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PubMed2002

Evasion of host immunity directed by papillomavirus-encoded proteins.

The nature of the interaction between papillomaviruses (PV) and their infected host has led to the identification of ways in which the viral oncoproteins can transform the infected host cells into cancer cells. As viral persistence is required for malignancy, and persistence requires avoidance of immune attack by the host, defining the relationship between PV and the immune system is also paramount in understanding tumorigenesis. It has emerged that PV have evolved several ways in which to prevent clearance by the host immune system. The limitation of the PV replication cycle to the epithelium, together with low level expression of the virus proteins and an absence of inflammation, minimises the exposure of virus to immune cells. In addition, more recently it has been shown that, like many other viruses, PV can directly subvert the immune response, including interference with the interferon pathway, modulation of antigen presentation, inhibition of interleukin-18 activity and down-regulation of major histocompatibility class I on infected cells. Collectively these mechanisms explain how PV lesions are able to persist for long periods of time in immunocompetent hosts.

Female↗
PubMed1987

Modulator effect of Toxoplasma lysate antigen in mice experimentally infected with Plasmodium berghei.

Normal mice were pretreated twice at an interval of 2 weeks with an emulsion of TLA (Toxoplasma lysate antigen), PLA (Plasmodium lysate antigen) or both in LMO (light mineral oil) or with a combination of the emulsion and Obioactin or Tp-LKs (Toxoplasma lymphokines) as an immunopotentiator. They were then given Obioactin or Tp-LKs 3 and 25 days after the first treatment and were further given parasitized erythrocytes with 1 X 10(2)-10(4) P. berghei 2 weeks after the second treatment. Thirty (3/10, number of survival/number of examined) per cent of mice treated with TLA, 50 (5/10)% of those treated with a combination of TLA and Tp-LKs and 60 (6/10)% of those treated with a combination of TLA and Obioactin survived as long as 20 days postinfection while none of untreated controls survived more than 15 days postinfection. Only 18.2 (2/11)% of mice treated with PLA or TLA + PLA survived and 20 (2/10), 18.2 (2/11) and 60 (6/10)% of those treated with TLA + Obioactin, PLA + Obioactin or TLA + PLA + Obioactin survived throughout the experiment, respectively while none of controls survived more than 13 days postinfection. Five mice of each group were killed right before infection, and 5, 10 and 15 days postinfection. In mice treated with TLA + Obioactin, more macrophage phagocytosis and macrophage migration inhibition induced by sensitized T-cells were observed than in those treated otherwise. No appreciable differences were noted according to the method of treatment in blood examination values. Cross immunities between Toxoplasma and Plasmodium antigens were tested by counter-immunoelectrophoresis and indirect fluorescent antibody technique. By using counter-immunoelectrophoresis, a specific precipitin line was observed between TLA and anti-PLA which was absorbed by mouse erythrocytes, leucocytes and liver powder. By the indirect fluorescent antibody technique, anti-Plasmodium IgM and IgG titers were detected in sera from mice treated with TLA or TLA-Obioactin before infection.

Adjuvants, Immunologic↗
PubMed2000

Modulation of HLA-G antigens expression in myelomonocytic cells.

As trophoblast cells and macrophages share cellular characteristics, we investigated the expression of HLA-G antigens during the myelomonocytic differentiation. Analyses with the 87G and 16G1 monoclonal antibodies demonstrated that HLA-G was not expressed in peripheral blood monocytes, in in vitro differentiated dendritic cells and macrophages, and in resident mononuclear phagocytes infiltrating healthy tissues. Conversely, activated macrophages and dendritic cells localized in tumoral biopsies of some lung carcinomas expressed HLA-G antigens. Induction of HLA-G expression at the cell surface of the monohistiocytic cell line U 937 with different cytokines strongly suggests that cytokines secreted during inflammation may be involved in this specific upregulation. Bronchoalveolar macrophages collected from patients suffering from acute HCMV pneumonitis also expressed HLA-G molecules. In vitro, we thus demonstrated that HLA-G antigens are produced during viral reactivation in the macrophages generated after allogeneic stimulation of HCMV latently infected monocytes. Our data suggest that inflammatory processes in lung tissues, like tumoral transformation and HCMV acute infection, are likely to induce HLA-G molecules in infiltrating macrophages and dendritic cells. The expression of molecules capable of downregulating both the innate and adoptive immunity could be a mechanism that helps tumoral and HCMV infected cells to escape immune response.

Acute Disease↗
PubMed1983

Cell culture density modulates the incorporation of HLA antigens by enveloped viruses.

Uninfected, as well as feline leukemia virus (FeLV) infected human cells cultured under high cell density conditions undergo changes in the expression of major histocompatibility complex (MHC) antigens, as determined by indirect trace binding radio immunoassay (RIA) using monoclonal anti-HLA antibodies and by decreased sensitivity to complement mediated cytotoxicity by anti-HLA alloantibodies. FeLV particles produced by the viral infected cells are also sensitive to neutralization by anti-HLA antibodies, suggesting that enveloped viral particles incorporated MHC antigens in the viral envelope. The amount of HLA antigens expressed in the viral enveloped, closely reflects the expression of HLA antigens by the virus-producer lymphoid cells. FeLV-infected HsB-2 (T) and SB (B) lymphoid cells cultured under high cell concentration condition show decreased expression of some HLA antigens (A2, B12, B17), and the viral particles produced by those cells also incorporate lower amounts of such antigens. Our results, based on the findings that human lymphoid cells (uninfected, as well as FeLV infected) show decreased expression of some HLA membrane determinants when grown under high cell density conditions, indicate that no viral selective mechanism operates in the incorporation of HLA determinants by enveloped viruses. Instead, our results suggest that viruses pick up MHC antigens from the host cell membrane according to the concentration of those antigens on the surface of the cells at the time of virus budding.

Animals↗
PubMed2003

Analysis of the role of vaccine adjuvants in modulating dendritic cell activation and antigen presentation in vitro.

We have studied the effects of adjuvant formulations on the activation and antigen-presenting functions of bone marrow-derived dendritic cells (DCs). While LPS could induce high-level expression of MHC Class II and co-stimulator molecules on DCs, it did not enhance antigen presentation to co-stimulation independent DO11.GFP T hybridoma cells. In contrast, alum, NISV and PLGA formulations failed to activate DCs, but NISV and PLGA could enhance antigen-presentation efficiency by 10-100-fold. Irrespective of the previously described antigen release characteristics of each adjuvant, antigen presentation peaked at 6h and waned thereafter for all formulations. Given the importance of DCs in the activation of nai;ve T cell responses, these studies suggest that as yet undefined pathways of DC activation in vivo may underlie the activity of alum, PLGA and NISV adjuvants. Furthermore, as NISV and PLGA do not appear to act as slow-release systems in DCs, the ability of these particulate systems to induce high levels of antigen presentation by DCs probably has a more significant role in their adjuvant activity.

Adjuvants, Immunologic↗
PubMed1997

Effect of IL-4 and IL-12 liposomal formulations on the induction of immune response to bovine herpesvirus type-1 glycoprotein D.

Activation of different T-helper (Th) responses following immunisation has profound and specific influences on the development of the immune response and on the ability of a vaccine to confer protection. Since cytokines are capable of influencing the stimulation of distinct T-cell responses, their encapsulation in vaccines should modulate antigen-specific immune responses. Unfortunately, the use of cytokines in vivo is hampered by their rapid clearance and inactivation. One possible solution to this problem is the use of liposomes to entrap both cytokines and antigen. This approach will not only protect the cytokine but will also deliver the two components simultaneously to the same site. The authors examined, therefore, the immune responses elicited by systemic immunisation of mice with liposome formulations containing a truncated form of bovine herpesvirus type-1 glycoprotein D (tgD) together with IL-4 or IL-12. Subcutaneous immunisation with liposomes containing tgD and IL-12 significantly enhanced the induction of antigen-specific cellular and humoral immune responses. These responses were characterised by an increase in IFN-gamma secreting cells and the induction of tgD-specific IgG2a antibodies. In contrast, encapsulation of IL-4 into tgD-liposomes did not enhance the humoral immune response to gD but significantly influenced the development of antigen-specific IL-4 secreting cells. Our results indicated that encapsulation of IL-12 into the liposomes was necessary for the systemic adjuvant effect and demonstrated the feasibility of using liposome technology and cytokines to manipulate the development of different antigen-specific Th subsets in vivo.

Animals↗
PubMed2003

Prolactin enhances production of interferon-gamma, interleukin-12, and interleukin-10, but not of tumor necrosis factor-alpha, in a stimulus-specific manner.

Prolactin, an anterior pituitary hormone, has been shown to have a role in immunomodulation. Some reports have shown the importance of prolactin in activating lymphocytes and macrophages, while in hyperprolactinemia patients, prolactin was found to decrease lymphocyte activation and natural killer function. In the present work, at physiological (15ng/ml) and stress-induced levels (30ng/ml) of prolactin, interferon-gamma (IFN-gamma) and interleukin (IL)-12 p70 levels, but not of IL-10 and tumor necrosis factor-alpha (TNF-alpha), increased significantly (p<0.05-0.006) in phytohemeagglutinin (PHA)+lipopolysaccharide (LPS)-stimulated whole blood. However, no such effect was observed at high concentrations of prolactin (100-300ng/ml). In addition, 15ng/ml of prolactin reversed hydrocortisone suppressive effect on IFN-gamma, IL-12 p70, and IL-10 production in PHA+LPS-stimulated whole blood. On the other hand, in LPS-stimulated whole blood, prolactin enhanced significantly (p=0.027) the production levels of IL-10, but not of IFN-gamma, IL-12 p70, and TNF-alpha, in non-concentration-dependent manner. These results suggest that prolactin modulates cytokine response during antigenic response, and this modulation is stimulus specific.

Adult↗
PubMed2002

Cell membrane modification for rapid display of proteins as a novel means of immunomodulation: FasL-decorated cells prevent islet graft rejection.

Long-term display of exogenous proteins on the cell surface may have important research and therapeutic implications. We report a novel method for the cell-surface display of proteins that involves generation of a chimeric protein with core streptavidin, biotinylation of cells, and "decoration" with the protein. A chimeric protein with the extracellular portions of FasL (SA-FasL) was efficiently displayed on the cell surface within 2 hr without detectable cellular toxicity. Biotin and SA-FasL persisted on the cell surface for weeks in vitro and in vivo. Immunomodulation with SA-FasL-decorated splenocytes effectively blocked alloreactive responses in naive and presensitized rodents and prevented the rejection of allogeneic pancreatic islets. This approach may serve as an alternative to gene transfer-based expression with broad research and therapeutic applications.

Animals↗
PubMed2003

Expression of CD94-NKG2A inhibitory receptor is restricted to a subset of CD8+ T cells.

Natural killer (NK)-cell receptors (NKRs) on CD8+ T cells can modulate antigen-specific T-cell activity but their function and rules that govern their expression remain unclear. Recent work has provided new insight into CD94-NKG2A expression on T cells. Whereas upregulation on the cell surface is induced following T-cell receptor (TCR) engagement, commitment to CD94-NKG2A expression is a clonal attribute. NKRs can therefore shape cytotoxic T-lymphocyte (CTL) responses and should be considered in designing vaccine therapies.

Animals↗
PubMed1999

Modulatory effects of alveolar macrophages on CD4+ T-cell IL-5 responses correlate with IL-1beta, IL-6, and IL-12 production.

Increasing evidence suggests that the pattern of T-cell cytokine production can be modulated by antigen presenting cell (APC)-derived factors during the cell interactions. Recently, it has been shown that alveolar macrophages (AMs) from atopic asthmatics (AA) but not atopic nonasthmatics (AN) enhance interleukin (IL)-5 production by CD4+ T-cells. The present study compared AM production of IL-1beta, IL-6, and IL-12, as well as their associated functional capacity to influence IL-5 production by allergen-specific CD4+ T-cells in 10 AA, 10 AN, and nine nonatopic control subjects (C). AMs from AA showed a relatively high production of IL-1beta and IL-6 (p<0.05) and a relatively low secretion of IL-12 compared to C, whereas AMs from AN and C behaved similarly. This study confirmed previous findings that co-culture with AMs augments IL-5 production from allergen-stimulated CD4+ T-cells only in AA and not in nonasthmatics even if they are atopic. On the other hand, stimulation with allergen alone did not enhance IL-5 production by CD4+ T-cells in either AA nor AN. AM-induced changes in CD4+ T-cell IL-5 production upon allergen stimulation significantly correlated with their ability to produce IL-1beta (r=0.59, p<0.01), IL-6 (r=0.56, p<0.01), and inversely with IL-12 (r=-64, p=0.002) in all atopic subjects, and even more closely with the ratio of IL-12/IL-1beta (r=-0.75, p<0.001) and IL-12/IL-6 production (r=-0.81, p<0.001) in these subjects. These findings suggest that the role of alveolar macrophages from atopic asthmatics in enhancing interleukin-5 production by allergen-specific CD4+ T-cells is due, at least partly, to their aberrant production of interleukin-1beta, interleukin-6, and particularly of interleukin-12.

Adult↗
PubMed2000

Serum antibody titers to Bacteroides forsythus in elderly subjects with gingivitis or periodontitis.

BACKGROUND: The risks for periodontal disease appear to increase with age. STUDY PURPOSE: To determine associations between clinical findings, the presence of specific bacteria in periodontal pockets, and serum antibody titers. 10 older subjects (mean age=73.0 years SD+/-4.9) with confirmed gingivitis only (gingivitis group) and 10 subjects with periodontitis (mean age: 76.1 years, SD+/-10.4) (periodontitis group) were studied. RESULTS: The mean group differences for probing depth and clinical attachment levels were 4.1 mm and 5.6 mm, respectively, and were significantly different (p<0.001). Both groups had high plaque scores (>60% surfaces with plaque). DNA probes demonstrated that B. forsythus was present in 8/10 samples from the periodontitis group and in 7/10 samples from the gingivitis group. The B. forsythus isolates studied were found in four of the subjects with periodontitis and from 2 of the subjects with gingivitis. Serum antibody titers to 6 ribotypes of B. forsythus were studied. Western blots, gradient gels, and pulsed field gel electrophoresis concurrently demonstrated that the B. forsythus isolates were genotypically, and phenotypically unique for each subject. Antibody titers to two selected B. forsythus isolates were significantly higher in the periodontitis group (p<0.01, Mann-Whitney test). The study confirmed that antibody serum titers to the six different ribotypes of B. forsythus varied greatly between older individuals with gingivitis or periodontitis. Not all strains of B. forsythus elicited higher titers in periodontitis affected subjects. CONCLUSIONS: The results of the present study suggest genotype variation of B. forsythus that is unique to the individual and that serotype variation can be expected. It is possible that B. forsythus under specific host conditions can modulate surface antigen factors to evade the host immune response.

Age Factors↗
PubMed2002

Recognition of the carbohydrate modifications to the RgpA protease of Porphyromonas gingivalis by periodontal patient serum IgG.

Periodontal infections by Porphyromonas gingivalis are associated with a sustained systemic IgG antibody response and elevations in local antibody synthesis to this organism. One of the targets of this response is a protease, RgpAcat, which is an important virulence determinant of this organism. Recently, we demonstrated that this molecule is glycosylated and that the glycan chains are immunologically related to P. gingivalis lipopolysaccharide (LPS) (Curtis et al., Infect Immun 1999;62:3816-3823). In the present study, we examined the role of these glycan additions in the immune recognition of RgpAcat, by sera from adult periodontal patients (n = 25). Serum IgG antibody levels to P. gingivalis W50, RgpAcat and LPS and to recombinant RgpA were determined by enzyme-linked immunosorbant assay (ELISA). No correlation was observed between the antibody levels to RgpAcat from P. gingivalis and the recombinant form of this enzyme expressed in Escherichia coli. However, a strong association was found between the recognition of LPS and the wild-type enzyme (R = 0.8926; p = 0.0005). Incorporation of LPS into the ELISA led to a significant reduction (mean 25%; range 0.8-43%, SD = 15; p < 0.05) in the recognition of RgpAcat, but had no effect on the recognition of control antigens. Deglycosylation of RgpAcat led to the abolition of immune recognition by patient serum IgG, which suggests that the glycan additions to this molecule are the principal targets of the immune response. Therefore, glycosylation of the RgpAcat protease may play an important role in immune evasion by shielding the primary structure from immune recognition.

Adhesins, Bacterial↗
PubMed2001

Costimulation of CD8alphabeta T cells by NKG2D via engagement by MIC induced on virus-infected cells.

NKG2D is an activating receptor that stimulates innate immune responses by natural killer cells upon engagement by MIC ligands, which are induced by cellular stress. Because NKG2D is also present on most CD8alphabeta T cells, it may modulate antigen-specific T cell responses, depending on whether MIC molecules--distant homologs of major histocompatibility complex (MHC) class I with no function in antigen presentation--are induced on the surface of pathogen-infected cells. We found that infection by cytomegalovirus (CMV) resulted in substantial increases in MIC on cultured fibroblast and endothelial cells and was associated with induced MIC expression in interstitial pneumonia. MIC engagement of NKG2D potently augmented T cell antigen receptor (TCR)-dependent cytolytic and cytokine responses by CMV-specific CD28- CD8alphabeta T cells. This function overcame viral interference with MHC class I antigen presentation. Combined triggering of TCR-CD3 complexes and NKG2D induced interleukin 2 production and T cell proliferation. Thus NKG2D functioned as a costimulatory receptor that can substitute for CD28.

CD8-Positive T-Lymphocytes↗