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PubMed1984

Crossed immunoelectrophoresis for the detection of split products of the third complement component in dengue hemorrhagic fever. II. In vitro activation by dengue viral antigen.

The ability of dengue viral antigen(s) from different sources, and performed antigen-antibody complexes, to activate the third component of human complement (C3) in vitro was demonstrated by using split products of human C3. Dengue type 2 viral antigen(s) from suckling mouse brain and from infected monocytes activated C3 via the alternative pathway, while performed soluble dengue-2 antibody complex activated mainly the classical pathway. The implications of this finding for the pathogenesis of dengue hemorrhagic fever are discussed.

Animals↗
PubMed1991

[Differential diagnosis of kidney transplant rejection and ciclosporin nephrotoxicity by urine cytology].

To make the differentiation of kidney transplant acute rejection and ciclosporin (CS) nephrotoxicity urine cytology by classical Papanicolaou with immunocytochemical stain has been performed. Increased numbers of renal tubular cells with lymphocytes and monocytes were found in both rejections and CS toxicities. CS toxicities were associated with increased numbers of proximal tubular cells. In immunocytochemical stain, increased numbers of CD25 and CD8 positive cells as well as increased ratio of HLA-DR/cytokeratin positive cells were typically found in rejections. It is concluded that the proposed analysis of urine cytology is a non-invasive and reliable method for daily graft monitoring of acute rejection and CS toxicity.

CD8 Antigens↗
PubMed2003

Regulated secretion of macrophage migration inhibitory factor is mediated by a non-classical pathway involving an ABC transporter.

The cytokine macrophage migration inhibitory factor (MIF) is inducibly secreted by immune cells and certain other cell types to critically participate in the regulation of the host immune response. However, MIF does not contain a N-terminal signal sequence and the mechanism of MIF secretion is unknown. Here we show in a model of endotoxin-stimulated THP-1 monocytes that MIF does not enter the endoplasmatic reticulum and that MIF secretion is not inhibited by monensin or brefeldin A, demonstrating that MIF secretion occurs via a non-classical export route. Glyburide and probenicide but not other typical inhibitors of non-classical protein export strongly block MIF secretion, indicating that the export pathway of MIF involves an ABCA1 transporter.

ATP Binding Cassette Transporter 1↗
PubMed1983

Analysis of chemotactic factor generation in C1q-deficient sera.

The roles of the classical and alternative complement pathways in the formation of chemotactic factors in normal human serum and in sera from patients with an inherited selective deficiency of C1q were studied. Monocytic chemotaxis was evaluated in serum activated by zymosan, endotoxin, cobra venom factor, aggregated human IgG and immune complexes. Chemotactic activity was only impaired when the C1q-deficient serum concentration was low or the period of exposure to zymosan, endotoxin or immune complexes was short. No effect was demonstrated when cobra venom factor and aggregated human IgG were used as activating agents even at limited serum concentrations. Chemotactic activity was also impaired when deficient sera were chelated with EGTA and activated with immune complexes during 7 and 60 min. The addition of normal human serum or purified human C1q to the assay resulted in improvement or normalization of the chemotactic function. The observation that the formation of chemotactic factors via the alternative pathway requires a higher serum concentration and/or longer activation time, points out the necessity for an intact classical pathway in order to achieve optimal activation of the alternative pathway.

Antigen-Antibody Complex↗
PubMed1981

Pseudo-lymphocyte monocytes--the memory cells responsible for the development of epitheloid cell granulomata. A new hypothesis.

This hypothesis proposes that, in individuals with an appropriate genetic background, monocyte memory cells are formed when histiocytes and macrophages undergo mitosis following first exposure to a granulomagenic agent and circulate as pseudolymphocytes in the lymphocyte null cell population. It is proposed that epithelioid cell granulomata develop from a clone of cells formed from monocyte memory cells on the second or subsequent exposure to the same granulomagenic agent. Epithelioid cell granuloma formation is therefore not dependent on T-cell function, although the cellular nature of the granuloma appears to depend upon the nature of a concomitant but independent classical immune response. The implications of pseudolymphocyte memory cells on the development of granulomata of both exogenous and endogenous origin, and the relationships between lymphocytes and cells of the monocytic phagocyte series are discussed.

Animals↗
PubMed2001

Lipopolysaccharide and phorbol 12-myristate 13-acetate both impair monocyte differentiation, relating cellular function to virus susceptibility.

Both lipopolysaccharide (LPS) and phorbol 12-myristate 13-acetate (PMA) impeded monocyte to macrophage differentiation with respect to typical phenotypic modulation and certain phagocyte-related processes. The down-regulation of the porcine monocyte marker SWC1, and up-regulation of the SWC9 macrophage marker were retarded, but not inhibited, as was the differentiation-associated down-regulation of p53 and myeloperoxidase. Despite this clear impairment of macrophage differentiation, not all cellular functions were equally susceptible. Both agents inhibited phagocytosis, but not low-density lipoprotein receptor-associated endocytosis. Only LPS inhibited tartrate-resistant acid phosphatase up-regulation. In contrast, increase of vacuolar acidification rates was more susceptible to PMA. The activity of certain endosomal/lysosomal enzymes - esterase, nucleotidase, peroxidase and cathepsins - was generally enhanced by both LPS and PMA. This contrasted with autophagosomal activity, detected through the induction of an antiviral state. Disruption of autophagosomes and lysosomes (methionine-O-methyl ester), but not lysosomes alone (glycyl-L-phenylalanine) reversed LPS-induced inhibition of virus replication, without influencing the PMA-induced antiviral effect. Thus, PMA is similar to LPS in inhibiting monocyte to macrophage differentiation, when primary blood monocytes are employed, but not all pathways are equally susceptible. The analyses demonstrate that the pathways modulated during monocyte differentiation function somewhat independently. Moreover, certain functions of monocytic cells are more important with respect to the outcome of virus infection, with autophagosomal activities in particular favouring cell survival.

African Swine Fever Virus↗
PubMed2006

Increased proteolysis of diphtheria toxin by human monocytes after heat shock: a subsidiary role for heat-shock protein 70 in antigen processing.

The expression of heat-shock proteins (hsp) increases after exposure to various stresses including elevated temperatures, oxidative injury, infection and inflammation. As molecular chaperones, hsp have been shown to participate in antigen processing and presentation, in part through increasing the stability and expression of major histocompatibility complex molecules. Heat shock selectively increases human T-cell responses to processed antigen, but does not affect T-cell proliferation induced by non-processed antigens. Here, we have analysed the mechanisms by which stress such as heat shock, and the ensuing hsp over-expression affect the processing of diphtheria toxin (DT) in peripheral blood monocytes. We found that heat shock increased DT proteolysis in endosomes and lysosomes while the activities of the cathepsins B and D, classically involved in DT proteolysis, were decreased. These effects correlated with the heat-shock-mediated increase in hsp 70 expression observed in endosomes and lysosomes. Actinomycin D or blocking anti-hsp 70 antibodies abolished the heat-shock-mediated increase in DT proteolysis. These data indicate that the increased expression of hsp 70 constitutes a subsidiary mechanism that facilitates antigen proteolysis in stressed cells. Confirming these data, presentation by formaldehyde-fixed cells of DT proteolysates that were obtained with endosomes and lysosomes from heat-shocked peripheral blood monocytes showed higher stimulation of T cells than those generated with endosomes and lysosomes from control peripheral blood monocytes.

Antigen Presentation↗
PubMed2004

IFN-gamma induces gp91phox expression in human monocytes via protein kinase C-dependent phosphorylation of PU.1.

We previously reported that the stimulation of human blood monocytes with IFN-gamma induces the binding of PU.1 to the gp91(phox) promoter and the consequent expression of gp91(phox). In this study, we show that the effect of IFN-gamma is reproduced by the serine phosphatase inhibitor, okadaic acid, and this suggests that serine kinases could be involved in gp91(phox) expression. We also show that IFN-gamma induces the serine/threonine phosphorylation of PU.1 in cultured monocytes. This phosphorylation, as well as the IFN-gamma-induced PU.1 binding and gp91(phox) protein synthesis, is slightly affected by the casein kinase II inhibitor, daidzein, but is abrogated by the protein kinase C (PKC) -alpha and -beta inhibitor, Go6976, and by synthetic peptides with sequences based on the endogenous pseudosubstrate region of the classical PKC alpha and beta isoforms. In contrast, peptides reproducing the pseudosubstrate region of PKC epsilon were without effect. Moreover, we found that the treatment of monocytes with IFN-gamma induces the nuclear translocation and the activation of PKC alpha and beta I, but not of PKC beta II, and that the IFN-gamma-induced phosphorylation of PU.1 was greatly reduced by LY333531, a selective inhibitor of PKC beta isoforms. Finally, nuclear run-on assays demonstrated that while the PKC inhibitors, Go6976 and LY333531, decrease the IFN-gamma-induced gp91(phox) transcription, the serine phosphatase inhibitor, okadaic acid, enhances the gp91(phox) gene transcription. Our results indicate that in cultured monocytes, IFN-gamma induces the binding of PU.1 to the gp91(phox) promoter and the expression of gp91(phox) by phosphorylation of PU.1 via activation of PKC alpha and/or beta I.

Active Transport, Cell Nucleus↗
PubMed2003

[Role of coronary risk factors in blood thrombogenicity and acute coronary syndromes].

Recent advances in basic science have linked some systemic risk factors to endothelial dysfunction which gives rise to atherosclerotic disease and triggers the progression of thrombotic complications. Superficial erosion of the stenotic plaque can be observed in one-third of acute coronary syndromes (ACS). In these cases the presence of classic risk factors such as diabetes mellitus, hypercholesterolemia and smoking favor a state of "vulnerable blood" or high risk. Increased thrombogenicity can exacerbate thrombus formation and is able to trigger an ACS. The vessel endothelium regulates contractile, mitogenic and thrombotic activities of the vessel wall. Risk factors impair both homeostasis and hemostasis of the vessel wall and promote inflammatory signals. Platelet and monocyte activation favors the expression of tissue factor (TF), thus triggering the coagulation cascade with thrombin generation and clot formation. Increased blood thrombogenicity linked to classic risk factors may be associated with circulating TF levels which are much higher than those observed in healthy subjects without risk factors. These observations not only emphasize the usefulness of aggressive management of risk factors but open a new avenue for future studies to devise therapeutic strategies to treat ACS by inhibiting TF expression.

Acute Disease↗
PubMed2000

Functional characterization of HLA-F and binding of HLA-F tetramers to ILT2 and ILT4 receptors.

HLA-F is a human non-classical MHC molecule. Recombinant HLA-F heavy chain was refolded with 2-microglobulin to form a stable complex. This complex was used as an immunogen to produce a highly specific, high-affinity monoclonal antibody (FG1) that was used to study directly the cellular biology and tissue distribution of HLA-F. HLA-F has a restricted pattern of tissue expression in tonsil, spleen, and thymus. HLA-F could be immunoprecipitated from B cell lines and from HUT-78, a T cell line. HLA-F binds TAP, but unlike the classical human class I molecules, was undetected at the cell surface. HLA-F tetramers stain peripheral blood monocytes and B cells. HLA-F tetramer binding could be conferred on non-binding cells by transfection with the inhibitory receptors ILT2 and ILT4. Surface plasmon resonance studies demonstrated a direct molecular interaction of HLA-F with ILT2 and ILT4. These results, together with structural predictions based on the sequence of HLA-F, suggest that HLA-F may be a peptide binding molecule and may reach the cell surface under favorable conditions, which may include the presence of specific peptide or peptides. At the cell surface it would be capable of interacting with LIR1 (ILT2) and LIR2 (ILT4) receptors and so altering the activation threshold of immune effector cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

CD154+ graft antigen-specific CD4+ T cells are sufficient for chronic rejection of minor antigen incompatible heart grafts.

We used a defined model system to address the role of minor histocompatibility antigen-specific CD4+ T cells in chronic rejection. The coronary arteries of vascularized heart grafts expressing the model antigen ovalbumin developed intimal hyperplasia in normal recipients and those lacking CD8+ T cells but not in those lacking CD4+ T cells. Furthermore, purified ovalbumin-specific CD4+ T cells from T-cell antigen receptor transgenic mice caused intimal hyperplasia in ovalbumin-expressing heart grafts in lymphocyte-deficient mice. The graft antigen-specific CD4+ T cells only caused intimal hyperplasia when expressing CD154 and were found in the intima of the affected coronary arteries along with CD40+ cells, CD11c+ dendritic cells and CD11b+, Gr-1+ monocytes. These results show that minor histocompatibility antigen-specific CD4+ T cells are required to cause the classical vascular changes of chronic rejection. They are capable of doing so without contributions from other lymphocytes, and may cause intimal hyperplasia by using CD154 to stimulate other non-lymphoid cells in the intima.

Animals↗
PubMed2000

Quantitation of CD95 and CD95L mRNA expression in chronic and acute HIV-1 infection by competitive RT-PCR.

Human immunodeficiency virus-type 1 (HIV-1) infection is characterized by increased immune cell apoptosis. Apoptosis can be triggered by signals that arise from within the cell, or by signals that are elicited by binding of extracellular "death ligands" to their "death receptors," most of which belong to the tumor necrosis factor (TNF)-receptor family, such as CD95 (Fas/Apo-1). In immune cells the oligomerization of CD95, induced by its ligand CD95L, and the recruitment of different intracytoplasmic molecules that in turn activate FLICE/caspase 8 are crucial. To study the role of CD95/CD95L interactions during HIV-1 infection, we developed an original method based upon quantitative-competitive (QC) RT-PCR that allowed us to quantify the amounts of mRNA coding for the total (tCD95) and membrane (mCD95) forms of CD95. We first studied the expression of different forms of CD95 mRNA in a classical model of chronic HIV infection using two infected cell lines of different origin--lymphocytic (ACH-2) or monocytic (U1). We have shown that infected cells of monocytic origin preferentially produce the "protective" (soluble) form of CD95, and no detectable CD95L mRNA, while lymphoid cells produce more mRNA for the membrane form of CD95 (which triggers apoptosis) along with low but detectable amounts of CD95L mRNA. One can hypothesize that a complex balance exists between pro-apoptotic events, perhaps triggered by the host to limit viral production, and anti-apoptotic events likely triggered by the virus to increase its production and survival. In cells of monocytic origin, which act as a reservoir for the virus, the anti-apoptotic molecules are favored; in cells of lymphocytic origin, molecules with an apoptotic meaning are prevalent.

Apoptosis↗
PubMed2005

Shiga toxin 2 and lipopolysaccharide induce human microvascular endothelial cells to release chemokines and factors that stimulate platelet function.

Shiga toxins (Stxs) produced by Shigella dysenteriae type 1 and enterohemorrhagic Escherichia coli are the most common cause of hemolytic-uremic syndrome (HUS). It is well established that vascular endothelial cells, mainly those located in the renal microvasculature, are targets for Stxs. The aim of the present research was to evaluate whether E. coli-derived Shiga toxin 2 (Stx2) incubated with human microvascular endothelial cells (HMEC-1) induces release of chemokines and other factors that might stimulate platelet function. HMEC-1 were exposed for 24 h in vitro to Stx2, lipopolysaccharide (LPS), or the Stx2-LPS combination, and chemokine production was assessed by immunoassay. More interleukin-8 was released than stromal cell-derived factor 1alpha (SDF-1alpha) or SDF-1beta and RANTES. The Stx2-LPS combination potentiated chemokine release, but Stx2 alone caused more release of SDF-1alpha at 24 h than LPS or Stx2-LPS did. In the presence of low ADP levels, HMEC-1 supernatants activated platelet function assessed by classical aggregometry, single-particle counting, granule secretion, P-selectin exposure, and the formation of platelet-monocyte aggregates. Supernatants from HMEC-1 exposed only to Stx2 exhibited enhanced exposure of platelet P-selectin and platelet-THP-1 cell interactions. Blockade of platelet cyclooxygenase by indomethacin prevented functional activation. The chemokine RANTES enhanced platelet aggregation induced by SDF-1alpha, macrophage-derived chemokine, or thymus and activation-regulated chemokine in the presence of very low ADP levels. These data support the hypothesis that microvascular endothelial cells exposed to E. coli O157:H7-derived Stx2 and LPS release chemokines and other factors, which when combined with low levels of primary agonists, such as ADP, cause platelet activation and promote the renal thrombosis associated with HUS.

Blood Platelets↗
PubMed1996

In vitro He-Ne laser effect on some immunological functions of the polymorphonuclears and monocytes in rabbits.

The aim of this study is to evaluate in vitro the effect of Helium-Neon (He-Ne) laser irradiation on the viability, adherence, phagocytic activity of the polymorphonuclears and monocytes. Also the level of metabolic processes in phagocytizing blood cells, monocytes and polymorphonuclears was estimated and evaluated by the INT-test. Evaluation of the leukocyte adherence, the method of MacGregor was used. Phagocytic activity was examined by classical method using microspherical hydrophilic particles (Hema-particles). He-Ne laser in a small dosage (< or = 0.8 J) increases the leukocyte adherence, after higher laser irradiation dosage (> 1.2 J) the leukocyte adherence is decreased. The laser effect on the phagocytic activity of both types of blood cells, polymorphonuclears and monocytes is similar. Small dosage of the laser irradiation increases the phagocytic activity, and after higher laser irradiation phagocytic activity is decreased. Also the changes of the level of metabolic processes in the phagocytizing cells are very similar with the changes of phagocytic activity. The viability of the blood cells examined after higher laser irradiation is gradually decreased.

Animals↗
PubMedDate not supplied

Immunoregulating properties of peptides related to tumor rejection antigens: effect on human monocytes and natural killer cells.

The authors analyzed the effect of several 15-amino acid peptides with sequences related to tumor-rejection antigens, tyrosinase, and the MAGE family on peripheral blood mononuclear cells from healthy donors cultured for periods of 1 to 7 days. Some of these peptides promoted stimulation of monocytes, manifested by phenotypic changes, release of interleukin (IL)-1a, IL-6, and tumor necrosis factor-alpha, and induction of nitric oxide synthase on differentiated CD14++/+ CD16+ DR++ monocytes. An increase in the percentage of cytotoxic monocytes (CD14+/- CD16+) containing granule-associated DNase activity was also observed. Active peptides induced the release of IL-2 and interferon-gamma. Nonspecific natural killer and lymphokine-activated killer cell-mediated cytotoxicity was also observed against classical target cell lines (K-562 and Daudi) and allogenic melanoma cell lines AC and BB, together with an increase in granule-associated DNase in the natural killer cell-enriched population. Monocytes were needed to enhance this innate response, because peptides failed to induce the release of IL-2 on monocyte-depleted peripheral blood mononuclear cells. Data show an enhancement of the rapid innate immune response by peptides related to tumor rejection antigens and suggest that they could also determine the nature of a slow and more definitive specific immune response against tumor cells.

Adjuvants, Immunologic↗
PubMed1991

Monocyte chemotactic activity in sera after hypnotically induced emotional states.

In a number of studies it has been shown that psychological factors in general and specifically emotional factors can be correlated to changes in immunological function and defence mechanisms. Although the mediating pathways between the central nervous system and the immune system still remain unclear, it is known that some of the 'classical stress hormones' such as cortisol and catecholamines have modulatory effects on different immunological parameters. In this investigation we wished to study the effect of brief hypnotically induced emotional states on monocyte chemotaxis and endocrinological parameters. Eleven highly hypnotically susceptible volunteers were, while in a deep trance, given suggestions to re-experience earlier life experiences involving intense anger and depression in random order. Before concluding hypnosis subjects were given suggestions to re-experience a feeling of happiness and well-being. Monocyte chemotactic activity in sera and serum levels of cortisol, as well as venous plasma levels of the catecholamines epinephrine, norepinephrine, DOPA and DOPAC, were measured before hypnosis, after each emotional state and immediately after hypnosis. The results showed a significant differences (P less than 0.02) in chemotactic activity between the angry and the depressed emotional states, the depressed state exhibiting a decreased chemotactic index compared with the angry state. Chemotactic index after the happy relaxed emotional state also showed a significant (P less than 0.01) increase compared with both chemotactic index before hypnosis and chemotactic activity after the angry and depressed state. Though there were significant differences between emotions and between emotions and the before-hypnosis-condition, no clear-cut significant differences between the emotional states of anger and depression could be detected for serum cortisol levels and catecholamine plasma levels. Significant positive correlations (P less than 0.01) for differences in chemotactic activity and differences in plasma DOPA levels between emotional states was found. When investigated in vitro, DOPA did not in itself exhibit monocyte chemotactic properties. No other significant correlations between differences in chemotactic activity and other endocrinological parameters could be detected. Soluble interleukin-2 receptors in serum were also measured. No significant differences were found.

Anger↗
PubMed2006

[Expression of fragile histidine triad (FHIT) protein and its significance in diagnosing classical Hodgkin lymphoma].

OBJECTIVE: To study the expression of FHIT protein and its potential application in diagnosing classic Hodgkin lymphoma. METHODS: Immunohistochemical study using EnVision method for FHIT tumor suppressor protein, hematopoietic stem cell markers CD133/AC133 and CD34, B-cell marker CD20, T-cell marker CD3 and oncoprotein c-erbB2 was performed on 33 cases of classic Hodgkin lymphoma. RESULTS: Thirty-three of the Hodgkin lymphoma cases (90.9%) expressed FHIT protein. The antigen was mainly located in the cytoplasm, nucleus and membrane of classic Reed-Sternberg and Reed-Sternberg-like cells. Normal B and T lymphocytes, as well as their malignant counterparts, were negative for FHIT protein; whereas monocytes, histiocytes and dendritic cells were positive. All the cases studied were negative for CD133/AC133, CD34, CD3 and c-erbB-2. Two of the 33 cases showed positive staining for CD20 in some of the Reed-Sternberg cells. CONCLUSION: The expression of FHIT protein can be used as a useful adjunct in diagnosing classic Hodgkin lymphoma.

AC133 Antigen↗