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At least 1,099 records · Page 61Linked to original sources
PubMed2006

Human immunodeficiency virus (HIV) type 1 Vpr induces differential regulation of T cell costimulatory molecules: direct effect of Vpr on T cell activation and immune function.

Human immunodeficiency virus type 1 (HIV-1) viral proteins disrupt the normal host cellular immune pathways thus exploiting the cellular machinery for replication, survival and to escape host immune attack. Here we evaluated the direct effects of HIV-1 Vpr-mediated immune modulation of infected T cells. Vpr specifically downregulated the expression of CD28 and increased the expression of CTLA-4, whereas no significant difference in the expression of CD25 and HLA-DR was observed. Interferon gamma (IFN-gamma) production in T cells was evaluated as a measure of the downstream effector functions. Results indicate that Vpr significantly inhibited IFN-gamma production and this may, in part, due to Vpr's ability to inhibit the nuclear translocation of NF-kappaB, and its transcriptional regulation. Together these results support that HIV-1 Vpr selectively dysregulates the immune functions at multiple levels and exerts its inhibitory effects in the presence of other viral proteins.

Antigens, CD↗
PubMed2005

[Comparative study on the treatment effects with rhIL-11 and rhG-CSF in combination or alone on immune function].

OBJECTIVE: To investigate the effect of in vivo administration of rhG-CSF and/or rhIL-11 on mice immune system function. METHODS: T cell subgroups, suppressor T cells (CD8+ CD28-, CD4+ CD25+, CD3+ CD4- CD8- T cells), expression of CD28 on T cells, and spleen T cells intracellular IL4/IFN-gamma secretion were determined by multicolor flow cytometry. MTT was used to determine the T cell proliferation capacity and mixed lymphocyte reactions. RESULTS: In vivo administration of cytokines decreased the percentage of lymphocytes (P < 0.05), rhIL-11 and rhG-CSF in combination significantly decreased the CD4+/CD8+ ratio and increased the percentage of CD8+ CD28- suppressor T cells compared to either cytokine alone (P < 0.01). There was no difference in the percentage of CD3+ CD4- CD8- and CD4+ CD25+ suppressor T cells between either of the cytokines. Furthermore, cytokines treatments significantly decreased the capacities of splenic T cells proliferation and the response to alloantigens compared with the PBS treatment (P < 0.05), the combination group being more significantly decreased (P < 0.01). And cytokines treatment significantly decreased the production of IFN-gamma and increased the production of IL-4 compared with the PBS treatment(P < 0.05). The ratio of IFN-gamma/IL-4 were significantly decreased after the combination compared with either of them alone. CONCLUSION: The combination of rhIL-11 and rhG-CSF is potentially synergistic in the induction of immune tolerance by their effects on the proliferation capacity and function of T lymphocytes.

Animals↗
PubMed1996

Critical amino acids in the lymphocyte function-associated antigen-1 I domain mediate intercellular adhesion molecule 3 binding and immune function.

We have identified amino acid residues within the evolutionarily conserved I domain of the alpha-chain (CD11a) of the leukocyte integrin leukocyte function-associated antigen (LFA) 1 that are critical for intercellular adhesion molecule (ICAM) 3 (CD50) binding. ICAM-3, a ligand of LFA-1, is thought to mediate intercellular adhesion essential for the initiation of immune responses. Using a panel of human/murine I domain chimeras and point mutants, we observed that the Ile-Lys-Gly-Asn motif, located in the NH2-terminal part of the CD11a I domain, is required for ICAM-3 but not ICAM-1 binding. These findings demonstrate that the I domain of CD11a contains distinct functional subdomains for ligand specific binding. An aspartic acid located at position 137, which is essential to ICAM-1/LFA-1 interactions (Edwards, C.P., M. Champe, T. Gonzalez, M.E. Wessinger, S.A. Spencer, L.G. Presta, P.W. Berman, and S.C. Bodary. 1995. J. Biol. Chem. 270:12635-12640), was also critical for ICAM-3 binding, whereas Ser at position 139 did not effect ICAM-1 or ICAM-3 binding. A synthetic peptide containing the Ile-Lys-Gly-Asn motif inhibited ICAM-3-dependent adhesion and proliferation of T cells at micromolar concentrations, suggesting that this peptide interferes with immune recognition. These observations underscore the importance of ICAM-3 in leukocyte function, and may lead to development of a new category of immunosuppressive agents.

Amino Acid Sequence↗
PubMed1996

The huPBL-SCID mouse as a means to examine human immune function in vivo.

The transfer of human peripheral blood lymphocytes (huPBL) into mice with severe combined immune deficiency (SCID) has allowed for the generation of a model in which it is possible to examine human immune cell function in vivo. This model also provides the researcher an invaluable tool with which to examine human disease states and to evaluate potential therapies using human cells and reagents under more physiological conditions. However, it is clear that there are still significant obstacles that need to be addressed to optimize this model. The primary problem with the huPBL-SCID mouse is the tremendous variability in the extent of human cell engraftment which can vary from donor to donor and even from mouse to mouse using the same huPBL donor. This variability currently limits attempts to standardize this model among investigators and subsequently, various laboratories have employed different methods to optimize and ascertain the extent of human cell engraftment. In addition, there appears to be significant xenogeneic host-versus-graft and graft-versus-host reactions, as well as lethal EBV-induced B-cell lymphomas that can spontaneously arise which may further complicate the interpretation of human immunological studies performed in these mice. Despite these obstacles, the huPBL-SCID model has the potential to serve as a model for the examination of human lymphoid cells in an in-vivo setting and has been usefully applied to the study of various human disease states including AIDS, transplantations, autoimmunity and cancer.

Animals↗
PubMed2000

In vitro effects of interleukin-10, prednisolone, and GM-CSF on the non-specific immune function of human polymorphonuclear leucocytes and monocytes.

A wide range of immune-modulating effects make IL-10 a potential therapeutic option in the treatment of numerous diseases pathophysiological based on a dysregulation of cytokine production. The background of this study was to investigate, whether the beneficial effects of a therapeutic immunosuppression with IL-10 may be countered by an increased risk for infections due to impaired effector cell functions of unspecific immunity. We demonstrated the in vitro effects of IL-10 on phagocytosis (P), intracellular killing (K), and chemotactic activity (C) by human neutrophils (PMN) and monocytes (MON) using Candida albicans as test strain and compared the results to the effects of prednisolone and GM-CSF. IL-10 reduced significantly the intracellular killing rate of PMN compared to untreated phagocytes (60 +/- 16% versus 68 +/- 13%, mean +/- SD, p = 0.0002). High dose IL-10 (100 ng/ml) had a stimulating effect on the percentage of phagocytizing MON (70.2 +/- 12.7% vs. 66.9 +/- 14.2%, p = 0.0436), without impairing intracellular killing. Prednisolone reduced significantly the Candida uptake by MON (57 +/- 18.1% vs. 66. 9 +/- 14.2%, p = 0.0019). In contrast to prednisolone, neither MON nor PMN chemotaxis was suppressed by IL-10. In conclusion, IL-10 had only marginal immunosuppressive effects on the unspecific immunity compared to prednisolone.

Anti-Inflammatory Agents↗
PubMed2004

Immune function and organochlorine pollutants in Arctic breeding glaucous gulls.

Organochlorine contaminants (OCs) are known to affect the immune systems of wildlife, and in this study we assessed the relationship between blood concentration of different OCs and measurements relevant to immune status and function in arctic breeding glaucous gulls (Larus hyperboreus). In 1997 and 2001, we counted white blood cells (heterophils and lymphocytes) from blood smears, and in 2000 and 2001 we injected two novel nonpathogenic antigens (diphtheria and tetanus toxoids) into the pectoral muscle of gulls and measured the primary antibody responses. We then related these measurements to the blood concentrations of three pesticides (hexachlorobenzene [HCB], oxychlordane, and p,p'-dichlorodiphenyldichloroethylene) and seven different polychlorinated biphenyl congeners (PCB 101, 99, 118, 153, 138, 180, and 170). There were significant or near significant positive relationships (0.1 > p > 0.001) between most persistent OCs and the levels of heterophils in the blood for both sexes in 1997 and for male gulls in 2001. Similarly, levels of all persistent OCs and lymphocytes were positively related (0.1 > p > 0.001) in both sexes in 1997. This suggests that OCs are causing alterations to immune systems, which may decrease their efficiency and make the birds more susceptible to parasites and diseases. In female gulls, the antibody response to the diphtheria toxoid was significant and negative for HCB (p < 0.01) and weaker, but significant, for oxychlordane (p < 0.05), suggesting that OCs were causing an impairment of the humoral immunity. Various OCs have been linked to negative effects in our study population, including decreased survival and reproduction, and this study suggests that such compounds also affect immune status and function.

Animals↗
PubMedDate not supplied

The role of the growth and lactogenic hormone family in immune function.

The influence of various members of the growth and lactogenic hormone family on the immune system is reviewed. A general hypothesis is proposed for growth control in higher animals. It is suggested that immune reactions, which are based on lymphocyte proliferation, obey the general rules of growth control in vertebrate animals. Growth and lactogenic hormones (GLH) are required for the development and function of the immune system and are suggested to deliver the first signal that prepares the cell for proliferation, differentiation and function. This signal has already been designated by other as the competence signal which initiates the cell cycle. Second signals are delivered through the antigen receptor, and/or by some other cell surface receptors (adhesion molecules) and always involve cell-to-cell ('bridging') and/or cell-to-matrix interaction. This category of signals is designated as stromal or adherence signals. The lymphocyte adhesion molecules that mediate second signals have evolved form organ- and tissue-specific recognition/regulatory molecules. The antigen receptors have been perfected during evolution from self recognition to specific-antigen recognition. Apart from this exquisitely specific mechanism of immune recognition, there is evidence for other less specific means of recognition by adherence molecules that mediate the activation of the immune system during nonspecific injury and also play a role in the elimination of degenerated and neoplastic cells. Signals delivered through adhesion molecules have the power to commit the cell to a given activity which is executed by the delivery of third signals in the form of soluble cytokines, usually, but not always, by the same cell delivering the second signal(s). The combination of these three groups of signals will ultimately determine whether or not the cell will proliferate, differentiate, maintain function or, perhaps, be committed to apoptosis. Therefore, GLH maintain immunocompetence which enables the immune system to respond to specific antigenic and tissue-derived stimuli in a self-regulated fashion. The adrenocorticotropic hormone-adrenal axis antagonizes the immunostimulatory effect of GLH. This basic pattern of lymphocyte regulation is influenced further by additional hormones, neurotransmitters and neuropeptides, mostly by the modulation of signal delivery. The constant interaction of neuroendocrine and internal immunoregulatory mechanisms assures the fine tuning of the immune system, so that it is able to function in homeostasis and harmony with the organism.

Animals↗
PubMed1998

Signs of infections and reduced immune functions at weaning of conventionally reared and specific pathogen free pigs.

The growth rate and several immune parameters were recorded to monitor the performance, health and immune status of 40 piglets in a conventional farrow to finish herd. In addition, effects of weaning on immune parameters were studied under minimal influence of infections in 20 specific pathogen free (SPF) pigs. The growth rate of the conventionally reared pigs decreased after weaning and after allocation of pigs to new premises. Around weaning a considerable number of pigs displayed interferon-alpha (IFN-alpha) in serum, indicating the spread of viral infections. Bacterial infections were indicated by elevated numbers of circulating neutrophilic granulocytes during the weaning period. Functional in vitro tests of peripheral blood mononuclear cells (PBMC) revealed that the Concanavalin A (Con A) induced proliferation decreased both after weaning and after transfer of the conventionally reared pigs to the finishing unit. The decreased proliferation observed after weaning was accompanied by decreased interleukin-2 (IL-2) production in response to the mitogen. A reduced IL-2 producing capacity after weaning was confirmed with PBMC obtained from the SPF pigs. Flow cytometric analyses of these cells showed that the proportion of PBMC expressing IL-2 receptors (IL-2R+) was decreased 3 and 6 days after weaning when cultured in the absence of mitogen while the proportion of IL-2R+ cells was unaltered in Con A stimulated cultures. Thus indications of reduced immune function coincided in time with signs of infections, especially around weaning.

Animals↗
PubMed1995

Cell-mediated immune function and the outcome of chronic fatigue syndrome.

This study examined the importance of cell-mediated immunity in determining the long-term outcome of patients diagnosed with chronic fatigue syndrome (CSF). A total of 103 patients (74%) of 139 previously enrolled in one of two treatment trials conducted within a university hospital referral center was reviewed a mean of 3.2 yr after trial entry. Ongoing symptom severity, levels of disability and immunological function were assessed at follow-up. The relationship between immunological function at trial entry and measures of outcome was also evaluated. Sixty-five patients (63%) had improved, while only 6 (6%) reported no current symptoms. Thirty-one subjects (30%) were unable to perform any form of work and 26 (25%) were on a disability benefit directly attributable to CFS. Cell-mediated immune function, as measured at trial entry or follow-up, did not appear to affect outcome. Whilst improvement occurred in the majority of patients with CFS, a substantial proportion (37%) remained functionally impaired. Impairment of cell-mediated immunological function measured during the course of the illness may not be an important factor in determining long-term outcome.

Adult↗
PubMed2006

Soy isoflavones modulate immune function in healthy postmenopausal women.

BACKGROUND: The immune system may be compromised after menopause because of the effects of aging and diminishing concentrations of estrogen, an immune-modulating hormone. Isoflavones, plant-derived compounds with estrogenic and antioxidant properties, may offer immunologic benefits to women during this stage of life. OBJECTIVE: The objective of this study was to evaluate the effects of soy isoflavones, both in soymilk and in supplement form, on markers of immunity and oxidative stress in postmenopausal women. DESIGN: Postmenopausal women aged 50-65 y (n = 52) enrolled in this 16-wk double-blind, placebo-controlled trial were randomly assigned to 1 of 3 experimental groups: 1) control, 706 mL cow milk/d plus a placebo supplement; 2) soymilk, 71.6 mg isoflavones derived from 706 mL soymilk/d plus a placebo supplement; and 3) supplement, 70 mg isoflavones in a supplement plus 706 mL cow milk/d. Plasma and 24-h urine samples were obtained at baseline and at 16 wk. Immune variables included lymphocyte subsets, cytokine production, and markers of inflammation and oxidative damage. RESULTS: Isoflavone intervention in postmenopausal women resulted in higher (P < 0.05) B cell populations and lower (P < 0.05) plasma concentrations of 8-hydroxy-2-deoxy-guanosine, an oxidative marker of DNA damage. Isoflavone treatment did not significantly influence concentrations of interferon gamma, interleukin 2, tumor necrosis factor alpha, or C-reactive protein in plasma or of 8-isoprostane in urine. CONCLUSIONS: Soymilk and supplemental isoflavones modulate B cell populations and appear to be protective against DNA damage in postmenopausal women.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1973

Altered immune function in hypercholesterolemic monkeys.

Humoral and cellular immune responses to several antigens were compared in control and hypercholesterolemic groups of monkeys. Chronic hypercholesterolemia, with concomitant hyperphospholipidemia and hypotriglyceridemia, was produced experimentally by feeding monkeys a high-fat, high-cholesterol diet. When studied prior to infection, hypercholesterolemic monkeys exhibited impaired development of precipitating antibodies against ovalbumin, enhanced sensitivity to tuberculin antigen (stimulated apparently by mycobacterial components in complete Freund adjuvant), and an increased rate of clearance of colloidal carbon from blood. During pneumococcal infection the ability of neutrophiles from hypercholesterolemic monkeys to reduce nitroblue tetrazolium dye showed an increase greater than that of control monkeys; both groups exhibited increased but comparable final clearance rates of colloidal carbon, although the increment of increase was smaller in hypercholesterolemic monkeys.

Animals↗
PubMed2001

Immune function of astrocytes.

Astrocytes are the major glial cell within the central nervous system (CNS) and have a number of important physiological properties related to CNS homeostasis. The aspect of astrocyte biology addressed in this review article is the astrocyte as an immunocompetent cell within the brain. The capacity of astrocytes to express class II major histocompatibility complex (MHC) antigens and costimulatory molecules (B7 and CD40) that are critical for antigen presentation and T-cell activation are discussed. The functional role of astrocytes as immune effector cells and how this may influence aspects of inflammation and immune reactivity within the brain follows, emphasizing the involvement of astrocytes in promoting Th2 responses. The ability of astrocytes to produce a wide array of chemokines and cytokines is discussed, with an emphasis on the immunological properties of these mediators. The significance of astrocytic antigen presentation and chemokine/cytokine production to neurological diseases with an immunological component is described.

Animals↗
PubMed2001

Membrane estrogen and glucocorticoid receptors--implications for hormonal control of immune function and autoimmunity.

Membrane steroid receptors (mSRs) have recently re-emerged as candidates for mediating steroid effects which do not fit the paradigm of nuclear transcription factor mechanisms. We have studied two steroid-binding classes of mSRs, and have noted striking similarities in their characteristics (immunocytochemical appearance, biochemical properties, proteolytic sensitivity, signaling pathways, regulation, and molecular origins). These observations strengthen the conclusion that mSRs can be modified versions of intracellular steroid receptors. The membrane estrogen receptors (mERs) we studied are involved in estrogen-induced release of prolactin. Membrane glucocorticoid receptors (mGRs) in both mouse and human lymphoma cells are necessary for the initiation of glucocorticoid-induced therapeutic apoptosis which is related to the developmental phenomenon of thymic involution. Diseases of autoimmunity such as systemic lupus erythematosus and arthritis are related to estrogen status. Since both of these mSRs have recently been found in both normal and cancerous lymphoid cells, actions of these mSRs may have important consequences for functions and diseases of the immune system. Therefore, the study of these forms of steroid receptors may present novel therapeutic opportunities for the use of steroids and steroid analogs.

Animals↗
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↗
PubMed2006

MyD88 innate immune function in a zebrafish embryo infection model.

Innate immunity signaling mechanisms during vertebrate embryogenesis are largely unknown. To study Toll-like receptor (TLR) signaling function in the zebrafish embryo model, we designed an experimental setup for antisense morpholino knockdown under conditions of bacterial infection. Clearance of Salmonella enterica serovar Typhimurium Ra bacteria was significantly impaired after knockdown of myeloid differentiation factor 88 (MyD88), a common adaptor protein in TLR and interleukin-1 receptor signaling. Thereby, we demonstrate for the first time that the innate immune response of the developing embryo involves MyD88-dependent signaling, which further establishes the zebrafish embryo as a model for the study of vertebrate innate immunity.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Pituitary hormones and immune function.

The pituitary gland plays a key role in the regulation of growth, differentiation and function of all cells in the body, including immunocytes. Immune reactions are generated through the proliferation of antigen-specific lymphocyte clones. Growth hormone and prolactin are required for the development of mature lymphocytes and for the maintenance of immunocompetence. These hormones enable lymphocytes to respond to antigen, which is delivered as an adherence signal in the context of major histocompatibility surface molecules of antigen-presenting cells. Numerous other adhesion molecules play a role in the regulation of lymphocyte activation. The activation process is completed by cytokine signalling, after which lymphocyte proliferation, differentiation and functional maturation take place. Interleukins, hormones and growth factors may all function as cytokines. Many lymphocytes exist in the body in a quiescent state, with minimal metabolic activities. These cells are maintained by competence hormones and insulin-like growth factor 1, which are present in the systemic and local environment. Apparently, some steroid hormones, opioid peptides and catecholamines are capable of modulating delivery of the signal from the lymphocyte membrane receptor to the nucleus. Steroid and thyroid hormones control nuclear transcription factors as their receptors, and thus are powerful regulators of lymphocyte signalling at the nuclear level. The bioactive forms of thyroid hormone and of several steroid hormones are generated locally by immunocytes. These important hormonal immunoregulators function both at systemic and local levels. Glucocorticoids are major regulators of cytokine production, and alpha-melanocyte-stimulating hormone functions as a powerful cytokine antagonist. The hormones secreted or regulated by the pituitary gland therefore regulate every level of immune activity, including the competence of lymphocytes to respond to immune/inflammatory stimuli, signal transduction, gene activation, the production and activity of cytokines and other immune effector functions.

Animals↗