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At least 163 records · Page 9Linked to original sources
PubMed1988

Effect of lithium carbonate in HIV-infected patients with immune dysfunction.

Ten homosexual men received oral lithium carbonate at doses that maintained their serum lithium concentrations between 0.5 and 1.5 mEq/L. Prior to treatment all patients had HIV isolated from PHA-activated peripheral blood lymphocytes (PBLs) using a quantitative antigen-capture enzyme-linked immunosorbent assay (ELISA) assay for detection, and had an absolute number of CD4 (helper) lymphocytes of less than 300/mm3. Eight of 10 patients developed symptoms of drug toxicity requiring discontinuation of the drug in 7 patients. Two patients completed only 4-5 weeks of lithium therapy, and 5 patients received 7-8 weeks. All patients remained culture positive for HIV during the trial, and viral titers as measured by the antigen capture assay were unchanged or increased. There were no significant changes in the absolute number of CD4 lymphocytes, CD4/CD8 ratio, or phytohemagglutinin (PHA) or tetanus toxoid induced proliferative responses. There was a significant decrease in mixed lymphocyte reaction (MLR). Lithium carbonate demonstrated no immunorestorative or antiviral activity when given in therapeutic doses. Drug toxicity limited therapy in the majority of patients.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Immune dysfunction in primary biliary cirrhosis (PBC): I. Increased sensitivity of PHA stimulated lymphocyte cultures to indomethacin.

A reduced responsiveness of peripheral blood lymphocytes from PBC patients to phytohaemagglutinin (PHA) was observed. Such an alteration may be related either to an intrinsic defect of T cells to proliferate or to a derangement of endogenously secreted mediators with regulatory functions, i.e., prostaglandins (PG). The role of the PG mediated suppressor system in 14 PBC patients and in 12 age and sex matched controls was evaluated. After the addition of indomethacin, the lymphocyte responsiveness to PHA increased in both controls and in PBC patients. However, this increment was statistically significantly only in PBC patients. The addition of PGE1 and PGE2 to PHA stimulated cultures decreased the lymphocyte proliferative activity. No differential sensitivity to PGEs was detectable in lymphocytes from PBC patients. Our data suggest, that, after polyclonal stimulation, mononuclear cells from PBC patient may release increased levels of PGEs which in turn affect the proliferative activity of mitogen activated lymphocytes.

Adult↗
PubMed1989

AIDS: a syndrome of immune dysregulation, dysfunction, and deficiency.

Acquired immune deficiency syndrome (AIDS) is a disease caused by the human immunodeficiency virus (HIV) in which cellular immune functions are severely impaired. Acute infection and subsequent destruction of helper T cells, although occurring readily in cell cultures, do not appear to be the only mechanisms mediating helper T cell loss. Other mechanisms that may account for the loss of helper T cells include: T cell syncytia formation, decreased T cell production, and autoimmune-related destruction of helper T cells. Immune abnormalities seen early in the course of HIV infection include immune hyperactivation and autoimmune phenomena suggestive of immune dysregulation rather than immune deficiency. Many changes in immune function are, in fact, seen in HIV-seropositive patients who possess a normal number of helper T cells. Mechanisms (other than the loss of helper T cells) that may contribute to the immune abnormalities seen in these patients include noninfectious effects of HIV and HIV proteins, effects of HIV on non-T cells, autoimmune-related manifestations of HIV infection, and HIV-induced activation of normal immunosuppressive circuits.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Trauma-induced suppression of antigen presentation and expression of major histocompatibility class II antigen complex in leukocytes.

The immune response to trauma, shock, and/or sepsis appears to exhibit a bimodal response, in which there is an early exaggerated inflammatory response, giving way over time to a state of hyporesponsiveness or immune dysfunction. This state of immune dysfunction is frequently associated with increased infectious complications and/or mortality, seen following shock or trauma. In this article, we present an overview of some of those changes that have been seen with respect to the process of major histocompatibility class II (MHC class II) antigen presentation by macrophage, a key component of the overall host immune response to foreign bacterial and/or fungal pathogens encountered following shock/trauma (with a particular emphasis on hemorrhagic shock as a component of traumatic shock). With respect to the overall process of antigen presentation, defects (dysfunction) are evident not only in models of shock and sepsis, but also in traumatized patients. Studies of the capacity of a monocyte's/macrophage's ability to present antigen indicate that defects can be detected, not only in those steps involved in antigenic processing, but also in MHC class II molecule expression and accessory molecule function (or its inhibition) following shock. Those changes in the macrophage's capacity to process antigen seen during the first 24 h after hemorrhagic shock appear to be associated with the cell's metabolic response to regional hypoxia and/or the shift to proinflammatory mediator release (tumor necrosis factor, interleukin [IL]-1, IL-6, etc.). This initial acute response to shock appears to act as the nidus for chronic anti-inflammatory mediator release (prostaglandin E2, transforming growth factor-beta, IL-10, IL-4, nitric oxide, etc.), which may mediate the sustained depression of the antigen-presenting cell's function.

Animals↗
PubMed1994

Deficient type I protein kinase A isozyme activity in systemic lupus erythematosus T lymphocytes.

Systemic lupus erythematosus (SLE) is an autoimmune disorder of indeterminate etiology characterized by a dysfunctional cellular immune response. We have previously identified a metabolic disorder of the adenylate cyclase/cAMP/protein kinase A (AC/cAMP/PKA) pathway characterized by impaired cAMP-inducible, PKA-catalyzed protein phosphorylation in intact T lymphocytes from subjects with severe SLE disease activity. Because this metabolic disorder may contribute to abnormal T cell immune effector functions, we tested the hypothesis that impaired PKA-dependent protein phosphorylation is the result of a PKA isozyme deficiency in SLE T lymphocytes. Compared with healthy and rheumatoid arthritis (RA) controls, subjects with severe SLE activity exhibited reduced PKA-catalyzed phosphorylation of proteins in the T lymphocyte plasma membrane where the type I isozyme of PKA (PKA-I) is predominantly localized. Both silver staining and biosynthetic labeling of membrane-associated proteins with [35S]methionine demonstrated that reduced protein phosphorylation was not due to either an altered distribution of or absence of proteins. Moreover, phosphorylation of SLE membrane-associated proteins with the PKA catalytic (C) subunit showed a similar distribution and extent of phosphorylation compared with membrane proteins from healthy T cells, suggesting that SLE T cell membrane proteins could be phosphorylated. Sequential column chromatography of the type I and type II isozymes of PKA (PKA-I, PKA-II) demonstrated a deficiency of PKA-I isozyme activity. Compared with a ratio of PKA-I to PKA-II activity of 4.2:1 in healthy T cells, the activity ratio in T cells from subjects with severe SLE disease activity was 0.99:1 (P = 0.01, SLE versus healthy controls for PKA-I). The deficient PKA-I activity was associated with a significant increase of free C-subunit activity (P = 0.04, SLE versus healthy controls for C-subunit). T cells from subjects with mild/moderate SLE disease activity also exhibited diminished PKA-I activity, yielding a ratio of PKA-I to PKA-II activity of 2.4:1. By contrast, T cells from RA controls possessed increased PKA-I, PKA-II, and free C-subunit activities compared with healthy controls, resulting in a ratio of PKA-I to PKA-II activity of 3.6:1. We conclude that the reduced PKA-catalyzed protein phosphorylation in the plasma membrane of SLE T cells is the result of deficient PKA-I isozyme activity. This is the first identification of a deficiency of PKA activity in SLE T lymphocytes; the deficiency, resulting in diminished protein phosphorylation, may alter cellular homeostasis, contributing to the cellular immune dysfunctions observed in SLE.

Adult↗
PubMed1992

A prospective study of lymphocyte-initiated immunosuppression in normal pregnancy: evidence of a T-cell etiology for postpartum thyroid dysfunction.

Immune function in normal pregnancy and the postpartum period remains poorly defined. We hypothesized that a comparative study between pregnant women with normal and abnormal immune function would further our understanding of the immune mechanisms of pregnancy. We chose to study a cohort of pregnant women at risk for the development of postpartum thyroid dysfunction (PPTD) as well as a group of normal controls. We chose PPTD as the model for abnormal immune function because of the relative ease of monitoring disease development and the relatively high prevalence for PPTD reported in earlier studies. Five hundred and fifty-two women were screened for the presence of thyroid autoantibodies in the first trimester of pregnancy. Thirty-three thyroid autoantibody-positive women and 28 thyroid autoantibody-negative women were followed prospectively throughout pregnancy and 6 months into the postpartum period. Lymphocyte subset analyses, thyroid function tests, and thyroid autoantibodies (antihuman thyroglobulin and antithyroid peroxidase) were performed at defined intervals. All patients were HLA serotyped. Normal pregnancy was principally characterized by decreased CD4+ T-cells and increasing CD8+ T-cells, causing a significant fall in the CD4+/CD8+ ratio in late pregnancy and into the postpartum period. Women who developed PPTD had 1) a higher CD4+/CD8+ ratio (P = 0.04), 2) activation of T-cells in the postpartum period (P = 0.02), and 3) significantly higher thyroid autoantibody titers (antihuman thyroglobulin, P = 0.02; antithyroid peroxidase, P = 0.0018). We found an overall incidence for PPTD of 8.8%. These data demonstrated that women who were thyroid autoantibody positive in the first trimester of pregnancy had a one in three chance of developing PPTD. We observed a significant fall in the T-cell helper/suppressor ratio in normal pregnant women, which was associated with distinct T-cell subset changes. This pregnancy-initiated T-cell regulation reflected an overall suppression of immune function. The development of PPTD was a frequent postpartum event in our population and was associated with a triad of immune markers: a reduction in the normal immune suppression of pregnancy (as indicated by higher T-cell helper/suppressor ratios), enhanced postpartum T-cell activation, and elevated thyroid autoantibodies. The reduction in the degree of immune suppression was, therefore, a major factor in the development of PPTD. Our results define immunological changes that occur in normal pregnancy and distinct immunological abnormalities necessary for the development of PPTD.

Autoantibodies↗
PubMed1987

Immunotoxicology today.

Immunotoxicology is a science which deals with the effects of physical and chemical agents and other toxic substances on the immune system. The discipline includes study of the detection, occurrence, adverse effects, and mechanisms of chemically-induced immune dysfunction. Many drugs and chemicals are known to compromise the immune response of a host which is extremely vulnerable and sensitive to perturbation by these agents. The consequences of immune dysfunction may be expressed in reduced resistance to infectious and neoplastic diseases, or enhanced hypersensitivity and autoimmunity. The immunomodulating profiles of xenobiotics may be diverse, involving several components of the immune system, or they may selectively compromise an individual compartment of the immune response. Many drugs and chemicals are known to result in immune disregulation in animals, but a paucity of information is available to indicate the effects of xenobiotics on systemic immunity in humans. Epidemiological studies and research designed to assess chemical immunomodulation in man are necessary to confirm animal data. Further, a definitive diagnosis for chemically-induced immune dysfunction must include several etiologies and body organ systems, since a triad of reciprocal interactions exists between the immune, endocrine, and central nervous systems.

Animals↗
PubMed1994

Vaccinology, immunology, and comparative pathogenesis of measles in the quest for a preventative against AIDS.

Current approaches to the prevention and control of AIDS by vaccines and by chemotherapy have failed to provide satisfactory solutions to this important medical problem and have failed, in addition, to provide definitive guidelines for future research endeavor. Vaccine research must and will continue but it is possible that a safe and effective vaccine may never be developed and it may be timely to explore, in addition, alternative means for immunological intervention in AIDS. Both immunoprophylactic and immunotherapeutic efforts might be assisted by manipulating the T helper 1 (Th1) and T helper 2 (Th2) subsets of CD4+ T helper cells, which is therefore worthy of exploration. Selective control of immune response by the two T helper subsets is by release of different cytokines that promote either cellular or humoral immunity, the latter of which may be associated with inappropriate immune responses and with immune dysfunction. Discovery of the Th1 and Th2 subsets and definition of the cytokines they release provide a new avenue toward possible development of a safe and effective vaccine and an approach, in addition, to correction of immune dysfunction by selective cytokine administration or by cytokine ablation by antagonists or antibodies. AIDS pathogenesis and immune dysfunction are complex and understanding them may be overwhelmed by an excess of possibilities. Simplification of the endeavor might benefit from comparative studies of the pathogenesis of measles, in which there also is immune deficiency but usually with spontaneous viral clearance, reversal of immune dysfunction, and total recovery. In addition, measles presents as a single disease and is caused by antigenically stable virus. Identification of the process whereby measles immunodeficiency is spontaneously reversed might be of importance in attempting to devise means for similar reversal in AIDS.

AIDS Vaccines↗
PubMed1995

[Respective indications of enteral or parenteral nutrition during pre- and post-operative periods].

Denutrition is often associated with poor postoperative outcome. However, a large body of evidence, from studies comparing perioperative parenteral (PN) or enteral (EN) nutrition to the absence of perioperative nutrition, suggests that perioperative nutritional support provides significant improvements in both nutritional status and postoperative clinical outcome in selected patients who are or will become malnourished. The aim of this study was to select and review all relevant articles comparing perioperative parenteral and enteral nutritional support, either in terms of clinical outcome, or risks and costs, or in pathophysiological terms. Twelve clinical reports were reviewed. All contained methodological flaws, mainly type II statistical error due to an insufficient number of patients, inaccurate primary diagnosis, absence of blinding, and lack of objective criteria of judgement. These concerns warrant caution in interpreting the results. Moderately strong (grade B) recommendations can only be drawn from these studies: PN (compared to early EN) is associated with a higher rate of sepsis in patients following abdominal trauma; EN is as efficient as PN in patients following surgery; EN is safe and cheaper than PN. PN formulae lack many important nutrients (glutamine, arginine, cysteine, peptides, fibers, n-3 polyunsaturated fatty acids, and nucleotides). Many experimental (animal) and some clinical (in non surgical patients) studies showed that PN (compared to EN) induces gut mucosal atrophy, liver dysfunction, gut bacterial translocation and immune dysfunction. The final aim of PN and EN would therefore strikingly differ. The qualitatively imperfect PN would only supply the fasting patient with quantitative amounts of calories and proteins. Due to initially limited digestive tolerance, EN provides less nutrition than PN does, but would finally lead to the same or even better outcome, due to its ability to counteract stress induced gut and immune dysfunction. Current evidence therefore suggests that early EN is superior to PN in trauma patients, and not different from but cheaper (and therefore more cost-effective) than PN in surgical patients. Further controlled, randomised, and blinded studies including sufficient sizes of groups are required, especially in the surgical setting, to address a large number of still unanswered questions.

Enteral Nutrition↗
PubMed1989

[Cyto-dynamic observations on T lymphocytes and the CSF in Guillain-Barre syndrome].

We have examined by ANAL for 107 times in 45 cases and the cytology of CSF in 92 times for acute infectious polyneuritis. The count of T-lymphocytes in severe and most severe types had a marked decrease comparing with the light and moderate types. The patients with a course of disease less than seven days had a significant decreasing to comparing with the more than seven days. The immune complex (IgG, IgM, Cs) had a distinct decreasing. The cytology of CSF showed that the lymphocytes were decreasing but the monocytes and the macrophages increased. We considered that there were not only cellular immunity dysfunction, but also the humoral immunity dysfunction. Using of hormones in this disease is not suitable.

Adolescent↗
PubMed1996

Vitamins and immunomodulation in AIDS.

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a retrovirus infection and represents the end point in a progressive sequence of immunosuppressive changes. Vitamins can enhance disease resistance in animals and humans. As such they are important co-factors in optimal functioning of the immune systems. In this article, the immunological and nutritional modifications caused by AIDS are summarized. The effects of murine and human retrovirus infection on vitamin status are analyzed as co-factors in the development of severe immune dysfunction, AIDS. The properties of immunoenhancing antioxidative vitamins, vitamin A, B6, B12, C, E, and beta-carotene, which are frequently low in AIDS patients, are evaluated relative to the development of immunodeficiency during retrovirus infection. Vitamin A, E, and B12 deficiency accelerated the development of AIDS with low T cells, whereas their normalization retarded the development of immune dysfunction. The interactions between these vitamins and the immune system in human AIDS patients and animal models of AIDS are reviewed. Our purpose is to provide data on how retrovirus infection can cause nutritional deficiencies that accentuate immune damage and to evaluate the potential therapeutic role of vitamins in the treatment of immune dysfunctions in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1996

T-cell-receptor dose and the time of treatment during murine retrovirus infection for maintenance of immune function.

C57BL/6 mice were injected with different doses of human T-cell receptor (TCR) V beta 8.1 CDR1 peptide at different times after murine retrovirus (LP-BM5) infection. Injection with TCR V beta 8.1 CDR1 peptide largely prevented the retrovirus-induced reduction in B- and T-cell proliferation, and T-helper 1 (Th1) cytokines [interleukin-2 (IL-2) and interferon-gamma (IFN-gamma)] secretion. It also suppressed T-helper 2 (Th2) cytokines (IL-6 and IL-10) production, which was stimulated by retrovirus infection. These effects were accomplished using at least 100 micrograms of peptide per mouse and the most effective dose of peptide had to be given within 4 weeks after retrovirus infection. Immunization with doses above 100 micrograms/mouse as long as 4 weeks postinfection maintained natural killer (NK) cell activity during retrovirus infection. Reducing the dose of peptide or delaying it until the disease progressed towards early murine acquired immune deficiency syndrome (AIDS) allowed development of immune dysfunction. These studies provide data suggesting that immune dysfunction, induced by murine retrovirus infection, was largely prevented by TCR V beta CDR1 peptide injection.

Adjuvants, Immunologic↗