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Results for “immune modulation”

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At least 361 records · Page 20Linked to original sources
PubMed1997

Inhibition of protein kinase A and cyclic AMP response element (CRE)-specific transcription factor binding by delta9-tetrahydrocannabinol (delta9-THC): a putative mechanism of cannabinoid-induced immune modulation.

Delta9-Tetrahydrocannabinol (delta9-THC) binding to cannabinoid receptors induces an inhibition in adenylate cyclase activity through the engagement of a pertussis toxin-sensitive GTP-binding protein. In this study we investigated the ramifications of decreased cyclic AMP (cAMP) formation by delta9-THC on signaling events through the cAMP pathway distal to adenylate cyclase in mouse splenocytes. Delta9-THC treatment produced a marked and concentration-related decrease in forskolin-inducible protein kinase A (PKA) activity. This decrease in kinase activity was due to an inhibition in cAMP formation and not through a direct effect on the kinase as evidenced by the fact that PKA activity could not be modulated directly by delta9-THC in the presence of exogenous cAMP. One of the primary roles of PKA in this signaling pathway is to activate transcription factors for subsequent binding to cAMP response elements (CRE) present in the promoter region of cAMP-responsive genes. In the present studies, we observed that forskolin treatment of splenocytes resulted in a rapid activation of trans-acting factor binding to the CRE, which peaked at 30-60 min and whose binding was repressed concentration dependently in the presence of delta9-THC. As with forskolin, mitogenic stimulation including anti-CD3 mAb or phorbol ester plus ionomycin treatment of splenocytes induced CRE binding activity, which was maximal around 60 min and was suppressed by delta9-THC treatment. In conclusion, these data indicate that cAMP-mediated signal transduction is inhibited by delta9-THC and consequently leads to a decrease in the activation of transcription factors that bind to CRE regulatory sites.

Animals↗
PubMed1979

Effect of potential cytostatic and immune modulating chemicals on the plasma membrane of red blood cells (RBC) as revealed by osmotic hemolysis, cell electrophoresis and scanning electron microscopy (SEM).

The influence on red blood cells (RBC) of two cancerostatic-(ZIMET 3106 and ZIMET 3393) and two immunomodulating agents (ZIMET 3164 and ZIMET 86/76) administered subcutaneously, or intraperitoneally in case of the radiolabelled N-mustard compounds, to mice, was studied by means of measurements of the radiolabelled compounds in blood, by cell electrophoresis, filipin-induced hemolysis of pretreated RBC and by scanning electronmicroscopy. The portion of doses applied which binds to RBC-surface decreases in the sequence of ZIMET 3106, ZIMET 3164, ZIMET 3393 and ZIMET 86/76. However, the highest reduction of the electrophoretic mobility and protection from filipin-induced hemolysis of pretreated RBC was found with ZIMET 3164. In both tests ZIMET 86/76 proved to be ineffective. These findings are in good agreement with the modifications demonstrated in pretreated RBC after filipin-induced hemolysis by means of SEM. The results presented point to a N-mustard specific interaction between the cholesterol of the membrane and/or other membrane constituents. However, these fundamental differences found in binding affinity, surface-charges and membrane interactions caused by the chemically similar compounds cannot be attributed merely to the N-mustard group.

Animals↗
PubMed2003

IFN alpha-2a protects mice against a helminth infection of the liver and modulates immune responses.

BACKGROUND & AIMS: Hepatic alveolar echinococcosis (AE), caused by the larval growth of Echinococcus multilocularis, is one of the most lethal helminthic diseases with no satisfactory treatment. Advances in the understanding of the host's immune response (Th2 responses associated with a progressive form of AE), have driven the research towards immune stimulation as an alternative possibility to treat patients. We previously reported clinical stabilization associated with a shift from a Th2 to a Th1 cytokine profile in an AE patient treated with interferon (IFN)alpha. METHODS: The effects of recombinant IFN alpha-2a were analyzed in the susceptible C57BL/6J E. multilocularis infected mice. Parasitic burden, macrophage functions, and specific T-cell responses were studied 15, 45, and 90 days postinfection. RESULTS: After 90 days postinfection, 75% of infected IFN alpha-2a-treated mice had no hepatic lesions and half were fully protected. IFN alpha-2a treatment markedly decreased the abnormally elevated production of IL-10 in both spleen cell cultures and peritoneal macrophage cultures from infected mice and restored phagocytosis and oxidative metabolism of macrophages. It also inhibited IL-6 and IL-13 antigen-induced secretions in spleen cell cultures. CONCLUSIONS: Through its immunoregulatory properties, IFN alpha-2a may be effective in a helminthic liver infection and is a promising candidate for clinical application in AE.

Animals↗
PubMed2003

Major royal jelly protein 3 modulates immune responses in vitro and in vivo.

We have recently shown that royal jelly has potent antiallergic properties in a mouse model of immediate hypersensitivity. However, it is still unclear which components of royal jelly exhibit antiallergic activity. In this study, we have screened for antiallergic factors in royal jelly based on inhibition of IL-4 production by anti-CD3 stimulated spleen cells derived from OVA/alum-immunized mice. Using a series of column chromatographies, we purified a 70 kDa glycoprotein, major royal jelly protein 3 (MRJP3), that suppresses IL-4 production. In in vitro experiments, MRJP3 suppressed the production of not only IL-4 but also that of IL-2 and IFN-gamma by T cells concomitant with inhibition of proliferation. The MRJP3-mediated suppression of IL-4 production was also evident when lymph node cells from OVA/alum-immunized mice were stimulated with OVA plus antigen presenting cells. We next examined the purified suppressive factor on OVA/alum-induced allergic responses in mice. Interestingly, in spite of the antigenicity of MRJP3 itself as an extraneous foreign protein, intraperitoneal administration of MRJP3 inhibited serum anti-OVA IgE and IgG1 levels in immunized mice. In addition, heat-treated soluble MRJP3 treatment reduced its antigenicity while maintaining its inhibitory effects on antibody responses to OVA. These results indicate that MRJP3 can exhibit potent immunoregulatory effects in vitro and in vivo. Furthermore, considering the intriguing immunomodulatory effects of MRJP3, it may be of clinical significance to design MRJP3-derived antiallergic peptides by identifying the associated polypeptide regions.

Adjuvants, Immunologic↗
PubMed2003

Evidence for modulated immune response to Anaplasma phagocytophila sensu lato in cats with FIV-induced immunosuppression.

Human granulocytic ehrlichiosis (HGE) is an emerging infectious disease in which some patients experience unusual opportunistic infections. In this study, cats infected with the HGE agent, Anaplasma phagocytophila s.l., had clinical granulocytic ehrlichiosis (GE), anti-nuclear antibodies and increased IFN-gamma mRNA. In FIV-immunosuppressed cats with GE, there was upregulated IL-10 transcription but not IFN-gamma. Cats with FIV had poor response to vaccines, regardless of GE status. This preliminary report demonstrates that cats with FIV-infection make a good model of ehrlichiosis in an immunocompromised host, and that viral immunosuppression may not increase the severity of ehrlichiosis but may attenuate immune responses to the pathogen.

Anaplasma phagocytophilum↗
PubMed2000

Immunocalins: a lipocalin subfamily that modulates immune and inflammatory responses.

A subset of the lipocalins, notably alpha(1)-acid glycoprotein, alpha(1)-microglobulin, and glycodelin, exert significant immunomodulatory effects in vitro. Interestingly, all three are encoded from the q32-34 region of human chromosome 9, together with at least four other lipocalins (neutrophil gelatinase-associated lipocalin, complement factor gamma-subunit, tear prealbumin, and prostaglandin D synthase) that also may have anti-inflammatory and/or antimicrobial activity. This review addresses important features of this genetically linked subfamily of lipocalins (involvement with the acute phase response, immunomodulatory and anti-inflammatory properties, the tissue localization, complex formation with other proteins and receptors, etc.). It is likely that these proteins have evolved to be an integrated part of the body's defense system as part of the extended cytokine network. Its members exert a regulatory, dampening influence on the inflammatory cascade, thereby protecting against tissue damage from excessive inflammation. That most major mammalian allergens are lipocalins may reflect this connection of lipocalins with the immune system. We propose that this immunologically active lipocalin subset be named the 'immunocalins', signifying not only the structural homology and close genetic linkage of its members, but also their protective involvement with immunological and inflammatory processes. As immune mediators, immunocalins appear to use at least three interactive sites: the lipocalin 'pocket', binding sites for other plasma proteins, and binding sites for cell surface receptors.

Acute-Phase Reaction↗
PubMed1993

Immune modulation of adhesion molecules ICAM-1 (CD54) and LFA-3 (CD58) in human hepatocytic cell lines.

Interactions between leukocytes such as T cells and accessory or target cells are promoted by adhesion molecules, in particular intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-3 (LFA-3). Hepatocytes are usually negative for these surface membrane proteins which, however, may be up-regulated in inflammatory processes within the liver. Because the regulatory signals for, and tissue distribution of, these adhesion molecules vary among different tissues, expression of ICAM-1 and LFA-3 was studied in the Hep-G2 and SK-Hep-1 human hepatocytic cell lines in vitro. Low, constitutive membrane expression of the two molecules was detected in both cell lines. ICAM-1, but not LFA-3, was rapidly up-regulated by interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF), and to some extent by interferon-gamma (IFN) and IL-6, whereas IL-4 had variable low effects, if any. Considerable synergism on ICAM-1 protein levels was observed after stimulation with TNF, IL-1, and IFN, whereas co-incubation with actinomycin D abolished these effects. ICAM-1 mRNA levels increased 16-20 times after cytokine incubation. Our data indicated that hepatocytes share the regulatory pathways for ICAM-1 described for several other cell types. Absence of these molecules in vivo may reflect a dominance of negative modulation signals in the normal liver, which might also explain the low levels of HLA class I molecules.

Antigens, CD↗
PubMed1984

The use of three baseline values in intervention studies: application to evaluation of immune modulation therapies.

In studying the effects of a treatment intervention on immunological parameters, we have found that three baseline values are a practical number to obtain on each patient. Three baseline values 1) increase the chances of detecting a statistically significant effect of the intervention, 2) provide an assessment of the daily variability of the assay and patients, and 3) enable the identification of individual patients who demonstrate significant changes associated with the intervention.

Drug Evaluation↗
PubMed1982

Immune modulation by epidermal cell products: possible role of ETAF in inflammatory and neoplastic skin diseases.

Recent studies have indicated that the epidermis plays an important role in the modulation of immunologic reactions. The factors involved in these processes include not only Langerhans cells but also keratinocyte products. One of these products, ETAF (Epidermal cell derived Thymocyte Activating Factor), which is similar to the macrophage derived product interleukin 1 (IL-1), is reviewed. Speculations as to its possible role in skin diseases are presented.

Antigens↗
PubMed2001

Th1 genetic adjuvants modulate immune responses in neonates.

In these studies, we address the ability of DNA encoding Th1 cytokines to bias the isotype of antibody raised by neonatal or adult immunization with an influenza hemagglutinin expressing DNA (HA-DNA). Neonatal mice coimmunized with HA-DNA and either IL-12 or IFN-gamma-expressing DNA developed IgG2a-biased immune responses, regardless of inoculation method. In contrast, the Th1 genetic adjuvants had no effect on IgG subtype patterns in adults. In neonatal mice, the Th1 genetic adjuvants also shifted the pattern of lymphokine production by recall splenocytes from a mixed response of IFN-gamma and IL-5 to exclusively IFN-gamma. In adults, despite the failure to change the isotype pattern of the antibody response, a shift towards IFN-gamma production also occurred for recall splenocytes following coimmunzation with IL-12. Thus, coinoculation of Th1 genetic adjuvants had greater effects on the nature of the immune response in the neonate than in adults.

Adjuvants, Immunologic↗
PubMed2003

HLA-G modulates immune responses by diverse receptor interactions.

HLA-G regulates immune responses as it binds different receptors expressed on natural killer (NK) cells, T cells and myeloid cells. HLA-G1 can inhibit NK- and T-cell-mediated lysis of target cells by its interaction with the inhibitory receptors ILT2 and ILT4. Engaging KIR2DL4 triggers different reactions depending on the activation state of the effector cells. The indirect recognition of HLA-G as peptide presented by HLA-E and recognized by the CD94/NKG2 receptor family might further power the battle between the immune system and tumor cells. Secreted HLA-G5 can also bind CD8 and induces Fas/Fas ligand-mediated apoptosis in activated CD8+ lymphocytes.

Animals↗