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PubMed2006

Cancer immunosuppression and autoimmune disease: beyond immunosuppressive networks for tumour immunity.

Cancer immunosuppression evolves by constitution of an immunosuppressive network extending from a primary tumour site to secondary lymphoid organs and peripheral vessels and is mediated by several tumour-derived soluble factors (TDSFs) such as interleukin-10 (IL-10), transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF). TDSFs induce immature myeloid cells and regulatory T cells in accordance with tumour progression, resulting in the inhibition of dendritic cell maturation and T-cell activation in a tumour-specific immune response. Tumour cells grow by exploiting a pro-inflammatory situation in the tumour microenvironment, whereas immune cells are regulated by TDSFs during anti-inflammatory situations--mediated by impaired clearance of apoptotic cells--that cause the release of IL-10, TGF-beta, and prostaglandin E2 (PGE2) by macrophages. Accumulation of impaired apoptotic cells induces anti-DNA antibodies directed against self antigens, which resembles a pseudo-autoimmune status. Systemic lupus erythematosus is a prototype of autoimmune disease that is characterized by defective tolerance of self antigens, the presence of anti-DNA antibodies and a pro-inflammatory response. The anti-DNA antibodies can be produced by impaired clearance of apoptotic cells, which is the result of a hereditary deficiency of complements C1q, C3 and C4, which are involved in the recognition of phagocytosis by macrophages. Thus, it is likely that impaired clearance of apoptotic cells is able to provoke different types of immune dysfunction in cancer and autoimmune disease in which some are similar and others are critically different. This review discusses a comparison of immunological dysfunctions in cancer and autoimmune disease with the aim of exploring new insights beyond cancer immunosuppression in tumour immunity.

Animals↗
PubMed1995

Decreased lymphocyte responses in free-ranging bottlenose dolphins (Tursiops truncatus) are associated with increased concentrations of PCBs and DDT in peripheral blood.

Since 1987, large-scale mortalities of dolphins have been reported along the Atlantic coast of North America, in the Gulf of Mexico, and in the Mediterranean Sea. Autopsied bottlenose dolphins, Tursiops truncatus, which were collected from the large-scale mortality along the Atlantic coast in 1987 to 1988, exhibited opportunistic infections indicative of immune dysfunction. Further, these animals had high levels of chlorinated hydrocarbons, such as PCBs and DDT, that can suppress immune functions. The purpose of this study was to determine whether there is a relationship between chemical contaminant exposure and immune response in free-ranging dolphins. In June of 1991, peripheral blood was obtained from members of a bottlenose dolphin population that resides along the west coast of Florida. Peripheral blood lymphocyte responses to Concanavalin A (Con A) and phytohemagglutinin (PHA) were determined in vitro and compared by regression analysis with contaminant concentrations in whole blood from a small subset of these animals (n = 5). These data indicate that a reduced immune response in these bottlenose dolphins was correlated with increasing whole blood concentrations of several contaminants. Specifically, inverse correlations were found between Con A-induced lymphocyte proliferation and tetrachlorinated to octachlorinated biphenyls (r2 values ranged from 0.70 to 0.87). Con A-induced lymphocyte responses also correlated inversely with p,p'DDT (r2 values of 0.73 and 0.79); o.p'-DDE (r2 values of 0.93 and 0.96); and p,p'-DDE (r2 values of 0.73 and 0.81).

Animals↗
PubMed2001

A review on cancer--psychospiritual status interactions.

With the advances in the knowledge of neuroimmunomodulation, a new era of investigations about the chemical basis of the state of mind has been initiated. Both emotions and states of spiritual consciousness may influence immune functions and cancer growth. Stress, anxiety and depressive states are associated with immunosuppression and enhanced frequency of tumors. On the other hand, the states of sexual pleasure and spiritual joy enhance the immune efficacy, by counteracting tumor onset and dissemination. The biochemistry of pleasure and immunostimulation is mainly mediated by pineal indoles and cannabinergic substances, whereas that of stress, anxiety and depression is associated with enhanced production of adrenal steroids, opioids and catecholamines. The sexual repression would allow a progressive immunosuppression through a profound damage in the biochemistry of pleasure. Therefore, a better definition of psychospiritual status-associated neuroimmunochemistry could allow us to improve the immune dysfunction by acting on the same neuroendocrine secretions which are involved in mediating the psychic influence on the immunity, including that against cancer.

Emotions↗
PubMed1994

T helper cell dysfunction in systemic lupus erythematosus (SLE): relation to disease activity.

Patients with systemic lupus erythematosus (SLE) are known to have defects in both humoral and cellular immunity. The significance of defective T cell-mediated immunity and its relationship to disease activity have not been clearly established. We studied in vitro T helper cell (Th) function in 150 SLE outpatients and correlated Th function with validated measures of disease activity. Interleukin 2 (IL-2) production by peripheral blood mononuclear cells (PBMC) was measured after stimulation with the recall antigens influenza A virus (FLU) and tetanus toxoid (TET), irradiated allogeneic peripheral blood mononuclear cells (ALLO), and phytohemagglutinin (PHA). We observed three patterns of Th response: (1) 76 of 150 (50%) of patients responded to the recall antigens FLU and/or TET, ALLO, and PHA; (2) 62 of 150 (42%) of patients did not respond to recall antigens but responded to ALLO and PHA; and (3) 12 of 150 (8%) of patients did not respond to either recall antigens or ALLO antigens. This diminished T cell function was correlated with higher disease activity as measured by four scales of clinical activity, such that individuals who exhibited more in vitro immune dysfunction presented with significant increases in their clinical activity indices. The alterations in T cell function could not be accounted for by medication doses alone. Thus, SLE patients have multiple distinct defects at the level of the Th cell which are associated with clinical measures of disease activity.

Adult↗
PubMed1997

Nutritional modification of inflammatory diseases.

Regulation of the immune system is extremely complex. We are only starting to understand how the immune system coordinates the body's response to a disease or invading pathogen. Immunomodulation, as the term implies, can be used to designate either a suppression or an augmentation of an immune response. Suppressing the function of the immune system may be important in cases of inflammation and augmenting the immune response when increased resistance to disease is required. Nutrition does and can play an important role in modulation of the animal's immune system. The majority of scientific literature published on the interaction of nutrition and the immune system correlates the effects of nutrient deficiency and modulation of an immune response. These studies have evaluated deficiencies of protein; energy; the fat soluble vitamins A, D, and E; the B-complex vitamins; vitamin C; and the minerals selenium, iron, zinc, and copper and their relationship to immune dysfunction. Most recently, researchers have concentrated efforts on evaluating the impact specific fatty acids have on modulation of the immune system. Undoubtedly, the nutritional status of the animal plays an important role in resistance mechanisms against disease causing organisms and may influence the outcome of disease in infected animals. The focus of this chapter is to concentrate on the role specific polyunsaturated fatty acids have on the immune response of animals and to consider the potential for nutritional modification of diseases related to inflammation.

Adjuvants, Immunologic↗
PubMed2001

Using death to one's advantage: HIV modulation of apoptosis.

Infection by human immunodeficiency virus (HIV) is associated with an early immune dysfunction and progressive destruction of CD4+ T lymphocytes. This progressive disappearance of T cells leads to a lack of immune control of HIV replication and to the development of immune deficiency resulting in the increased occurrence of opportunistic infections associated with acquired immune deficiency syndrome (AIDS). The HIV-induced, premature destruction of lymphocytes is associated with the continuous production of HIV viral proteins that modulate apoptotic pathways. The viral proteins, such as Tat, Env, and Nef, are associated with chronic immune activation and the continuous induction of apoptotic factors. Viral protein expression predisposes lymphocytes, particularly CD4+ T cells, CD8+ T cells, and antigen-presenting cells, to evolve into effectors of apoptosis and as a result, to lead to the destruction of healthy, non-infected T cells. Tat and Nef, along with Vpu, can also protect HIV-infected cells from apoptosis by increasing anti-apoptotic proteins and down-regulating cell surface receptors recognized by immune system cells. This review will discuss the validity of the apoptosis hypothesis in HIV disease and the potential mechanism(s) that HIV proteins perform in the progressive T cell depletion observed in AIDS pathogenesis.

Apoptosis↗
PubMed2004

Case-control study of multiple chemical sensitivity, comparing haematology, biochemistry, vitamins and serum volatile organic compound measures.

BACKGROUND: Multiple chemical sensitivity (MCS), although poorly understood, is associated with considerable morbidity. AIM: To investigate potential biological mechanisms underlying MCS in a case-control study. METHODS: Two hundred and twenty-three MCS cases and 194 controls (urban females, aged 30-64 years) fulfilled reproducible eligibility criteria with discriminant validity. Routine laboratory results and serum levels of volatile organic compounds (VOCs) were compared. Dose-response relationships, a criterion for causality, were examined linking exposures to likelihood of case status. RESULTS: Routine laboratory investigations revealed clinically unimportant case-control differences in means. Confounder-adjusted odds ratios (OR) showed MCS was negatively associated with lymphocyte count and total plasma homocysteine, positively associated with mean cell haemoglobin concentration, alanine aminotransferase and serum vitamin B6, and not associated with thyroid stimulating hormone, folate or serum vitamin B12. More cases than controls had detectable serum chloroform (P = 0.001) with the OR for detectability 2.78 (95% confidence interval = 1.73-4.48, P < 0.001). Chloroform levels were higher in cases. However, cases had significantly lower means of detectable serum levels of ethylbenzene, m&p-xylene, 3-methylpentane and hexane, and means of all serum levels of 1,3,5- and 1,2,3-trimethylbenzene, 2- and 3-methylpentane, and m&p-xylene. CONCLUSIONS: Our findings are inconsistent with proposals that MCS is associated with vitamin deficiency or thyroid dysfunction, but the association of lower lymphocyte counts with an increased likelihood of MCS is consistent with theories of immune dysfunction in MCS. Whether avoidance of exposures or different metabolic pathways in cases explain the observed lower VOC levels or the higher chloroform levels should be investigated.

Adult↗
PubMed2000

The effects of tramadol and morphine on immune responses and pain after surgery in cancer patients.

UNLABELLED: There has been growing interest in determining the possible immune consequences of opioid administration for the management of postoperative pain. We studied the effects of morphine and tramadol on pain and immune function during the postoperative period in 30 patients undergoing abdominal surgery for uterine carcinoma. Phytohemoagglutinin-induced T lymphocyte proliferation and natural killer cell activity were evaluated immediately before and after surgery, and 2 h after the acute administration of either 10 mg of morphine IM or 100 mg tramadol IM for pain. In all patients, phytohemagglutinin-induced lymphoproliferation was significantly depressed by surgical stress. However, in the morphine-treated group, proliferative values remained lower than basal levels for 2 h after treatment, whereas in tramadol-administered patients proliferative values returned to basal levels. Natural killer cell activity was not significantly affected by surgery nor by morphine administration, whereas tramadol significantly enhanced the activity of natural killer cells. Both drugs produced a comparable reduction in postoperative pain. We conclude that, as previously observed in the experimental animal, tramadol and morphine, when administered in analgesic doses, induce different immune effects. IMPLICATIONS: Recent studies suggest that opioids can have an adverse impact on the immune system. Because surgical stress also induces immune dysfunction, the search for analgesic drugs devoid of immunosuppressive effects is of import. This study compared the effects on immune responses of morphine and of the atypical opioid analgesic, tramadol, given for postoperative pain to gynecological cancer patients. Tramadol and morphine showed comparable analgesic activity; however, tramadol, in contrast to morphine, induced an improvement of postoperative immunosuppression and, therefore, may be preferred to morphine for the treatment of postoperative pain.

Aged↗
PubMed1990

Zinc deficiency and immune function.

Zn deficiency can have marked effects on virtually all components of the immune system. That these effects can be functionally significant is demonstrated by the increased susceptibility of Zn-deficient animals to a number of bacterial, viral, and parasitic challenges. In addition, strong epidemiological data support the belief that Zn deficiency is a major factor underlying immune dysfunction in select human populations. Despite recognition of the importance of Zn in the ontogeny and functioning of the immune system, the biochemical lesions underlying the effects of Zn deficiency on immune responsivity have not been well characterized. Future efforts to delineate the effects of Zn on the production, release, and action of cytokines will likely produce significant advances in our understanding of the influence of this element on the immune system. The recent observation that Zn may be critical for the activity and binding of protein kinase C in lymphocyte membranes suggests that another fruitful area of research will involve examination of the influence of Zn deficiency on lymphocyte membrane structure and function. Finally, the recent recognition that Zn may be a critical factor in the activation/inactivation of immunoregulatory genes provides us with yet another avenue of research.

Animals↗
PubMed1991

A comparative study of immune status in panic disorder patients and controls.

Alterations of immunocompetence in various mental disorders have been reported. We studied white blood cell counts and immunoglobulin levels in 59 panic disorder patients and 30 controls. The significantly increased IgA levels and tendency toward increase in other immunoglobulins in panic disorder patients suggest an immune dysfunction.

Adult↗
PubMed1989

The immune system in minimal change nephrotic syndrome.

Numerous examples of abnormal immune responsiveness have been described in minimal change nephrotic syndrome (MCNS). The of MCNS with allergy and with certain genetic markers of immune responsiveness, as well as the excellent response of proteinuria to immunomodulatory agents, has suggested a causal relationship between the immunological and renal abnormalities. However, the nature of this relationship is uncertain. Before it can be clarified, the basic mechanism(s) involved in disturbed immunity in patients with MCNS must be better characterized. Studies of humoral and cellular immune function support the hypothesis that immune regulation is abnormal. However, conclusive evidence of participation by a defined immunoregulatory system in the events leading to immune dysfunction has not been obtained. Thus, considerable work remains to be done in determining the nature and cause of abnormal immunity in MCNS prior to investigating its potential role in the pathogenesis of proteinuria.

Antibody Formation↗
PubMed1983

Anti-laminin antibodies in workers exposed to mercury vapour.

In 62 male workers exposed to mercury vapour for 5.5 years on average, the results of several renal parameters were not significantly different from those found in a well-matched control group (n = 60). Circulating anti-laminin antibodies were found, however, in 8 workers exposed to mercury vapour but in none of the control workers. These results suggest that occupational exposure to mercury vapour may lead to immune dysfunction in a certain percentage of the exposed population. Whether such a finding is predictive of the occurrence of an immune glomerulonephritis remains to be evaluated.

Antibodies↗
PubMed2004

Immune response in burn patients in relation to HIV infection and sepsis.

The post-burn immune dysfunction predisposes patients to sepsis and multiple organ failure leading to increased mortality. HIV infection also results in a depressed immune response. The combination of burn injury and HIV might therefore lead to an increased morbidity and mortality as compared to non-HIV infected burn patients. Twenty burn patients and 10 healthy volunteers were included in a prospective study. To evaluate their immune status, CD4+ and CD8+ T-lymphocyte counts were determined in peripheral blood. HIV serology samples were obtained on admission. Bacteriological cultures were obtained from wound surface samples and wound tissue biopsies. Six burn patients were HIV infected. Clinical signs of sepsis were observed in 10 patients. The number of CD4+ T-lymphocytes were lower in burn patients compared to healthy volunteers (P < 0.05). HIV infected burn patients had lower CD4+ lymphocyte counts than non-HIV infected patients (P < 0.05). Patients with clinical signs of sepsis had lower CD4+ counts compared to patients without sepsis (P < 0.05). There was no difference in the mortality rate or the length of hospitalisation between patient groups. Burn injury, HIV infection and sepsis independently result in immunosuppression.

Adult↗
PubMed2003

Suppressive effect of iron on concanavalin A-induced multinucleated giant cell formation by human monocytes.

Immune dysfunction in patients with iron overload has been reported. Iron disturbed CD2 expression on T-cells, cell-mediated immunity by Th1 cells and monocyte functions including phagocytosis and natural killer activity. In the present study, we examined the effects of iron and desferrioxamine (DFX, an iron chelator) on generation of multinucleated giant cells (MGC) by human monocytes in vitro. Human monocytes were isolated from venous blood and cultured with concanavalin A (Con A) stimulation with additives, ferric citrate (Fe-citrate) or sodium citrate (Na-citrate) or DFX for 4 days. The cells were fixed and subjected to Wright staining. MGC formation was observed under light microscopy. Con A induced MGC formation in a dose-dependent manner, and reached a plateau after 3 days of incubation. MGC formation was suppressed when Con A-stimulated monocytes were cultured with the co-addition of Fe-citrate but not Na-citrate only in the early phase of culture (less than 24 hours). DFX also suppressed MGC formation in a dose-dependent manner. Using flow cytometry analysis, the co-addition of Fe-citrate significantly suppressed CD18 (beta2 integrin) and CD54 (ICAM-I) but not CD11a (alpha integrin) expression on Con A-stimulated monocytes. Iron supressed the generation of MGC by human monocytes in vitro. These observations suggested that iron might affect MGC generation by down-regulation of adhesion molecule expression on monocytes.

Acid Phosphatase↗
PubMed2002

[Cellular aspect of neuroinflammation in Guillain-Barré syndrome: a key to a new therapeutic option?].

Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating neuropathy associated with long-lasting morbidity and substantial risk of mortality. The two reference treatments (plasma exchange-PE and intravenous immunoglobulins-IVIGs) do not change the functional prognosis in patients with very severe disease. Pathogenesis of GBS associates recently characterized humoral and cellular immune dysfunctions. Antibodies against nerve antigens may participate in complement activation, antibody-dependent macrophage cytotoxicity, and reversible conduction failure. Cellular immune reaction is associated with an increase of proinflammatory cytokines (for exemple TNF-alpha), a decrease of anti-inflammatory cytokines (such as TGF-B1), an increase of matrix metalloproteinases (MMP-9-gelatinase B), all abnomalities favoring adhesion to and transmigration across endothelium of immune cells, a key phenomenon in GBS. Recovery of GBS is characterized by the normalization of these abnormalities. Experimental allergic neuritis (EAN), the experimental model of GBS has strikingly similar immunological abnormalities. The treatments of GBS, PE and IVIGs, mainly target the humoral component of the immune response. IFN-B is a cellular immunomodulator that inhibits antigen presentation, TNF-alpha production and binding, modulates macrophages properties. IFN-B increases anti-inflammatory T cell functions and cytokines, such as TGF-B1. IFN-B has important properties on leukodiapedesis by modulating expression of cell adhesion molecules and the MMP-9 proteinase. IFN-B has been used with success in EAN, in some patients with acute exacerbation of chronic inflammatory demyelinating polyneuropathy, and in one patient with GBS. Pathophysiology of GBS, IFN-B properties, and experimental studies support the initiation of a trial of IFN-B in GBS.

Guillain-Barre Syndrome↗
PubMed1987

[Clinico-immunologic parallels of patients with circulatory insufficiency].

T cell and lymphocyte subpopulation counts measured by surface markers (T helpers and T suppressors), lymphocyte blast transformation with FHA, IgA, IgM and IgG levels and phagocytosis were evaluated in 45 patients with circulatory insufficiency (CI), including 30 with coronary heart disease (CHD) and 15 with dilatation cardiomyopathy (DCMP). Three patterns of immunologic response were identified: the first one (intact immunity) was found in normal subjects, coronary patients without CI and those with first-stage CI; the second pattern (immune dysfunction) was detected in coronary patients with CI, stage 2A and DCMP patients with CI, stage 2B; the third pattern (immune deficiency) was present in coronary and DCMP patients with CI, stage 2B-3. The extent of immunologic reactivity disturbance is shown to depend on the severity of CI. DCMP was associated with a deficiency of T suppressors that may be useful as an additional diagnostic sign of this condition.

Adult↗
PubMed1986

[Does oral zinc improve the cellular immunity of patients with alcoholic cirrhosis?].

A depressed response to delayed hypersensitivity skin tests is frequent in patients with alcoholic cirrhosis. Immune dysfunction in these patients is presumably dependent on nutritional factors. Zinc deficiency, a common finding in alcoholic cirrhosis, inhibits cellular immunity and might be one of these factors. The aim of our study was to show that zinc supplementation may improve cellular immunity in patients with alcoholic cirrhosis. We therefore compared 2 groups of patients: patients in the treated group (n = 18) had a daily oral intake of zinc-sulfate, 200 mg, during 2 months, patients in the non treated group (n = 20) received no supplementation. Both groups had a free diet. Delayed hypersensitivity skin tests to 7 antigens were performed with the Multitest IMC System at the beginning and at the end of the study. The immunity score was determined by the number of tests producing a skin induration greater than 2 mm. The evolutive index, calculated in each patient, was the difference between the final and initial immunity scores. The 2 groups were similar for all studied parameters. Cumulated immunity scores improved from 35 to 53 in treated patients (p less than 0.02), and from 42 to 44 (NS) in non treated patients. The evolutive index was 1 +/- 1.4 in treated patients and 0.1 +/- 1 in non treated patients (p less than 0.05). We conclude that in patients with alcoholic cirrhosis, daily intake of zinc sulfate, 200 mg, improves responsiveness to delayed hypersensitivity skin tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗