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At least 667 records · Page 37Linked to original sources
PubMed1999

Antigen-specific cytokine and antibody isotype profiles induced by mucosal and systemic immunization with recombinant adenoviruses.

We investigated antigen-specific antibody and T-cell responses in mice immunized with human adenovirus type 5 (HAd5) vectors expressing either the authentic or truncated form of glycoprotein D (gD and tgD, respectively) of bovine herpesvirus type 1 (BHV-1). We also tested whether different routes of immunization influenced the level and type of immunity. Immunization intranasally (i.n.) stimulated higher levels of gD-specific IgA in the lung and nasal washes and induced a higher frequency of gD-specific antibody secreting cells (CSs) in the lung than did immunization subcutaneously (s.c.). In addition, immunization i.n. stimulated gD-specific systemic antibody responses of a higher IgG1/IgG2a ratio and lower numbers of gD-specific interferon (IFN)-gamma SCs in the spleen than did immunization s.c. HAd5-specific responses also depended on the route of immunization and were characterized by lower IFN-gamma interleukin (IL)-4 ratios than gD-specific responses. Immunization with the tgD-expressing vector induced generally lower antibody and cytokine responses than the gD-expressing vector. Higher numbers of antigen-specific IgA SCs in the lung as measured by enzyme-linked immunospot (ELISPOT) assay correlated with higher levels of IgA in the respiratory tract as measured by enzyme-linked immunosorbent (ELISA) assay, although there was no such correlation for IgG responses of any isotype. In conclusion, the route of immunization and form of antigen had an impact on the level and type of immune responses induced by adenovirus vectors.

Adenoviruses, Human↗
PubMedDate not supplied

Serum lipid profile and its relationship with host immunity in carcinomas of the breast and uterine cervix.

Carcinomas of the uterine cervix and breast, which have a different etiopathogenesis, are the most common malignancies among Indian women. Between these two cancers a comparative study was undertaken in which serum lipids were assessed along with host immunity. Thirty randomly selected cases each of breast and cervical carcinoma, and 20 matched healthy control women were studied by means of standard procedures. Significantly higher (P < 0.001) mean levels of triglycerides (x = 192.1 mg/dl, SD +/- 113.5) and total cholesterol (x = 212.9 mg/dl, SD +/- 49.78) were observed in breast cancer as compared to controls or cervical cancer patients. Patients with cervical cancer had low mean values of all lipid fractions. Women with the above malignancies also showed a significantly decreased CD3+ and CD4+ population (P < 0.001), while there was a significant increase in CD8+ cells (P < 0.005) compared to normal controls. Interestingly, a significant relationship (P < 0.05) was observed between CD8+ cells and LDL-cholesterol among the cancer patients (r = 0.3652 and r = 0.4298 for carcinomas of breast and cervix, respectively.

Adult↗
PubMed2004

Antigen-specific gene expression profiles of peripheral blood mononuclear cells do not reflect those of T-lymphocyte subsets.

Advances in microarray technology have allowed for the monitoring of thousands of genes simultaneously. This technology is of particular interest to immunologists studying infectious diseases, because it provides tremendous potential for investigating host-pathogen interactions at the level of immune gene expression. To date, many studies have focused either on cell lines, where the physiological relevance is questionable, or on mixed cell populations, where the contributions of individual subpopulations are unknown. In the present study, we perform an intrasubject comparison of antigen-stimulated immune gene expression profiles between a mixed population of peripheral blood mononuclear cells (PBMC) and the two predominant cell types found in PBMC, CD4+ and CD8+ T lymphocytes. We show that the microarray profiles of CD4+ and CD8+ T lymphocytes differ from each other as well as from that of the mixed cell population. The independence of the gene expression profiles of different cell types is demonstrated with a ubiquitous antigen (Candida albicans) as well as with a disease-specific antigen (human immunodeficiency virus p24). This study has important implications for microarray studies of host immunity and underscores the importance of profiling the expression of specific cell types.

Antigens↗
PubMed2003

In vivo expression of recombinant pregnancy-specific glycoprotein 1a induces alternative activation of monocytes and enhances Th2-type immune response.

It has been proposed that pregnancy-specific factors could be responsible for shift the balance of cytokine profiles during maternal immune response from Th1-type reactivity into a "less-damaging" Th2-type reactivity. In the present work, we investigated the in vivo function of human pregnancy-specific glycoprotein (PSG)1a, the major variant of PSG polypeptides released into the circulation during pregnancy, on the modulation of the innate and adaptive immune response. For this, BALB/c mice were injected with a vaccinia virus-based vector harboring the human PSG1a cDNA (Vac-PSG1a) 4 days before immunization with ovalbumin (OVA) in complete Freund's adjuvant, and the early specific T cell response against OVA was evaluated 8 days post-immunization. We also studied the activation status of spleen and peritoneal monocytes/macrophages (Mo) populations from Vac-PSG1a-treated mice, and explored whether PSG1a-targeted Mo could affect the Th-type commitment by investigating their impact on the differentiation of naive T cells. Our data show that the treatment with Vac-PSG1a is able to induce a state of alternative activation on Mo. Furthermore, the generation of the immune response in the context of these alternatively activated antigen-presenting cells may shift T cell differentiation to Th2-type immunity which is more compatible with a successful pregnancy.

Animals↗
PubMed2002

Influence of the polyclonal activation induced by Plasmodium chabaudi on ongoing OVA-specific B- and T-cell responses.

Infection by Plasmodium chabaudi results in polyclonal activation, massive proliferation and differentiation of lymphocytes with parasite-unrelated specificities. To verify if polyclonal activation includes experienced B and T lymphocytes and if it modifies pre-established cytokine and Ig-isotype patterns, mice were immunized with ovalbumin (OVA) in alum, a condition that favours T helper 2/immunoglobulin G1 (Th2/IgG1) responses, and infected with P. chabaudi 7 or 80 days later. Polyclonal activation markedly increased the number of anti-OVA Ig-secreting cells in the spleen, an effect more patent in mice infected 7 days after OVA immunization, but also evident in mice infected after 80 days. The Ig-isotype profile predefined by immunization was not qualitatively modified by polyclonal activation. Thus, although P. chabaudi infection preferentially induces IgG2a, the expanded anti-OVA response is dominated by IgG1. Polyclonal expansion of the anti-OVA response did not yield an enlarged memory B-cell pool that could be recalled months later by OVA boosting. Moreover, polyclonal activation of anti-OVA IgG1-secreting cells did not increase this antibody in serum, a probable consequence of the high Ig turnover observed during infection. When OVA-specific T-cell cytokines were evaluated, we observed an increase of both interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in mice infected 7 days after immunization, whereas in those infected after 80 days, only IL-4 was augmented. These results suggest that polyclonal activation expands experienced B- and T-cell compartments, preserving their antibody and cytokine patterns.

Animals↗
PubMed2005

Immune Responses to Ethanol Metabolites and Cytokine Profiles Differentiate Alcoholics with or without Liver Disease.

OBJECTIVES: Excessive alcohol consumption is associated with the generation of antibodies against neoantigens induced by ethanol metabolism. However, the associations between such immune responses, ethanol consumption, and liver injury remain unclear. METHODS: Eight-six male alcoholics with (n=54) or without (n=32) liver disease, and 20 male volunteers (6 abstainers, 14 moderate drinkers) underwent clinical, morphological, and biochemical assessments of liver status and ethanol consumption. RESULTS: Antiacetaldehyde adduct IgAs in both groups of alcoholics were significantly higher than those in the controls. Elevated IgGs occurred in patients with liver disease, whereas IgMs were high in the heavy drinkers without apparent liver disease. Liver disease patients had high levels of both proinflammatory (IL-2, IL-6, IL-8, TNF-alpha) and antiinflammatory (IL-10) cytokines, whereas those without liver disease showed elevated IL-6, IL-8, and IL-10 only. Ethanol consumption correlated significantly with antiadduct IgA and IL-6 levels, which also showed parallel changes upon abstinence. CONCLUSIONS: Alcoholic liver disease is associated with the generation of IgAs and IgGs against acetaldehyde-derived antigens and enhanced levels of both pro- and antiinflammatory cytokines, whereas elevated IgA, IL-6, and IL-10 characterize alcoholics without liver disease. These data suggest that immunological mechanisms may play a role in the sequence of events leading to liver disease in some patients with excessive drinking.

Acetaldehyde↗
PubMed1984

A general theory for the precipitin reaction--based on Fc-mediated precipitation.

Fc-mediated immune precipitation is studied theoretically by computer simulation of precipitin curves and of zonal profiles of soluble immune complexes. Comparison with experiments indicates that Fc-mediated immune precipitation is caused by Fc-Fc interactions with association constants ranging from 10(5) to 10(7) liters/mole. The Langmuir adsorption isotherm is used for evaluation of these interactions. A general theory for the precipitin reaction is formulated, assuming it to be a three-stage process: 1st stage Formation of immune complexes, 2nd stage Precipitation due to coalescence of antibody-rich immune complexes, and 3rd stage Fc-mediated immune precipitation.

Antigen-Antibody Complex↗
PubMed1995

Stimulus-dependent production of cytokines and pterins by peripheral blood mononuclear cells.

The cytokine profiles produced by peripheral blood mononuclear cell (PBMC) cultures were dependent upon the nature of the stimulus used. Powerful lymphocyte activators such as mitogens induced rapid cell proliferation together with the production of both inflammatory (IL-1 alpha, IL-1 beta, IL-6 and TNF alpha) and immune (IFN-gamma, TNF-alpha and TNF-beta) cytokines, and immune activation markers (soluble IL-2 receptor, neopterin and xanthopterin). Bacterial endotoxin failed to induce cell proliferation but resulted in the rapid production of inflammatory cytokines together with a short burst of IFN-gamma production, without the production of the other immune cytokines or activation markers. Alloantigen stimulation gave a typical immune cytokine and marker profile, with little or no production of inflammatory cytokines. Re-call antigens (candida and PPD) induced maximal cell proliferation at days 5 to 6, but induced little or no production of inflammatory cytokines. Markedly different immune cytokine profiles were obtained with these re-call antigens. Candida induced an early burst of IFN-gamma production on day 1 followed by later production of TNF-alpha. In cultures stimulated with PPD, both IFN-gamma and TNF-alpha were detected from day 2. With both re-call antigens, the levels of production of the activation markers were equivalent to the proliferative responses obtained.

Biopterins↗
PubMedDate not supplied

[Characteristics of urogenital and post-enterocolitis reactive arthritides].

The immune status and profile of HLA antigens of loci A and B were evaluated in 159 patients with reactive arthritis. Reactive arthritis was caused by urogenital chlamydial infection in 64.2% of cases and by Shigella, Salmonella and Yersinia enterocolitica infection in 18.9% of cases. In patients with different etiology of the disease some variations in its course and outcome, immune status as well as in the HLA antigen profile were established that is indicative of genetic determination of the immune response character. The established specific variations in the immune and immunogenetic status of patients with reactive arthritis of different etiology may be used for improving diagnosis and treatment efficacy.

Adult↗
PubMed2026

Spatial Omics in High-Grade Gliomas: Mapping Immune-Tumor Niches for Precision Therapy.

High-grade gliomas (HGGs), particularly glioblastoma (GBM), remain among the most lethal human cancers despite decades of molecular profiling and therapeutic innovation. A primary reason for treatment failure is that HGG biology is spatial: malignant cell states, immune suppression, metabolic stress, and therapeutic resistance are organized into distinct anatomical and functional niches. Spatial omics technologies now enable high-dimensional mapping of gene expression, protein signaling, immune architecture, and metabolic activity within intact tumor tissue. These approaches reveal how proneural and mesenchymal transcriptional states coexist yet localize to distinct regions, alongside hypoxic, invasive, and stem-enriched niches. Spatial analyses show that key clinical determinants, including O6-methylguanine-DNA methyltransferase (MGMT)-associated temozolomide resistance, radiotherapy tolerance in hypoxic regions, and immunotherapy failure driven by myeloid-dominated immune exclusion, are influenced not only by molecular programs but also by cellular location. Beyond biological insight, spatial omics is reshaping clinical paradigms by enabling region-specific patient stratification, early assessment of treatment response, and identification of therapy-resistant reservoirs that seed recurrence. Prior bulk and single-cell studies defined HGG cell states and pathways but often treated resistance as tumor-wide. This review presents a spatially explicit framework that synthesizes spatial transcriptomic and immune-profiling studies to identify tumor-immune niches and spatial bottlenecks that drive therapeutic failure and recurrence.

Humans↗
PubMed2004

Serologic assessment of type 1 and type 2 immunity in healthy Japanese adults.

We assessed the informativeness of several serologic biomarkers of immune function using serum specimens collected in the Miyazaki Cohort Study from subjects who were seronegative for anti-human T-cell lymphotrophic virus I and anti-hepatitis C virus. To broadly characterize type 1 immune status, we measured EBV antibody titers, because titer profiles associated with cellular immune suppression are well described. We also tested for three type 2 biomarkers: total serum IgE, soluble CD23, and soluble CD30. Nonreactivity to a tuberculin purified protein derivative (PPD) skin test is indicative of diminished delayed-type hypersensitivity (type 1) responsiveness in the study population due to a history of tuberculosis exposure or Bacillus Calmette-Guérin vaccination. We therefore evaluated the serologic markers as predictors of PPD nonreactivity using logistic regression. Subjects whose EBV antibody profiles were consistent with deficient type 1 immunity were more than thrice as likely to be PPD nonreactive as persons with "normal" antibody titers. Elevated total IgE was also strongly associated with PPD nonreactivity (odds ratio 3.4, 95% confidence interval 1.2-9.9); elevated soluble CD23 had a weaker, but positive, odds ratio, whereas soluble CD30 levels were not predictive of PPD status. Therefore, PPD nonreactivity is associated, in this population, with a pattern of serum biomarkers that is indicative of diminished type 1 and elevated type 2 immunity. We conclude that, with the exception of soluble CD30, the serologic markers are informative for the characterization of type 1/type 2 immune status using archived sera from study populations of healthy adults.

Adult↗
PubMedDate not supplied

Low-tar and high-tar cigarettes.

Mice were exposed for 7 to 8 minutes on weekdays to fresh smoke from high-tar (HT) or low-tar (LT) cigarettes for varying periods of up to 36 weeks. Mice exposed to HT cigarettes exhibited more marked alterations in humoral immune responsiveness, hematological profiles, and pulmonary pathologic findings than those exposed to LT cigarettes. However, cell-mediated immune responsiveness to both bacterial and tumor-specific antigens was depressed similarly in animals exposed to HT or LT cigarettes. Furthermore, the growth rates of subcutaneously established tumors were enhanced similarly in the two groups, with respect to those in control animals.

Animals↗
PubMed2005

Recipient-specific tolerance after HLA-mismatched umbilical cord blood stem cell transplantation.

BACKGROUND: Lower incidence and severity of acute graft versus host disease (GVHD) has been observed in leukemia patients receiving HLA-mismatched umbilical cord (UCB) transplants. However, despite the increased use of UCB in stem cell transplantation, the mechanisms underlying these favorable outcomes are not well delineated. METHODS: We analyzed antigen specific lymphocyte responses after transplant to determine whether the decreased allogeneic responsiveness of UCB lymphocytes is attributable to pan-unresponsiveness, lymphocyte repressive or recipient-specific tolerance. RESULTS: Circulating lymphocytes collected early (3 months) after UCB transplant demonstrate a less naïve phenotype compared with that in the infused graft. Additionally, after transplant, circulating peripheral blood UCB-derived lymphocytes produced normal levels of interferon-gamma and proliferated normally when stimulated with mitogen or third party alloantigen. In contrast, when stimulated with recipient antigen, circulating lymphocytes emerging posttransplant did not proliferate nor produce interferon-gamma. Moreover, analysis of interleukin-4 production revealed a Th2 response to recipient antigens. These data indicate early induction of immune tolerance of naïve UCB graft lymphocytes with skewing of transplant recipient-specific immune response towards Th2 cytokine profile. CONCLUSIONS: UCB graft lymphocyte immune naivety and observed early tolerance induction may contribute to the observed favorable GVHD incidence, despite infusion of HLA mismatch grafts in the unrelated allogeneic setting.

Adult↗
PubMed1997

Infection with Salmonella typhimurium modulates the immune response to Schistosoma mansoni glutathione-S-transferase.

Immune response polarization is controlled by several factors, including cytokines, antigen-presenting cells, antigen dose, and others. We have previously shown that adjuvants and live vectors play a critical role in polarization. Thus, immunization with the Schistosoma mansoni 28-kDa glutathione-S-transferase (Sm28-GST) in aluminum hydroxide induced a type 2 cytokine profile and the production of immunoglobulin G1 (IgG1)- and IgE-specific antibodies. In contrast, mice infected with recombinant Salmonella typhimurium expressing Sm28-GST developed a type 1 cytokine profile and produced IgG2a-specific antibodies against Sm28-GST and Salmonella antigens. In this study, to determine if S. typhimurium not expressing Sm28-GST would still influence the type of the response against this antigen, we compared the profiles of the immune responses generated against Sm28-GST administered in alum in mice infected and not infected with S. typhimurium. Infected mice generated both IgG1 and IgG2a antibodies against Sm28-GST, while noninfected mice produced only IgG1 anti-Sm28-GST antibodies. Moreover, interleukin-4 (IL-4) mRNA expression in infected mice was near background levels, while gamma interferon (IFN-gamma) mRNA expression in coinfected mice was significantly higher than in mice immunized with Sm28-GST in alum only. However, after antigen-specific stimulation in vitro with Sm28-GST, levels of IL-4 and IFN-gamma cytokine production were similar in the two groups of mice. These results suggest that (i) the immune milieu produced during an infection may modify the response against an irrelevant antigen and (ii) isotype switching may be influenced by the cytokine environment of a bystander immune response, even though the specific antigen-driven cytokine production is not modified. Thus, the isotypic profile is not always an absolute reflection of the cytokines produced by antigen-specific Th cells.

Animals↗
PubMed1993

Effect of level of supplemental chromium on performance, serum constituents, and immune status of stressed feeder calves.

The effects of level of supplemental Cr from high-Cr yeast on performance, blood chemistry profile, morbidity, and immune status were investigated using 84 Charolais-crossed steer calves in a completely randomized design. Calves of 236-kg average weight, after transportation from Saskatchewan to Ontario, were randomly assigned to four treatments; 0, .2, .5, and 1 ppm of supplemental Cr, incorporated into a corn-silage diet. Blood was collected via jugular venipuncture at d 0, 7, 14, 21, and 28 and analyzed for metabolites, minerals, immunoglobulins, hematocrit (Hct), and leucocyte counts. Hemagglutinating antibody titers to human red blood cells (HRBC) were quantified after immunizations on d 0 and 14. Contact sensitivity after sensitization and challenge with dinitrochlorobenzene was also measured. A 27% increase (P < .05) in ADG was observed at d 30 for calves that were fed .2 and 1 ppm of supplemental Cr. Dry matter intake also increased (P < .05) for the .2- and 1-ppm Cr treatments. A linear decrease (P < .05) in serum cortisol with increasing Cr level was observed at d 28. Chromium supplementation decreased (P < .05) morbidity, as well as rectal temperatures at d 2 and 5. Peak primary antibody titers to HRBC (P < .05) and immunoglobulin G1 concentrations (P = .06) at d 14 were higher for steers that received the Cr supplementation. However, Cr treatment had no effect on expression of contact sensitivity. Chromium supplementation increased (P < .05) Hct on d 14 and 21 and serum Ca and Mg on d 7.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed2002

Protective roles of pulmonary surfactant proteins, SP-A and SP-D, against lung allergy and infection caused by Aspergillus fumigatus.

Pulmonary surfactant proteins, SP-A and SP-D, are immune molecules which can directly interact with pathogens and allergens, stimulate immune cells and manipulate cytokine and chemokine profiles during host's immune response. Using an opportunistic fungal pathogen Aspergillus fumigatus (Afu), we have attempted to understand participation of SP-A and SP-D in the host immunity. Afu causes a systemic infection via lungs, called invasive aspergillosis (IPA) in immunocompromised subjects. In the immunocompetent subjects, it can cause an allergic disorder, called allergic bronchopulmonary aspergillosis (ABPA). Therapeutic administration of these proteins in a murine model of IPA can rescue mice from death. Treating mice, having ABPA, can suppress IgE levels, eosinophilia, pulmonary cellular infiltration and cause a marked shift from a pathogenic Th2 to a protective Th1 cytokine profile. These results highlight the potential of SP-A, SP-D and their recombinant forms, as novel therapeutics for lung allergy and infection.

Animals↗
PubMed2000

Parasite-secreted products regulate the host response to larval Taenia crassiceps.

Parasite-induced immunosuppression is believed to play a significant role in the pathology of cysticercosis, a disease caused by the larval stage of cestode parasites. The biochemical basis for immunoregulation by Taenia crassiceps in experimental cysicercosis is unknown. In order to determine whether or not excretory/secretory (E/S) products from the parasite have the ability to regulate host immune function, the activity of these products was examined. Excretory/secretory products from larvae early in the infection were found to suppress T cell proliferative responses in vitro as well as the production of IFN-gamma and IL-4. In contrast, E/S products secreted from larvae harvested late in infection were not suppressive. Electrophoretic analysis of E/S products revealed both qualitative and quantitative differences in the pattern of proteins produced by larvae taken from an early infection versus those taken from a chronic infection. The viability of parasites taken from an early infection was greatly reduced compared to those taken from chronically infected mice, suggesting a change in the nature of the host immune response to the parasite during the course of the infection. The proliferative activity and cytokine profiles of host immune cells were examined. Both mesenteric lymph node cells and peritoneal exudate cells were found to produce high levels of both IFN-gamma and IL-4, consistent with the high levels of these cytokines in sera of chronically infected animals. Chronic infection with Taenia crassiceps therefore is characterized by high levels of production of both Th1 and Th2 cytokines by host cells.

Age Factors↗