD8 ratios and were unable to respond to the polyclonal activators Con A and LPS. The mitogen unresponsiveness was at least partially due to the presence of a suppressor cell, because proliferation of normal spleen cells to Con A and LPS was suppressed upon addition of C.B-20----F1 spleen cells. Further immune dysfunction was evident by the inability of T cells from mice with GVHD to generate a CTL response to H-2 alloantigens. Addition of C.B-20----F1 spleen cells to F1 responder cells at the induction of culture did not prevent generation of CTL, indicating that a suppressor cell was not responsible for the lack of CTL activity. In this setting of GVHD, F1 recipients were able to reject BCL1 upon adoptive transfer of C.B-20 anti-BCL1 effector cells. These data indicate that GVHD-induced immune dysfunction does not inhibit the activity of antileukemia T cells.

Animals↗