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PubMed2002

Performance enhancement with maintenance of resting immune status after intensified cycle training.

BACKGROUND: Unaccustomed intense endurance exercise is associated with short-term suppression of natural immunity. However, it is not established whether intensified endurance training alters resting immune status or increases the risk of upper respiratory infection (URI). PURPOSE: This study examined the effect of intensified endurance training for performance enhancement on resting immune status in nine healthy, male competitive cyclists. DESIGN: Data were collected during 4 weeks of usual training (baseline), followed by prescribed cycle training that consisted of volume-building at customary training intensity (V phase, 6 weeks), unaccustomed very high intensity interval training at 100% maximal heart rate (I phase, 18 days), and an unloading taper (U phase, 10 days). METHODS: The main performance criterion was a simulated 20 km time-trial. Aerobic capacity measures included power output at ventilatory threshold (POT(vent)) and maximal oxygen uptake (VO(2max)). Markers of immune status (lymphocyte subset counts, serum cytokine levels, and new URI cases) and physiological indicators of training stress (cycling economy, 24-hour urinary cortisol excretion, and serum testosterone concentration) were evaluated in the rested state, 36 to 44 hours postexercise, during baseline, and after each training phase. RESULTS: Time-trial performance, POT9(vent), VO(2max), and cycling economy improved significantly (p < 0.001) after the V phase, and remained higher than baseline (p < 0.001) after the I and U phases. As compared with the V phase, performance time was faster after the U phase (p < 0.01). In contrast, lymphocyte counts, cytokine levels, incidence of URI, cortisol excretion, and serum testosterone concentration were not significantly different from baseline in any phase. CONCLUSIONS: Cycling efficiency and performance improved while resting immune status was maintained throughout the 10-week training program. This study provides encouraging data in support of immunological robustness during intensified endurance training.

Adult↗
PubMed2004

Functional regulatory immune responses against human cartilage glycoprotein-39 in health vs. proinflammatory responses in rheumatoid arthritis.

The class of immune response against autoantigens could profoundly influence the onset and/or outcome of autoimmune diseases. Until now, there is only limited information on the antigen-specific balance between proinflammatory and regulatory responses in humans. Here we analyzed the natural immune response against a candidate autoantigen in rheumatoid arthritis, human cartilage glycoprotein-39 (HC gp-39). Peripheral blood mononuclear cells from healthy individuals reacted against HC gp-39 with the production of IL-10 but not IFN-gamma. Ex vivo assays indicated that the naturally occurring HC gp-39-specific immune response in bulk is powerful enough to suppress antigen-specific recall responses, demonstrating that rather than being unresponsive, the HC gp-39-directed immune response in healthy individuals shows a strong bias toward a regulatory phenotype. Moreover, CD4(+) T cell lines directed against HC gp-39 expressed CD25, glucocorticoid-induced tumor necrosis factor receptor, and Foxp3 molecules and were capable of suppressing antigen-specific T cell responses. Cell-cell contact was required for this suppression. As opposed to healthy individuals, the HC gp-39-directed immune response in 50% of patients with rheumatoid arthritis exhibits polarization toward a proinflammatory T helper 1 phenotype and is significantly less powerful in suppressing antigen-specific recall responses. Together these findings indicate that the presence of HC gp-39-specific immune responses in healthy individuals may have an inhibitory effect on inflammatory responses in areas where HC gp-39 is present. Furthermore, these data indicate that the class of HC gp-39-directed immune response in rheumatoid arthritis patients has shifted from an antiinflammatory toward a proinflammatory phenotype.

Adipokines↗
PubMed1975

Specific susceptibility of sensitized (memory) B cells to suppression and antigenic alteration by murine leukemia virus.

Mice infected with murine oncogenic RNA viruses, either Friend virus (FV) or Moloney leukemia virus (MuLV-M) reacted well to a primary immunization with antigen(s) of Vibrio cholerae; both the kinetics and magnitude of the direct (IgM) primary vibriolytic antibody plaque forming cell (PFC) response in the spleen was the same as in non-infected control mice. In contrast, the anamnestic PFC (IgM) response of mice preimmunized with cholera and later (2 to 9 months following priming) infected with either FV or MuLV-M, before the secondary challenge, was inhibited 90% or more when compared to the anamnestic response of controls. Hemolytic PFC response to a single (primary) immunization with sheep red blood cells (sRBC, an antigen to which laboratory mice have a natural immune background) was suppressed by infection with both viruses in a manner similar to the suppression of the secondary vibiolytic response. The suppressive effect of FV, and the lack of it, on these different immune responses was correlated with the appearance of FV-induced cell membrane antigen, FVMA, on respective individual PFC from the spleen. FVMA was detected by inhibition of PFC in the presence of specific antiserum, anti-FVMA, and complement (C). In particular, about 80% of the FV-infected mice with an anamnestic response to a secondary challenge with cholera antigen had a significant decline in the proportion of PFC (33% or more) following incubation with anti-FVMA plus C. A similar degree of inhibition was found with hemolytic (anti-sRBC) PFC from FV-infected mice. In contrast, primary vibriolytic PFC from FV-infected mice were not inhibited by anti-FVMA, i.e., they did not carry the virus-induced antigen. These results indicate absolute correlation between viral suppression of a given clone of immunocompetent cells, and antigenic alteration of individual antibody-forming cells due to the virus-infection. Furthermore, the absence of both functional inhibition and virus-induced antigen(s) in the primary immunocompetent cells and the presence of both these virus-related functions in the memory cells (either experimentally sensitized cholera memory cells or naturally sensitized sRBC memory cells) strongly suggested that the latter are selectively susceptible to oncornavirus.

Animals↗
PubMed1983

Native and inducible levels of natural cytotoxicity in lymph nodes draining mammary carcinoma.

Lymphocytes isolated from axillary nodes draining breast carcinoma possess variable natural cytotoxic capacity. Augmentation of lymph node cell (LNC) cytotoxicity by interferon (IFN) is also variable, with only some populations displaying potentiated lysis following exposure to either IFN-a or gene-cloned IFN-a2. Where present the IFN-induced augmentation of LNC cytotoxicity was invariably weaker than that observed following similar treatment of autochthonous peripheral blood mononuclear cells (PBMC). Irrespective of their responsiveness to IFN the cytotoxic activity of all LNC preparations examined was significantly increased following pre-incubation with either staphylococcal enterotoxin A (SEA) or factors elaborated by lectin-pulsed allogeneic LNC. THe induction or amplification fo LNC-mediated natural cytotoxicity by lymphokines may provide a local potentiation of natural immune function at the host : tumour interface.

Breast Neoplasms↗
PubMed1993

Role of NK cells in immunomodulator-mediated resistance to herpesvirus infection.

Seven chemically diverse biological response modifiers (BRM) were compared for antiviral activity in intact and NK cell-depleted CD-1 mice. Both spontaneous and BRM-induced splenic NK cell cytotoxicity were depleted for at least 5 days following treatment with the monoclonal antibody NK1.1. Antiviral protection of standard doses of MVE-2, pIC, pICLC, rmIFN-tau and CL246,738 against lethal MCMV or HSV-2 infections was not abrogated by NK cell depletion, demonstrating that NK cells are not required for BRM-induced antiviral activity against these herpesviruses. When mice were treated with 100,000 U of rHuIFN-alpha B/D, NK cells were not required for activity against MCMV, while at a dose of 25,000 U, NK cells appeared to be partially required against MCMV. At lower doses, the activity of rHuIFN-alpha B/D against MCMV appeared dependent upon the presence of NK cells. A similar dose-related requirement for NK cells was observed for activity of OK-432. Thus, at higher doses of rHuIFN-alpha B/D and OK-432, elements of the natural immune system in addition to or other than NK cells are apparently involved, while at lower doses NK cells appear to play a more important role in antiviral protection against MCMV infection.

Adjuvants, Immunologic↗
PubMed2005

Supernatural T cells: genetic modification of T cells for cancer therapy.

Immunotherapy is receiving much attention as a means of treating cancer, but complete, durable responses remain rare for most malignancies. The natural immune system seems to have limitations and deficiencies that might affect its ability to control malignant disease. An alternative to relying on endogenous components in the immune repertoire is to generate lymphocytes with abilities that are greater than those of natural T cells, through genetic modification to produce 'supernatural' T cells. This Review describes how such T cells can circumvent many of the barriers that are inherent in the tumour microenvironment while optimizing T-cell specificity, activation, homing and antitumour function.

Animals↗
PubMed2006

Biology of longevity: role of the innate immune system.

Genetic factors play a relevant role in the attainment of longevity because they are involved in cell maintenance systems, including the immune system. In fact, longevity may be correlated with optimal functioning of clonotypic and natural immunity. The aging of the immune system, known as immunosenescence, is the consequence of the continuous attrition caused by chronic antigenic overload. The antigenic load results in the progressive generation of inflammatory responses involved in age-related diseases. Most of the parameters influencing immunosenescence appear to be under genetic control, and immunosenescence fits with the basic assumptions of evolutionary theories of aging, such as antagonistic pleiotropy. In fact, by neutralizing infectious agents the immune system plays a beneficial role until reproduction and parenting. However, by determining chronic inflammation, it can be detrimental later in life, a period largely unforeseen by evolution. In particular, the data coming from the long-lived male population under study show that genetic polymorphisms responsible for a low inflammatory response might result in an increased chance of long lifespan in an environment with a reduced pathogen burden. Such a modern and healthy environment also permits a lower grade of survivable atherogenic inflammatory response.

Aged, 80 and over↗
PubMed1986

A comprehensive investigation of immunity to poliomyelitis in a developing country.

A comprehensive nationwide surveillance program of serologic immunity of two-year-old black children, combined with evaluation of vaccine quality and distribution, was carried out in South Africa during 1983-1984. Sera were randomly collected from urban and rural groups and cluster samples collected from the semi-urban group. The sample represented 0.23% of the total target population. Satisfactory levels of immunity were found in the urban (80%) and semi-urban (71%) groups but a disquietingly low level was found for the rural group (59%). Individual districts in the rural group could be singled out for directed cluster sampling at a later stage. History and documentation of immunization corresponded well to serologic findings and revealed also a fairly substantial level of natural immunization among individuals who, on history, had received no vaccine. Some 95% of random samples of vaccine recalled from the field showed satisfactory levels of potency. An immunity surveillance program such as this is ideally suited and highly cost-effective for developing countries with incomplete immunization to prevent large-scale buildup of immunity deficit. The technique, however, is too insensitive to detect localized community immunity defects.

Antibodies, Viral↗
PubMed2000

Mast cells and basophils.

Mast cells and basophils are effector cells in IgE-associated immune responses, such as those that contribute to asthma and other allergic diseases and to host resistance to parasites. Recent work shows that mast cells can also participate in innate immunity to bacterial infection and that the expression of such mast cell-dependent natural immunity can be significantly enhanced by long-term treatment of mice with the kit ligand, stem cell factor. However, mast cells may also influence many other biologic responses, including tissue remodeling and angiogenesis. This review discusses certain recent findings about the differentiation, phenotype, and function of basophils and mast cells, as well as briefly considering evolving concepts about the roles of these cells in health and disease.

Animals↗
PubMed1996

Oxidative burst response of neutrophils primed with PreS1 antigen of hepatitis B virus in patients with chronic hepatitis B and convalescents.

The pathogenesis of liver damage in the course of hepatitis B virus (HBV) infection depends on the host's specific and non-specific immune response to various viral antigens. The role of polymorphonuclear neutrophils (PMN) in the natural immune reaction and during secondary microbial infections is well documented. Increased free radical production is associated with many pathological conditions such as shock, ischaemia or chronic inflammatory diseases. We studied the oxidative metabolism of neutrophils in patients with chronic HBV and after recovery (convalescents). The effect of the PreS1 fragment of HBV antigen on some neutrophil functions in vitro was also examined. There were significant differences in the values of spontaneous and stimulated oxidative burst of neutrophils, measured using luminol-chemiluminescence, in patients with HBV when compared with the convalescents. PreS1 antigen did not by itself induce the respiratory burst in human neutrophils but it potentiated their response to a second stimulus. Hence we observed a priming of neutrophils, for an enhanced respiratory burst, by PreS1 antigen.

Adult↗
PubMed1980

Antiviral cell-mediated immune responses and effect of chromosome polymorphism in Herpesvirus saimiri-infected monkeys.

Herpesvirus saimiri is a horizontally transmitted virus of squirrel monkeys (Saimiri sciureus) which, when inoculated into owl monkeys (Aotus trivirgatus), induces fatal malignant lymphoma in 75 to 80% of the animals. Previous immunological and virological studies have not indicated why 20 to 25% of inoculated owl monkeys develop a chronic, disease-free H. saimiri infection. In the present study, we examined two parameters to explain why certain owl monkeys are resistant to H. saimiri-induced disease. The first possibility was that the animals in which H. saimiri established a chronic infection were all of the same karyotypic class. In studying four such animals, we found that three of the seven known karyotyes were represented, indicating that chromosome polymorphism does not explain disease resistance. The second possibility examined was that animals which develop disease do so as a result of a failure in specific anti-H. saimiri cell-mediated immunity. Naturally infected squirrel monkeys exhibited long-lasting, virus-specific cell-mediated immunity in a lymphocyte proliferation assay, whereas such reactivity could not be demonstrated either in chronically infected owl monkeys or in an owl monkey with a primary H. saimiri infection. The failure of owl monkeys to respond to viral antigens was not due to a basic immunological defect, since these animals gave normal responses to heterologous cells and were capable of being sensitized with the protein antigen keyhole limpet hemocyanin.

Animals↗
PubMed2005

Protection by natural human immunoglobulin M antibody to meningococcal serogroup B capsular polysaccharide in the infant rat protection assay is independent of complement-mediated bacterial lysis.

Neisseria meningitidis, an important cause of bacterial meningitis and septicemia worldwide, is associated with high mortality and serious sequelae. Natural immunity against meningococcal disease develops with age, but the specificity and functional activity of natural antibodies associated with protection are poorly understood. We addressed this question by using a selected subset of prevaccination sera (n = 26) with convergent or discrepant serum bactericidal activity (SBA) and infant rat protective activity (IRPA) against the serogroup B meningococcal strain 44/76-SL (B:15:P1.7,16) from Icelandic teenagers. The sera were analyzed by opsonophagocytic activity (OPA) assay, immunoblotting, immunoglobulin G (IgG) quantitation against live meningococcal cells by flow cytometry, and enzyme immunosorbent assay (EIA). High levels of SBA and OPA were reflected in distinct IgG binding to major outer membrane proteins and/or lipopolysaccharide in immunoblots. However, we could not detect any specific antibody patterns on blots that could explain IRPA. Only IgM antibody to group B capsular polysaccharide (B-PS), measured by EIA, correlated positively (r = 0.76, P < 0.001) with IRPA. Normal human sera (NHS; n = 20) from healthy Finnish children of different ages (7, 14, and 24 months and 10 years) supported this finding and showed an age-related increase in IRPA that coincided with the acquisition of B-PS specific IgM antibody. The protection was independent of complement-mediated bacterial lysis, as detected by the inability of NHS to augment SBA in the presence of human or infant rat complement and the equal protective activity of NHS in rat strains with fully functional or C6-deficient complement.

Age Factors↗
PubMed1992

Apparent ineffectiveness of natural killer cells vis-à-vis retrovirus-infected targets.

The role of NK cells in the defense against retroviral infections is ill defined. The discovery of the pathogenic human retroviruses and their epidemic spread have made more urgent a better understanding of how such infections may be naturally controlled. Therefore, a systematic study was undertaken to determine whether NK cells obtained from healthy individuals are able to recognize and lyse target cells that have been infected with HTLV-I, HTLV-II, or HIV. The studies demonstrated that NK cells can recognize retrovirus-infected cells as evidenced by rapid conjugation, but that neither freshly isolated, nor IL-2 stimulated cells cause lysis of such targets. As has been reported for NK-resistant tumor cells, removal of sialic acid residues rendered the retrovirus-infected target cells vulnerable to NK cell attack. Although these data do not suggest that boosting natural immunity would be a useful treatment modality for patients with AIDS or HTLV-related diseases, the observations may help to explain why the small number of cells that harbor retroviruses in patients with subclinical infection are not eliminated.

Cytotoxicity, Immunologic↗
PubMedDate not supplied

Proline-oxidase and hydroxypyroline-2-epimerase activities in experimental fibrosing granulomatous processes of the lung.

Three experimental fibrosing granulomatous processes of the lung (pulmonary granulomas induced by complete Freund adjuvant, viral pneumonitis induced by the A2 influenza virus, and tuberculosis induced in animals exposed to tobacco smoke) were produced in rabbits and the results confronted in view of establishing some relationships between mesenchymal cell accumulations, reticulin fibrillogenesis, and the enzymic activities of proline-oxidase (PO) and of hydroxyproline-2-epimerase (HEP), enzymes intervening in the control of hydroxyproline incorporation in the procollagen molecule. Histopathologic, histochemical and histoenzymic methods, quantification of cells and fibrils, statistical analyses, including the regression lines method, were used. The confrontation of the three processes made obvious that the cell accumulation invariably preceded the fibrillogenetic process, that the immune nature of the process was accompanied by larger cell accumulations than the non-immune one, that between cell accumulations and fibrillogenesis there existed highly significant correlations, and that the increase of the enzymic activities of proline-oxidase and of hydroxyproline-2-epimerase always accompanied these tissular changes, being topographically coincident with them (interlobular areas, alveolar walls).

Amino Acid Oxidoreductases↗
PubMed2003

[Immunobiology of dendritic cells and their application in clinical practice].

INTRODUCTION: Dendritic cells play a central role in the regulation of the immune responses towards cellular or humoral immunity. Several types of dendritic cells can be distinguished, which originate from different hematopoietic lineages, and differ from each other in function, morphology and localization within the organism. Immature dendritic cell-precursors originate from bone marrow haemopoietic stem cells, circulate in blood system and reach peripheral tissues, where they differentiate into active antigen capturing and processing cells. They have further maturation by the effect of adequate signals (antigen stimuli and inflammatory cytokines) and migrate into secondary lymphoid organs, presented cell surface MHC molecules-linked peptides from antigens which they have captured and processed, to T lymphocytes, induce immune reaction by T cell activation. Apart from the fact that dendritic cells as professional antigen presenting cells are essential to induction T cell-mediated immune responses, they influence activation and function of B lymphocytes and effector cells of natural immune system by cytokines and cell-cell interactions. CONCLUSIONS: Complex regulatory function of dendritic cells make a possibility for artificial alteration of immune processes by modification of dendritic cells: direct against definitive antigens, increase or decrease their intensity, hereby we can accomplish the immunotherapy of different diseases such as tumors, infection, autoimmune diseases, transplants' rejection.

Antigen Presentation↗
PubMed2003

4-1BB gene expression in peripheral blood mononuclear cells from orthotopic liver transplant recipients with graft acceptance.

OBJECTIVE: To investigate the gene expression of 4-1BB in peripheral blood mononuclear cells (PBMCs) and the possible significance of the 4-1BB pathway after clinical orthotopic liver transplantation (OLT). METHODS: 4-1BB mRNA levels in PBMCs from 22 OLT patients were analyzed by RT-PCR. 4-1BB protein expressed on the surface of CD(4)(+) and CD(8)(+) T cells were detected by flow cytometry, and visualized with direct immunofluorescence and confocal fluorescence microscopy. Patients with primary liver cancer (PLC) and healthy volunteers served as controls. Six cases of recently performed liver transplantation were also observed in this study. RESULTS: 4-1BB mRNA was detected in PBMCs from both liver transplant patients with long-term graft acceptance (22 cases) and from transplant patients on day 1 to day 3 post-transplantation (6 cases), but was not found in PBMCs from transplant patients on day 7 to day 30 post-transplantation (6 cases). 4-1BB mRNA was also not found in samples from 8 of the healthy controls and 7 of the PLC patients, though very low expression was detected in the other 4 healthy volunteers and 6 PLC patients. Simultaneously, 4-1BB protein was expressed at nearly undetectable levels on CD(4)(+) and CD(8)(+) T cells from healthy controls, PLC patients, as well as OLT patients within the first month post-transplantation (6 cases). However, 4-1BB expression was found on the surface of CD(4)(+) and CD(8)(+) T cells from liver transplant patients with long-term graft acceptance. Direct immunofluorescent staining and confocal fluorescence microscopy clearly revealed evidence of 4-1BB protein on cell membranes of CD(4)(+) and CD(8)(+) T cells from liver transplant patients with long-term graft acceptance. Simultaneously, a significantly higher percentage of CD(3)(+) CD(25)(+) T cells were found in liver transplant patients with long-term graft acceptance group as compared with the healthy control group (P < 0.05). The expression of 4-1BB protein on T cells did not correlate with the survival time of OLT patients postoperation. CONCLUSIONS: This study demonstrates that although patients remain in stable condition after liver transplantation under the treatment of immunosuppressants, activated T cells are present to some extent and 4-1BB protein may be involved in this process. Effector T-cells can exert permanent immunoresponses against grafts under these circumstances. Therefore, we conclude that a new immune response balance is established under the combination of both treatment with immunosuppressants and natural immune responses against alloantigens. Manipulation of the 4-1BB/4-1BBL pathway may provide a therapeutic technique for prolonging graft survival.

Adult↗
PubMed1977

Development of cellular anti-tumor immunity in chickens bearing tumors induced by Rous sarcoma virus.

The technique of peripheral lymphocyte stimulation in response to antigen was used to demonstrate the existence of cell-mediated anti-tumor immunity in chickens bearing tumors induced by avian sarcoma viruses. The expression of this anti-tumor response against virus-containing transformed cell culture supernatant fluids and cell extracts varied among animals in terms of time after inoculation with the oncogenic agent. Animals whose tumors had completely regressed rapidly lost the ability to mount such continuing immunity. In addition, we found evidence that some normal animals express endogenous levels of natural immunity against neoplasms induced by these viruses and/or against the viruses themselves.

Animals↗
PubMed1994

The origins of the NK cell, or a Canadian in King Ivan's court.

Before 1970, lymphocytes were classified as either of 2 cell types, T cells or B cells. Using the new T-cell antigen, Thy-1, the cytotoxic lymphocyte induced after alloimmunization was identified as a T cell. With the discovery that unimmunized lymphocytes could kill antibody-coated target cells, the search began to identify the effector cell. In 1973, while in Ivan Roitt's laboratory, we discovered "null" killer cells that were neither T nor B cells, indicating that a new class of killer lymphocytes exists. The following year, with John Playfair, we reported an unusual type of "spontaneous" cytotoxicity in which "null" lymphocytes kill target cells without prior immunization and without antibody. In 1975, Rolf Keissling and colleagues in Sweden described a similar natural cytotoxicity and determined that the killer cell was genetically regulated, and killed many types of tumours. Keissling named the effector cell a "natural" killer (NK) cell. In 1976, we proposed that resistance to tumours is T-cell independent and is mediated by a natural immune mechanism requiring NK cells. With the discovery of the NK-deficient "beige" (bg/bg) mouse, the importance of NK cells in control of hematogenous metastasis was confirmed.

Animals↗