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Results for “Immune function”

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At least 1,279 records · Page 71Linked to original sources
PubMed1987

Analysis of immune function in herpes zoster patients: demonstration and characterization of suppressor cells.

We sought to identify imbalances of immune regulatory cells that might contribute to the depression of cell-mediated immunity that occurs during an episode of herpes zoster. Peripheral blood mononuclear cells (PBMC) were obtained from patients with herpes zoster during the acute (less than 7 days after disease onset) and convalescent (more than 10 days after disease onset) phases of illness and from healthy seropositive donors. The PBMC were analyzed for: lymphoproliferative responses to varicella-zoster virus (VZV) antigens, Leu-3 (helper/inducer):Leu-2 (cytotoxic/suppressor) ratios, and percentages of suppressor cells as defined by coexpression of the Leu-2 and OKM1 antigens. Significantly depressed proliferative responses of VZV antigens and Leu-3:Leu-2 ratios, and increased percentages of Leu-2+ OKM1+ suppressor cells were observed in PBMC of acute phase herpes zoster patients as compared with the PBMC of convalescent patients or healthy donors. These differences were also observed in individual patients sequentially studied during both phases of disease. Cryopreserved acute phase PBMC suppressed the proliferative response of autologous convalescent phase PBMC to VZV antigens, but not to herpes simplex virus (HSV) antigens. The acute phase PBMC suppressor cell was radiation sensitive and was identified as a Leu-2+ cell by fluorescence-activated cell sorting. Thus, depression of cell-mediated immunity during the acute phase of herpes zoster was associated with a relative increase of lymphocytes expressing a suppressor cell phenotype and the activation of a radiosensitive Leu-2+ suppressor cell with some degree of antigen specificity.

Acute Disease↗
PubMed1981

Changes in immune function in patients with rheumatoid arthritis following treatment with sodium aurothiomalate.

The mitogenic response of peripheral blood lymphocytes from 21 patients with rheumatoid arthritis to concanavalin-A (con--A), phytohaemagglutinin (PHA), and pokeweed mitogen (PWM) was significantly lower than in 30 normal subjects. After 15--24 weeks' treatment with sodium aurothiomalate (GST) the response to these mitogens rose to within the normal range. Improvement over pretreatment values was significant for con-A and PWM measured as area under the dose response curve but only for con--A if response at optimal mitogen concentration is the sole criterion. The improvement in PHA response was not significant with either method of measurement. There was an improvement in disease activity by 15--24 weeks as measured by a fall in serum C-reactive protein (CRP), IgM rheumatoid factor (RF), Clq binding activity (ClqBA), and Ritchie articular index. Con--A lymphocyte responsiveness was inversely related to serum CRP levels, but measurements of disease activity were otherwise unrelated to lymphocyte mitogen responsiveness. The observed improvement in peripheral blood lymphocyte responsiveness during gold treatment contrasts with the suppressive effect of gold in vitro. We suggest that the improvement in lymphocyte function is due to the lessening of rheumatoid disease activity during gold treatment, and that the low serum gold levels in our patients were insufficient to mask this effect. Sera from some of our patients were capable of suppressing the function of normal lymphocytes, and this was less apparent after treatment. The suppressive effect of sera correlated with ClqBA. Suppressive factors in serum, including possibly immune complexes, may be one factor leading to suppression of lymphocyte function during rheumatoid arthritis. Such an inverse relationship between humoral and cellular immune mechanisms might influence the clinical expression of rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed2000

Improvement of immune functions in HIV infection by sulfur supplementation: two randomized trials.

To determine the therapeutic effect of sulfur amino acid supplementation in HIV infection we randomized 40 patients with antiretroviral therapy (ART; study 1) and 29 patients without ART (study 2) to treatment for 7 months with N-acetyl-cysteine or placebo at an individually adjusted dose according to a defined scheme. The main outcome measures were the change in immunological parameters including natural killer (NK) cell and T cell functions and the viral load. Both studies showed consistently that N-acetyl-cysteine causes a marked increase in immunological functions and plasma albumin concentrations. The effect of N-acetyl-cysteine on the viral load, in contrast, was not consistent and may warrant further studies. Our findings suggest that the impairment of immunological functions in HIV+ patients results at least partly from cysteine deficiency. Because immune reconstitution is a widely accepted aim of HIV treatment, N-acetyl-cysteine treatment may be recommended for patients with and without ART. Our previous report on the massive loss of sulfur in HIV-infected subjects and the present demonstration of the immunoreconstituting effect of cysteine supplementation indicate that the HIV-induced cysteine depletion is a novel mechanism by which a virus destroys the immune defense of the host and escapes immune elimination.

Acetylcysteine↗
PubMed1988

Opioid peptides modulate immune functions. A review.

In the past few years it has become evident that neuropeptides may be direct mediators in the modulation of the immune response and the unspecific defense by the brain. Lymphocytes have been thought to have opioid receptors and to respond to opioids with an increase in blastogenesis, cytotoxicity and factor release. Lymphocytes are said to release various neuropeptides. Furthermore, there are some unexplained effects of morphine on the immune system and of the immune system on morphine withdrawal. The purpose of this paper is to review what has been previously published in this field. The well established modulation of phagocyte functions by opioids will only be scanned.

Animals↗
PubMed2005

Seasonality of pineal gland activity and immune functions in chickens.

The immunomodulatory action of melatonin in different animal species is already well known, although the mechanism(s) by which the indoleamine influences the immune system have yet to be fully elucidated. Previously, we have shown both anti-inflammatory and opioid-mediated influence of exogenous melatonin on thioglycollate-induced peritonitis in young chickens. In the present study, the kinetics of peritonitis and splenocyte proliferation were compared in chickens reared in both seasons under the same L:D 12:12 conditions. These two aspects of the immune response were correlated with the diurnal rhythm of pineal gland function, measured by the activity of N-acetyltransferase (NAT), a key enzyme in melatonin biosynthesis. The results revealed seasonal changes in the circadian rhythm of pineal NAT activity occurring in parallel to the natural local geophysical seasons. These changes appeared to influence the development of peritonitis and splenocyte responsiveness to mitogenic stimulation in vitro. Moreover, the existence of bidirectional communication between the pineal gland and the activated immune system was supported by the decreased activity of pineal NAT in chickens with peritonitis compared with control birds.

Acyltransferases↗
PubMed1996

Hair cycle-dependent changes in skin immune functions: anagen-associated depression of sensitization for contact hypersensitivity in mice.

To assess whether hair follicle cycling influences skin immunity, we examined the association between highly synchronized hair follicle cycling and experimental contact hypersensitivity in C57BL/6 mice. Hair cycle synchronization was performed by depilation of hair shafts on the back with telogen skin. Mice were sensitized on the lower back skin with picryl chloride between 0 and 25 d, after anagen induction by depilation, and challenged on the earlobes with picryl chloride 5 d later. The magnitude of contact hypersensitivity was significantly decreased in mice sensitized on day 1, was minimal on day 3 (early anagen), and slowly increased thereafter, reaching level comparable to day 0 on day 25 (telogen). The significantly depressed contact hypersensitivity response in anagen skin was confirmed in mice with spontaneously developed follicles. Lymph node cells taken from mice sensitized with picryl chloride on days 0, 1, and 3 after depilation were cultured in vitro in the presence of syngeneic, haptenized, Langerhans cell-enriched epidermal cells. Marked proliferative responses of lymph node cells to haptenized cells were found in mice not only of day 0, but also of days 1 and 3, suggesting that immune T cells exist even lymph node cells of the low-responsive mice. Flow cytometric analyses demonstrated that the number of intraepidermal Langerhans cells and their functions, including the expression of major histocompatibility complex class II, CD54, and CD86, and mixed epidermal cell lymphocyte reactions, were not changed in skin on days 0,1, and 3. These findings demonstrated that contact hypersensitivity is induced most effectively via skin with telogen hair follicles and that the depressed response in early anagen skin is not simply due to failure in Langerhans cell function or sensitization of T cells.

Animals↗
PubMed1999

Effects of fentanyl on cellular immune functions in man.

In order to analyze the effects of the opioid agonist fentanyl on cells of the innate immune system, seven healthy individuals were treated intravenously with the opioid fentanyl and five subjects received a placebo. Respiratory burst of polymorphonuclear cells (PMNC) and phenotypes of peripheral blood lymphocytes (PBL) were analyzed from blood samples drawn before, 15 and 30 min after fentanyl or placebo application. In addition, in vitro effects of fentanyl on natural killer (NK) activity was assessed. Fentanyl administration affected neither superoxide production of PMNC nor circulating numbers of B-and T-lymphocytes. In contrast, NK cell (CD16+/CD56+) numbers significantly increased in response to fentanyl. However, no direct influence of fentanyl on NK cell function in vitro could be detected. These results suggest a transient effect of fentanyl on NK cell circulation which seemed to be centrally mediated rather than a direct effect of this opioid on NK cells.

Adult↗
PubMed1993

Glutathione depletion in rats impairs T-cell and macrophage immune function.

Critical illness is associated with both immunosuppression and glutathione deficiency. We determined if in vivo depletion of glutathione would adversely affect immune status. Rats with normal glutathione levels and those with glutathione stores depleted by diethyl maleate underwent analysis of splenocyte function and mesenteric lymph node lymphocyte function. Lymphocytes of the spleen and mesenteric lymph nodes were tested for concanavalin A proliferative response and interleukin 2 production. Tumor necrosis factor and interleukin 6 secretion by splenic adherent cells was also measured. Glutathione-depleted animals had significantly decreased lymphocyte proliferation and decreased production of tumor necrosis factor and interleukin 6 but unaltered interleukin 2 production. These findings indicate that in vivo glutathione deficiency impairs macrophage and T-cell function. Because glutathione depletion may occur in sepsis, trauma, and shock, treatments that help maintain glutathione levels may enhance immunocompetence and thus improve the ability of patients to recover from critical illness.

Animals↗
PubMed2002

Molecular mechanisms for protein kinase A-mediated modulation of immune function.

Protein kinase A (PKA) is a serine/threonine kinase that regulates a number of cellular processes important for immune activation and control. Modulation of signal transduction by PKA is a complex and diverse process, and differential isozyme expression, holoenzyme composition and subcellular localization contribute specificity to the PKA signalling pathway. In lymphocytes, phosphorylation by PKA has been demonstrated to regulate antigen receptor-induced signalling both by altering protein-protein interactions and by changing the enzymatic activity of target proteins. PKA substrates involved in immune activation include transcription factors, members of the MAP kinase pathway and phospholipases. The ability of PKA type I to regulate activation of signalling components important for formation of the immunological synapse, demonstrates that the cAMP signalling pathway can directly modulate proximal events in lymphocyte activation. Furthermore, the recent discovery that PKA regulates Src kinases through modulation of Csk, supports the notion that PKA is involved in the fine-tuning of immune receptor signalling in lipid rafts.

CSK Tyrosine-Protein Kinase↗