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PubMed1999

Can HIV infection be prevented with a vaccine?

The global human immunodeficiency virus type 1 (HIV-1) epidemic is devastating many communities and a well tolerated and effective vaccine is urgently required. Several lines of evident suggest that vaccine-induced protective immunity can be achieved. This evidence includes individuals shown to have natural immunity, and the partially effective immune responses that are generated during natural infection. However, the obstacles to HIV-1 vaccine development are enormous. The only substantially effective vaccine studied in pathogenic animal models (live, attenuated vaccines) is at present far too unsafe. The only HIV-1 vaccine to proceed to efficacy trials (an envelope protein approach) has been disappointing in its immunogenicity and efficacy in preliminary trials. The antigenic variability of HIV-1 strains is also a great obstacle. Unfortunately, commercial realities also do not favour the expensive development of HIV-1 vaccines required most urgently in less developed countries. Despite these obstacles, there is cause for cautious optimism. Better tolerated HIV-1 vaccine approaches are currently showing great promise in primate models and preliminary clinical trials. Many governments and the World Bank are now providing the political will and funding necessary to fast-track HIV-1 vaccine development. Given sufficient long term scientific and commercial commitment to the HIV-1 vaccine development process, it is ultimately likely that a preventative HIV-1 vaccine will emerge.

AIDS Vaccines↗
PubMed2003

Progress and new technologies for developing vaccines against gastrointestinal nematode parasites of sheep.

Despite the identification of highly effective native antigens for vaccination against Haemonchus contortus, particularly 'hidden' antigens derived from the intestine of adult worms, to date similar efficacy has not been shown with recombinant antigens. In addition, progress towards identification of protective antigens from other sheep gastrointestinal (GI) nematode species is limited. Coupled with this is an incomplete understanding of the mechanism of natural immunity to GI nematodes, making selection of appropriate immunization strategies and adjuvants for evaluation of candidate 'natural' antigens problematic. The current explosion in new high-throughput technologies, arising from human studies, for analysis of the genome, transcriptome, proteome and glycome offers the opportunity to gain a better understanding of the molecular pathways underlying pathogen biology, the host immune system and the host-pathogen interaction. An overview is provided on how these technologies can be applied to parasite research and how they may aid in overcoming some of the current problems in development of commercial vaccines against GI nematode parasites.

Animals↗
PubMed1990

The reactivity of naturally sensitized human CD4 cells and IgG antibodies to synthetic peptides derived from the amino terminal sequences of a 3800 MW Streptococcus mutans antigen.

Natural immunity to synthetic peptides (SP) derived from the sequences of a 3800 MW streptococcal antigen (SA) was found in human subjects. Significant serum IgG antibodies were detected both to the native SA and to peptides consisting of residues 3-13, 1-15 and 1-20. Inhibition studies confirmed cross-reactivity between the native SA and SP. A series of short peptides with deletions at the amino and carboxy termini were then tested to determine the sequence of B-cell epitopes. Residues 8-13 and 1-6 bound significant serum IgG antibodies, but residues 8-13 were more effective and consistent in inhibiting human antibodies than residues 1-6. These results suggest that residues 8-13 constitute a major B-cell epitope but that residues 1-6 may represent a minor B-cell epitope. The human CD4 subset of T cells was then examined by stimulating the cells with SA or SP and measuring the uptake of [3H]thymidine [( 3H]TdR). The cells were found to be sensitized in vivo to both the native SA and the SP and cross-reactivity between the SA and SP was shown by enrichment and depletion experiments on antigen-coated monocytes. As with the B-cell epitope, the series of short peptides was used to stimulate CD4 cells, in order to determine the T-cell epitope. Residues 6-15 were the shortest SP which stimulated significant [3H]TdR uptake and this peptide was designated as a T-cell epitope. The results suggest that natural oral immunization with Streptococcus mutans induces serum antibodies and T-cell sensitization to a peptide in which a T-cell epitope (residues 6-15) overlaps with a B-cell epitope (residues 8-13). Furthermore, a comparison between linear and cycled peptides suggests that unlike immunogenicity which is commonly enhanced by the more rigid cyclized peptides, antigenicity is favoured by linear peptides. This was evident not only for antibodies but also for T-cell proliferative responses.

Amino Acid Sequence↗
PubMed2006

The role of regulatory T cells in the control of natural killer cells: relevance during tumor progression.

Tumor immunosurveillance relies on cognate immune effectors [lymphocytes and interferon-gamma (IFN-gamma)] and innate immunity [natural killer (NK) cells, natural killer group 2, member D (NKG2D) ligands, perforin/granzyme, and tumor necrosis factor-related apoptosis-inducing ligand]. In parallel, tumor cells promote the expansion of CD4(+)CD25(+) regulatory T cells (Tregs) that counteract T-cell-based anti-tumor immunity. Moreover, accumulating evidence points to a critical role for Tregs in dampening NK cell immune responses. This review summarizes the findings showing that Tregs suppress NK cell effector functions in vitro and in vivo, i.e. homeostatic proliferation, cytotoxicity, and interleukin-12-mediated IFN-gamma production. The molecular mechanism involve selective expression of membrane-bound transforming growth factor-beta on Tregs, which downregulate NKG2D expression on NK cells in vitro and in vivo. The regulatory events dictating NK cell suppression by Tregs have been studied and are discussed. The pathological relevance of the Treg-NK cell interaction has been brought up in tumor models and in patients with cancer. Consequently, inhibition of Tregs through pharmacological interventions should be considered during NK-cell-based immunotherapy of cancer.

Animals↗
PubMed1982

Lymphotoxin enhances the susceptibility of neoplastic and preneoplastic cells to natural killer cell mediated destruction.

Treatment of neoplastic guinea-pig cells for 1-14 days with 300 units of guinea-pig lymphotoxin/ml medium enhanced 2- to 5-fold their susceptibility to natural killer (NK) cell-mediated cytotoxicity as measured by 4 h 51Cr and 72 h [3H]-thymidine-release assays. The NK susceptibility of human neoplastic and guinea-pig non-neoplastic cells refractory to guinea-pig lymphotoxin growth-inhibitory activity was unchanged after lymphotoxin treatment. Lymphotoxin preparations were free of detectable interferon and the enhancing activity copurified with lymphotoxin during diafiltration and isoelectric focusing. Treatment of NK cells with lymphotoxin preparations also augmented NK-mediated lysis but that activity did not copurify with lymphotoxin. As with neoplastic cells, lymphotoxin-sensitive preneoplastic cells previously treated with ultraviolet light, a chemical carcinogen, or carcinogen and the tumor-promoting agent tetradecanoylphorbol-acetate also exhibited lymphotoxin enhancement to NK-cell destruction. Thus, the immunologic hormone lymphotoxin enhances the susceptibility of lymphotoxin-sensitive cells to NK-cell destruction, indicating that these two natural immune mediators, lymphotoxin and NK cells, have the potential in concert to regulate carcinogenesis and neoplastic growth.

Animals↗
PubMed1991

Impact of changes in housing condition on mouse natural killer cell activity.

Various psychosocial stressors, such as housing condition and rotation, have been reported to influence tumour growth. This study assessed the influence of housing condition and change in housing condition on natural killer (NK) cell activity, an important component of natural immune defense against cancer. Mice which were individually housed for four weeks did not differ from group-housed mice in NK cell cytolytic activity against tumour targets in vitro or in the frequency of NK cells in the spleen. Switching of housing condition (group to individual, individual to group) for one week did not change the splenic NK cytolytic capacity relative to mice which were not switched. The two groups of mice which experienced a change in housing condition were, however, significantly different from each other. These data suggest that an acute change in housing condition, rather than the housing condition per se, has differential effects on the capacity to kill tumours by NK cells.

Animals↗
PubMed1996

A comparative study of immunomodulation produced by in vitro exposure to delta opioid receptor agonist peptides.

The present study assessed the direct immunomodulatory effect of a panel of synthetic peptides exhibiting delta-opioid receptor agonist activity. Murine splenic lymphocytes and peritoneal macrophages were cultured in vitro with peptides at concentrations of 0.00001-10 microM. Assessment was made of B-cell function by quantitating cellular proliferation, T-cell function by measuring cytokine production, natural immunity by quantitating basal and cytokine-augmented natural killer (NK) cell activity, and macrophage function by production of IL-6. These peptides had minimal effects on B-cell proliferation at any concentration examined. In comparison, enhancement of cytokine production by T-helper cells occurred following exposure to several of the compounds, to a significant extent with DPDPE, DPDPE-trifluoroacetate, or deltorphin-1 and most pronounced at concentrations between 0.00001 and 0.1 microM. Likewise, IL-6 production by macrophages was significantly augmented by exposure to these three peptides. NK cell function was significantly enhanced by in vitro exposure to several of the peptides, with enhancement generally noted at concentrations between 0.00001 and 0.01 microM. However, some of the peptides (most notably DADLE) greatly suppressed NK cell activity. These data suggest that delta opioid agonists are broadly immunomostimulatory.

Adjuvants, Immunologic↗
PubMed1998

Distinct T-cell subtypes induced with whole cell and acellular pertussis vaccines in children.

Recent clinical trials have demonstrated that new generation acellular pertussis vaccines can confer protection against whooping cough. However, the mechanism of protective immunity against Bordetella pertussis infection induced by vaccination remains to be defined. We have examined cellular immune responses in children immunized with a range of acellular and whole cell pertussis vaccines. Immunization of children with a potent whole-cell vaccine induced B. pertussis-specific T cells that secreted interferon-gamma (IFN-gamma), but not interleukin-5 (IL-5). In contrast, T cells from children immunized with acellular pertussis vaccines secreted IFN-gamma and/or IL-5 following stimulation with B. pertussis antigens in vitro. These observations suggest that protective immunity conferred by whole-cell vaccines, like natural immunity, is mediated by type 1 T cells, whereas the mechanism of immune protection generated with acellular vaccines may be more heterogeneous, involving T cells that secreted type 1 and type 2 cytokines.

Antigens, Bacterial↗
PubMed1998

Varicella-zoster virus IE63, a virion component expressed during latency and acute infection, elicits humoral and cellular immunity.

Varicella-zoster virus (VZV) latency in human dorsal root ganglia is characterized by the transcription of large regions of its genome and by the expression of large amounts of some polypeptides, which are also expressed during lytic cycles. The immediate early 63 protein (IE63) is a virion component expressed very early in cutaneous lesions and the first viral protein detected during latency. Immune response against IE63 has been evaluated among naturally immune adults with a history of chickenpox: Specific antibodies were detected in serum, and most subjects who had a T cell proliferation with unfractionated VZV antigens had T cell recognition of purified IE63. The cytotoxic T cell (CTL) response to IE63 was equivalent to CTL recognition of IE62, the major tegument component of VZV, whose immunogenicity has been previously described. T cell recognition of IE63 and other VZV proteins is one of the likely mechanisms involved in controlling VZV reactivation from latency.

Acute Disease↗
PubMed2003

A point of view: The need to identify an antigen in psyconeuroimmunological disorders.

Several lines of evidence support a mutual relationship between the nervous system and the immune system. Therefore, it is not surprising that some neuropsychiatric disorders are also characterized by immune abnormalities. In patients with phobic disorders and in patients with migraine without aura some common immune abnormalities have been detected and, in particular, natural immunity deficits, exaggerated release of proinflammatory cytokines and circulating bacterial endotoxins have been found. In other neurological disease, some etiologic factors have been detected as in the case of Guillain-Barrè syndrome in which molecular mimicry between Campylobacter jejuni endotoxin and GM1 ganglioside may cause an acute inflammatory polyneuropathy. On the other hand, attempts to identify an antigen have been made in patients with Alzheimer's disease and schizophrenia. Finally, the chronic fatigue syndrome, an old illness in search for an antigen, risk factors and precipitating agents have been described but evidence for a specific antigen is still lacking.

Antigens↗
PubMedDate not supplied

New roles for estrogens in rheumatoid arthritis.

Sex hormones appear to play an important role as modulators of autoimmune disease onset/perpetuation. Steroid hormones are implicated in the immune response, with estrogens as enhancers at least of humoral immunity, and androgens and progesterone (and glucocorticoids) as natural immune suppressors. Serum levels of estrogens have been found to be normal in rheumatoid arthritis (RA) patients. Synovial fluid levels (SF) of proinflammatory estrogens relative to androgens are significantly elevated in both male and female RA patients as compared to controls, which is most probably due to an increase in local aromatase activity. Thus, available steroid pre-hormones are rapidly converted to proinflammatory estrogens in the synovial tissue in the presence of inflammatory cytokines (i.e. TNF alpha, IL-1, IL-6). The increased estrogen concentrations observed in RA SF of both sexes are characterized mainly by the hydroxylated forms, in particular 16 alpha-hydroxyestrone, showing a mitogenic stimulating role. Indeed, recent studies by us indicate that 17-beta estradiol (E2) clearly enhanced the expression of markers of cell growth and proliferation, whereas testosterone (T) induced an increase in markers indicating DNA damage and apoptosis. In particular, our data further shows that the enhancing role of estrogens on the immune/inflammatory response is exerted by activating the NFkB complex. In conclusion, locally increased estrogens may exert activating effects on synovial cell proliferation, including macrophages and fibroblasts, suggesting new roles for estrogens in RA.

Adult↗
PubMed1992

[Epidemiological effectiveness of an inactivated three-component flu vaccine with an increased concentration of hemagglutinin in the inoculation dose].

The work presents the results of the evaluation of mass immunization of working adults with inactivated trivalent influenza vaccine under the conditions of an epidemic caused by influenza viruses A (H1N1), A (H3N2) and B. This immunization produced no effect on influenza morbidity in the groups of vaccinees in comparison with those of nonvaccinated persons. The index of effectiveness was 1.0 and less. The ineffectiveness of mass immunization was due to a high level of natural immunity to influenza and the extensive use of influenza vaccine in past years.

Hemagglutinins, Viral↗
PubMed1986

[Effect of different types of interferon on the natural cellular cytotoxicity of lung cancer patients].

The natural killer cell cytotoxicity was studied in the 4 hour and 18 hour cytotoxic reaction with cultured human tumour cells (K562 and lung adenocarcinoma) labelled by 51Cr. The natural killer cell activity of cancer patients was lowered only in 4 hour cytotoxic reaction with target cells K562. The natural and recombinant leucocyte interferon and natural immune interferon stimulated in vitro the activity of natural killer cells in most of the experiments (80.5 %) in the 4 hour and 18 hour cytotoxic reactions both from patients with initially lowered level, and with normal or high level of cytotoxic action of natural killer cells. In some experiments interferon preparations did not significantly influence the lysis of tumour cells or even suppressed the activity of effector cells. The heterogeneity of the population of natural killer cells and different immunomodulating effects of interferon were discussed.

Adenocarcinoma↗
PubMed1989

A novel cell type responsible for marrow graft rejection in mice. T cells with NK phenotype cause acute rejection of marrow grafts.

Acute rejection of allogeneic and semiallogeneic marrow grafts has long been considered to be a function of the natural immune system because it shares many features with NK activity in mice. With the use of a recently developed in vivo adoptive transfer assay in which spleen cells are transferred from mice able to reject a particular marrow graft into mice that fail to do so, we show that the cells responsible for induction of marrow graft rejection indeed display the phenotype of NK cells: they lack the T cell Ag CD4 and CD8 but express the NK Ag NK1 and ASGM1. The rejection induced by adoptively transferred cells is exquisitely specific--a feature that points to a specific recognition process by the transferred cells. To elucidate what the recognition structure on these cells may be we found that they express CD3 and most likely the beta-chain of the TCR. Highly purified responder cells with the NK1+, CD3+, CD4-, CD8- phenotype, when transferred into nonresponder recipients, cause specific marrow graft rejection. We conclude that the acute rejection of bone marrow grafts is caused by a cell that expresses NK phenotype but is of T cell lineage. This may suggest the specificity of acute marrow graft rejection is caused by a specific recognition process that involves TCR.

Animals↗
PubMed1979

Apparent identity of mechanisms of genetic resistance to marrow transplantation and natural killer cell activity.

Because the phenomenon of in vitro lysis of lymphoma cells by spleen natural killer (NK) cells bears genetic and effector cell resemblances to genetic resistance to bone marrow transplantation, they were compared for additional known unique characteristics of the latter phenomenon. Like GR to BMT, NK cell activity first appeared abruptly at about 3 weeks of post-natal age; was radioresistant to 1 100 R whole body irradiation, but was quantitatively diminished by higher exposures or delay of test post-irradiation; was suppressed by pretreatment with either cyclophosphamide, carrageenan, silica particles, anti-bone marrow serum or anti-thymus serum. The many unique identical characteristics of these two effector mechanisms indicates that they represent two manifestations of the same basic phenomenon of natural immunity. This is in accord with other data indicating that GR to BMT is directed at Hh antigens which, like TL antigens, may in some mouse strains appear on both leukemic cells and normal hemopoietic cells.

Animals↗
PubMed1979

[Change in the activity of specific and nonspecific immunity mechanisms in vitamin B1 deficiency].

The effect of thiamin deficiency on the immune response and activity of some mechanisms of natural immunity was studied in experimental mature rats. Thiamin deficiency was simulated by a single injection of hydroxythiamin (thiamin antagonists). Hydroxythiamin markedly decreased the complement activity, phagocytic activity of peripheral blood leucocytes, serum bactericidal activity as well as antibody production in response to sheep red blood cells. On the contrary, lysozyme activity increased. Vitamin B1 deficiency reduced 14C-leucine incorporation activity in the liver proteins.

Acute Disease↗
PubMed1986

Acquired resistance towards immune defense during metastatic progression represents a secondary phenomenon.

The role of natural immune defense in the control of metastatic spread of tumor cells was evaluated by adapting an s.c.-grown, antigenic, but non-immunogenic rat fibrosarcoma (Bsp6S) to ascitic growth (BSp6A) in the strain of origin (BDX), where peritoneal cells display a high level of NK and macrophage activity. Parallel tests were performed to determine whether tumor cells can selectively adapt to non-specific immune defense, i.e. whether antigenicity of the non-immunogenic tumor remains unaltered, and whether this is accompanied by metastatic progression. During adaptation to ascitic growth the tumor line gradually lost susceptibility to NK cells and macrophages. This was due to the appearance of an increasing number of resistant clones (BSp6S, none; BSp6A, 50% of clones), which had lost binding structures for NK cells and macrophages. No alteration could be observed in antigenicity of the BSp6A variant as revealed by clonal analysis using LD of CTL. Neither BSp6S nor BSp6A cells metastasized. When the ascitic variant was retransplanted s.c. (BSp6AS), susceptibility to NK cells and macrophages was further decreased, in the sense that all clones of the BSp6AS variant became resistant. Furthermore, the BSp6AS variant had lost some of the tumor-associated antigens (TAAs) found on BSp6S and A variants. More important, upon s.c. transplantation BSp6AS regularly metastasized to the draining LN, contrary to BSp6S and BSp6A. When locally growing tumors were excised, rats implanted with BSp6AS frequently died with metastatic tumor burdens in LNs and lung, while other animals survived after excision of BSp6S or BSp6A. The data indicate a correlation between resistance to lysis, morphology and metastatic capacity. But the initial loss of susceptibility to NK cells and macrophages during adaptation to ascitic growth, which can be considered as an escape mechanism, was not accompanied by increased metastatic capacity. Hence, we suppose that with respect to metastatic progression of the BSp6AS variant, resistance to lysis by loss of binding structures represents only a secondary, but not a causative, element.

Animals↗