The natural killer cell and its interaction with immune and non-immune cells. 2nd Meeting of the Society for Natural Immunity. Taormina, Italy, May 25-28, 1994. Abstracts.
Explore the source record for details and available documents.
Animals↗
SEARCH · Search PubMed
Results for “Immunity, Natural”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Duration and mechanisms of the increased natural cytotoxicity seen after chronic voluntary exercise in rats.
We have recently shown that in vivo natural cytotoxicity is enhanced after chronic exercise in spontaneously hypertensive rats (SHRs). In the present report, we have studied the duration of this augmentation and some possible mechanisms involved. Exercise consisted of voluntary running for 4-5 weeks, with the running distance ranging from 2.7-15.6 km day(-1) during the last week of running. In vivo cytotoxicity was measured as clearance of injected 51Cr-labelled YAC-1 lymphoma cells from the lungs. The in vivo natural cytotoxicity was increased in running SHRs, and also in SHRs that had their running wheel locked for 24 and 48 h prior to the experiment, and was still present after 96 h. The enhancement of in vivo cytotoxicity after 5 weeks of exercise was abolished after an acute injection of the beta-adrenergic receptor antagonist timolol (0.5 mg kg(-1) i.v.), indicating that catecholamines are involved in this augmentation. Interestingly, 24 h after the last exercise bout, the increased natural cytotoxicity could be blocked by timolol. The opioid receptor antagonist naloxone given subcutaneously for 7 days by osmotic pumps (6 mg kg(-1) h(-1)) could not reverse the increased in vivo cytotoxicity seen in the running SHRs, suggesting that opioid receptor mechanisms are not involved, or at least not the naloxone-sensitive mu-receptor. Natural immunity was not influenced by the histamine H2 receptor antagonist ranitidine, either in controls or in runners, indicating that the natural killer cell-regulatory effect of histamine is not present in SHRs and does not seem to be involved in the exercise-induced changes in natural immune function. We conclude that the augmentation of in vivo natural cytotoxicity after voluntary chronic exercise in rats is long-lasting and that the augmentation is partly mediated by beta-adrenergic receptors.
Adrenergic beta-Antagonists↗
Persistence of immunologic memory in long-term hemodialysis patients and healthcare workers given hepatitis B vaccine: role of a booster dose on antibody response.
Hepatitis B (HB) vaccine is effective in producing protection against HB virus infection, but the persistence of immunity remains largely unknown. Seventy-six hemodialysis (HD) patients (60 after primary HB vaccination and 16 with natural immunity) and 46 healthcare workers (32 after primary HB vaccination and 14 with natural immunity) were followed up for 10 years to evaluate the persistence of immunity. Ten years after vaccination, the analysis showed a lower seroconversion rate (38 vs. 75%, p < 0.001) in HD patients as compared with healthcare workers. In the follow-up period, the protective immunity developed through HB virus infection also showed a lower seroconversion rate (44 vs. 86%, p < 0.025) in HD patients as compared with healthcare workers. To assess the status of immunologic memory, we administered a booster dose of HB vaccine 3-12 years (mean 6.7 +/- 0.6 years) after primary vaccination in a selected group of 37 HD patients who presented a decline of their antibodies or were nonresponders. In another group of 12 healthcare workers who had a decline of their antibodies, we also administered a booster dose of HB vaccine 5-8 years (mean 5.8 +/- 0.3 years) after primary vaccination. Nineteen of the 37 HD patients (51%) presented an anamnestic response to the booster dose, and 15 of these (40%) were high responders. All of the healthcare workers responded to the booster dose with a high antibody response. We conclude that patients undergoing HD not only have lower rates of immunization to HB than healthy adults, but also that these are frequently transient. Booster doses after a primary course of vaccine are effective in about the half of HD patients who presented a decline of their antibodies or were nonresponders but whether they are necessary is unclear. The majority of healthcare workers continue to have high levels of protective HBs antibody for at least 10 years and routine boosters are not required.
Female↗
[New insights into cytotoxic effector cells].
Cytotoxic immune cells play a role against infectious or tumour invasion. There are two types of cytotoxic cells : those involved in innate or natural immunity (natural killer cells, Tgammadelta lymphocytes, NKT cells) and those involved in the adaptive or acquired immunity (cytotoxic T lymphocytes). Recent advances in immunology have allowed the characterisation of unconventional cytotoxic populations, to better individualise the real cytotoxic cells within the traditional CD8+ T-cell population, and finally to get more insights into the activation of the cytotoxicity properties, in particular with regard to NK cells. The data recently acquired concerning the effector cytotoxic cells contribute to a better understanding of the interactions between the immune system and tumour cells. This may provide rational basis for combined immunotherapy protocols.
Cytotoxicity, Immunologic↗
Immune and natural antibodies to syngeneic murine plasma cell tumors.
Cytotoxic antibody to a plasma cell tumor antigen was produced in syngeneic BALB mice by immunization with viable or inactivated plasma cell tumors. Antibody with the same specificity was found in the sera of normal BALB and other strains of mice. This natural antibody reacted with an antigen with characteristics indistinguishable from the previously described alloantigen, PC.1, and with viral envelope antigen, chiVEA. The incidence of cytotoxic reactivity and the antibody titers reached a peak in normal BALB mice at 3-4 months of age, and were lower in 9-12-month old mice. The sera of germfree mice had lower reactivity; but when the mice were transferred to conventional conditions, their sera soon became as active as those of conventional mice. A virus common to all plasma cell tumors, which is present in latent form in some normal tissues of BALB and other PC.1 positive strains, is suggested as the cause for the PC.1 antigen and for the appearance of natural antibody to it. The considerable evidence for the close association of a virus with plasma cell tumors is presented.
Animals↗
Distinct brain vascular cell types manifest inducible cyclooxygenase expression as a function of the strength and nature of immune insults.
Induced prostanoid synthesis by cells associated with the cerebral vasculature has been implicated in mediating immune system influences on the CNS, but the cell type(s) involved remain unsettled. To determine whether this might derive from differences in the nature and intensity of the stimuli used to model immune insults, immunochemical and hybridization histochemical methods were used to monitor cyclooxygenase-2 (COX-2) expression alone, or in conjunction with endothelial, perivascular, and glial cell markers, in brains of rats treated with varying doses of interleukin-1 (IL-1) or bacterial lipopolysaccharide (LPS). Vehicle-treated animals displayed weak COX-2 expression in the meninges, choroid plexus, and larger blood vessels. Rats challenged intravenously with IL-1beta (1.87-30 microgram/kg) showed a marked increase in the number of vascular-associated cells displaying COX-2-immunoreactivity (ir). More than 90% stained positively for the ED2 macrophage differentiation antigen, identifying them as perivascular cells, whereas none coexpressed endothelial or glial cell markers. Low doses of LPS (0.1 microgram/kg) elicited a similar response profile, but higher doses (2-100 microgram/kg) provoked COX-2 expression in a progressively greater number of cells exhibiting distinct round or multipolar morphologies, corresponding to cells expressing endothelial (RECA-1) or perivascular (ED2) cell antigens, respectively. Similarly, ultrastructural analysis localized COX-2-ir to the perinuclear region of endothelial cells of LPS-treated but not IL-1-treated rats. We conclude that perivascular cells exhibit the lower threshold to COX-2 expression in response to either IL-1 or endotoxin treatment, and that enzyme expression by endothelial cells requires one or more facets of the more complex immune stimulus presented by LPS.
Animals↗
How medical students in their pre-clinical year perceive their own hepatitis-B-virus status: the results of a study in a Thai medical school.
In 2000 all of the medical students of the Faculty of Medicine at Chulalongkorn University in Bangkok who were then in their pre-clinical year were interviewed about their hepatitis-B-virus (HBV) status. Of the 215 interviewees, 125 (58.2%) claimed to know their HBV status. Seventy (32.6%) of the subjects assumed they were immune because they had already been vaccinated against the virus, 32 (14.9%) claimed to have natural immunity following exposure to the virus, and 14 (6.5%) reported that they were HBV carriers. Another five (2.3%) of the subjects said they had been tested for HBV and found seronegative and the remaining four subjects (1.9%) who said they knew their status declined to give any more details. The 90 subjects who did not know their status were all offered HBV screening, and 62 agreed to be tested, both for the surface antigen of the virus (HBsAG) and antibody to the viral core (anti-HBc). These tests revealed that 37 subjects were seronegative (negative for both HBsAg and anti-HBc), 11 appeared to have natural immunity (negative for HBsAg but positive for anti-HBc) and the other 14 were carriers (positive for HBsAg but negative for anti-HBc). Four of the 14 carriers were also positive for the HBV 'e' antigen (HBeAg), indicating that they were highly infectious. Medical students form a high-risk group for infection with blood-borne pathogens, including HBV. That more than 40% of the pre-clinical students in the present study did not know their HBV status and fewer than 50% had been vaccinated against the virus are therefore causes for concern. Those students entering Thai medical schools for the first time clearly need to be better educated about hepatitis B and to be encouraged to be vaccinated before they begin any clinical practices.
Adult↗
Exercise training and mouse mammary tumour metastasis.
The present study was designed to address whether exercise influences the experimental metastasis of a mouse mammary tumour; a related issue was the impact of timing of exercise onset relative to tumour exposure on NK and LAK mediated cytotoxicity. After 8 weeks of forced treadmill exercise or voluntary wheel running or remaining sedentary, female BALB/c mice received an intravenous (i.v.) injection of female BALB/c mice received an intravenous (i.v.) injection of MMT line 66 tumour cells. Mice were then randomized into continuation of activity (TT, WW), cessation of activity (TS, WS), initiation of activity (ST, SW) and maintenance of sedentary condition (SS) for three weeks. Tumour control (TC) mice, who were matched to the SS mice for age, received an i.v. injection of heat-killed MMT 66 tumour cells. In total there were 8 groups including the tumour control. The average number of lung tumours did not differ by activity condition; however, the mice in the continuous treadmill group (TT) tended to have a higher tumour multiplicity (162 +/- 22) and those in the treadmill x sedentary condition (TS) tended to have lower tumour multiplicity (109 +/- 16) compared with the other groups except the SW group (95 +/- 15). The lymphokine activated killer activity in the spleen was significantly elevated in the TS (49 +/- 3%) and WS (44 +/- 3%) mice compared with the sedentary animals (30 +/- 3%) (p < 0.003 and 0.05, respectively). NK activity was lower in the mice that had stopped exercising (TS and WS) after injection of tumour compared with sedentary animals. These data suggest that although exercise training influences natural immune cytotoxic mechanisms in vitro, this may not translate into clinically significant changes in tumour burden. The dissociation between natural immunity and tumour outcome may reflect the relative resistance of the tumour line to lysis by natural killer cells. It remains to be tested if infusion of IL-2 (to induce LAK activity) in exercise trained animals results in fewer tumour metastases.
Animals↗
Effect of exercise on natural cytotoxicity and pulmonary tumor metastases in mice.
Exercise has been demonstrated to reduce experimental tumor formation in rodents when the exercise is present during the tumor initiation or promotion phases. This study evaluated whether exercise influenced the process of tumor metastasis and subsequent growth in a secondary implant site. Male C3H mice remained sedentary, were given free access to running wheels, ran on a treadmill (15 m.min-1, 30 min.d-1), or walked on a treadmill (5 m.min-1, 5 min.d-1)(N = 20/group). Following 9 wk of this protocol, exercise was discontinued. At this time all animals received a tumor cell dose (CIRAS 1, 3 x 10(5)) i.v., and remained sedentary until sacrificed 3 wk later. Splenic natural killer (NK) cell activity was elevated in the wheel running mice compared with sedentary controls 3 wk after cessation of exercise (F(3,74) = 6.266, P < 0.002). Exercised mice displayed lower tumor cell retention in the lungs relative to nonexercised mice (F(1,37) = 6.593, P < 0.02). Tumor incidence was not different across activity groups whereas tumor multiplicity was higher in mice that had been previously exposed to exercise. (However, it should be noted that the significant exercise-tumor effect was due to a small number of exercised mice with extreme multiplicity, > 200 foci/lung.) More extensive tumor colony formation was present in wheel-trained mice that displayed the greatest volumes of daily running. The results from this study suggest that exercise was able to augment natural immune cytotoxic function for up to 3 wk after cessation of activity. However, this augmentation of natural immune function was not associated with reduced tumor incidence in the exercised animals.
Animals↗
Impact of aging on innate immunity.
Immune responses in higher organisms are triggered by the recognition of a limited diversity of microbiological products by cells of the innate or "natural" immune system. As a result, in addition to the direct protective effect of natural immunity, antigen-presenting cells, particularly dendritic cells, are activated to process and present an enormous number of peptide antigens to the T lymphocytes of the adaptive immune system. These, together with the B lymphocytes, then mediate specific immune responses and maintain acquired immunological memory. The aging immune system is less well able to cope with infectious disease than the youthful immune system; this review will briefly consider what is known of the age-associated alterations in innate immunity, and how these may also impact on adaptive immunity.
Aging↗
Patients benefit from using own CD4 T-cells.
HIV researchers continue to explore novel ways to fight the disease and enhance the benefits of antiretroviral therapy. One new approach involves the transferring activated autologous CD4 T-cells into HIV-infected patients with the goal of augmenting natural immunity to HIV infection. Reconstituting CD4 helper cell activity, along with decreasing CCR5 expression, may augment natural immunity to HIV infection, according to a newly published study.
CD4-Positive T-Lymphocytes↗
Naturally acquired immunity to pneumonia due to Mycoplasma pneumoniae.
The immunity to Mycoplasma pneumoniae was studied by periodic collection of sera up to 15 years after infection. Sera were tested for antilipid antibodies by complement fixation. Antibody levels remained elevated for two to nine years after pneumonia but usually fell sharply after the second year in persons with milder symptoms. Infection rates were at least six times higher in comparison groups than in previous pneumonia patients. Schoolchildren with serologic evidence of infection, but without pneumonia, during the 1966-1967 epidemic were not protected during the next epidemic (1974). Children with evidence of infection during the first two years of life were at no higher risk of clinical pneumonia (immunopathological response) at school age than those without previous known exposure. The current study suggests that naturally acquired infection induces partial immunity which lasts longer after pneumonia than after mild infections.
Adolescent↗
Humoral and cell-mediated immunity in natural and experimental canine leishmaniasis.
This paper describes immunological and clinicopathological findings in dogs naturally and experimentally infected with progressive visceral leishmaniasis. Eight dogs were intravenously inoculated with 5 x 10(7) stationary phase promastigotes of Leishmania infantum (LEM 2002, ZMON-1). A further eight naturally infected dogs were diagnosed by parasitological and serological methods and selected according to their clinical and immunological condition. Clinical, hematological, pathological and parasitological examinations, including parasite burden and distribution, were included in the study. Antibody production was estimated by means of enzyme-linked immunosorbent assay and immunofluorescence assay techniques; the cellular immune response was studied by means of the skin test and the lymphocyte proliferation test. Experimentally infected dogs developed a chronic and progressive disease with the same clinical signs shown by naturally infected dogs. Both naturally and experimentally infected dogs developed the same histopathological reaction, but to differing degrees. Parasite burden and distribution were related to the extent of lesions, and were consequently less pronounced in experimentally infected dogs. The main feature of the immune response in experimental and natural infection was the lack of specific T-cell response to leishmanial antigen. Non-specific responses to mitogens were normal (i.e. as compared with healthy dogs) throughout the experimental infection, but were partially suppressed (65.3%) in naturally infected animals. A remarkable humoral response was evident in both natural and experimental infection: IgG-isotype antibodies were detected in experimental infection at 50-70 days post infection, and their production increased during the course of the infection. However, high titers were observed only in naturally infected dogs.
Animals↗
Interactions of commensal gut microbes with subsets of B- and T-cells in the murine host.
Although mechanisms operative in the induction and maintenance of specific, adaptive immunity, including 'cognate' B/T interactions, have been extensively studied and defined, we still know little about the mechanisms operative in developing and maintaining B- and T-cell dependent 'natural' immunity. Particularly, we are still rather ignorant concerning gut microbial/gut or systemic APC, T cell and B cell interactions that lead to lymphoid cell mediated 'natural' immunity: specific or broadly reactive, activation via TCR and BCR and/or via other receptors such as the TLR series, and whether T/B interactions are operative at this level? Here we will address: (1) the general role of gut microbes in the development and maintenance of the intestinal, humoral immune system; (2) the general role of gut microbes in the development of B1 cell mediated, 'natural' gut IgA and the dependence of these B1 cells on bystander T cell help; (3) the relative contributions of B1 versus B2 cells to gut 'natural' and specific IgA responses; (4) the role for particular 'normal' gut microbes in the initiation of inflammatory bowel diseases (IBD) in mice with a dysregulated immune system; and (5) the possible roles of gut microbes in facilitating oral tolerance, a mechanism likely operative in forestalling or ameliorating IBD. A central theme of this paper is to attempt to define the specificities of activated, functional CD4+ T cells in the gut for Ags of particular, usually benign gut microbes. We will also consider the still-unresolved issue of whether the contributions of B1-derived IgA in the gut to the 'natural' Ab pool are Ag-selected and driven to proliferation/differentiation or whether the main stimuli are not via BCRs but rather other receptors (TLRs, etc.). The main experimental approach has been to use antigen-free, germ-free, or gnotobiotic (mono- or oligo-associated with precisely known bacterial species) mice.
Animals↗
Xenotransplantation.
Transplantation of solid organs (heart, lung, liver, and kidney) from swine to humans would solve the current critical shortage of cadaver organs needed by patients with end-stage disease of these organs. In addition, transplantation between distant species (discordant xenografting) will require an understanding of a number of unique immunologic features. Discordant xenografts are rejected within minutes to hours after transplantation. This rejection is due to natural immunity by recipients never before exposed to the xenografts. In some species combinations, this fulminant rejection is due to naturally occurring pre-existing antibodies against the xenograft endothelium. In other species combinations, the xenograft activates the alternative pathway of complement. The swine to human species combination is the most clinically relevant. In this combination, natural human and private antibodies recognize alpha-galactosyl residues of glycoproteins and glycolipids. Potential future therapeutic measures to prevent natural immunity include the genetic engineering of human complement inhibitors into swine cell membranes or genetic "knock out" of the enzymes responsible for placing alpha-galactosyl residues on swine cell surfaces. There are also special considerations in acquired immunity against xenografts. Cytokines and adhesion molecules may not work across species lines. Xenograft antigens may have to be processed by host antigen-presenting cells in order to effectively stimulate the immune system.
Animals↗
Development of immunity in natural Plasmodium falciparum malaria: antibodies to the falciparum sporozoite vaccine 1 antigen (R32tet32).
Antibodies that reacted with a candidate sporozoite vaccine antigen (R32tet32) were found in 20 of 21 patients treated for acute infection with Plasmodium falciparum and monitored longitudinally over 67 days. R32tet32 contains 32 tandem copies of a tetrapeptide sequence that constitutes the immunodominant epitope of the circumsporozoite surface protein. The magnitude of the antibody response varied considerably among individuals and appeared to be independent of the number of previous clinical infections. Recrudescence of infection or infection with Plasmodium vivax had no demonstrable effect on antibody levels, although reinfection with P. falciparum produced a rapid rise in antibody titer. Antibody levels were observed to decline rapidly after treatment of clinical infection with mefloquine. The apparent antibody half-life was 27 days, which is comparable to the half-life of circulating immunoglobulin G in humans. The data suggest that antisporozoite antibody production ceased on about day 4 after treatment of acute infection. A similar pattern of response was observed for antibodies against the erythrocytic forms of the parasite. The cessation of antibody synthesis was interpreted as being due to immunosuppression induced by the presence of intraerythrocytic parasites and may explain in part why protective immunity is poorly developed in natural malaria infections.
Acute Disease↗
Unique T cell effector functions elicited by Plasmodium falciparum epitopes in malaria-exposed Africans tested by three T cell assays.
Natural immunity to malaria is characterized by low level CD4 T cell reactivity detected by either lymphoproliferation or IFN-gamma secretion. Here we show a doubling in the detection rate of responders to the carboxyl terminus of circumsporozoite protein (CS) of Plasmodium falciparum by employing three T cell assays simultaneously: rapid IFN-gamma secretion (ex vivo ELISPOT), IFN-gamma secretion after reactivation of memory T cells and expansion in vitro (cultured ELISPOT), and lymphoproliferation. Remarkably, for no individual peptide did a positive response for one T cell effector function correlate with any other. Thus these CS epitopes elicited unique T cell response patterns in malaria-exposed donors. Novel or important epitope responses may therefore be missed if only one T cell assay is employed. A borderline correlation was found between anti-CS Ab levels and proliferative responses, but no correlation was found with ex vivo or cultured IFN-gamma responses. This suggested that the proliferating population, but not the IFN-gamma-secreting cells, contained cells that provide help for Ab production. The data suggest that natural immunity to malaria is a complex function of T cell subgroups with different effector functions and has important implications for future studies of natural T cell immunity.
Adult↗
[Current status of the problem on child immunity. 1. Natural, nonspecific protective factors in the child's body].
Explore the source record for details and available documents.
Complement System Proteins↗