SEARCH · Search PubMed

Results for “immune profiling”

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.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

PubMed2004

Chronic immune activation associated with chronic helminthic and human immunodeficiency virus infections: role of hyporesponsiveness and anergy.

Chronic immune activation is one of the hallmarks of human immunodeficiency virus (HIV) infection. It is present also, with very similar characteristics, in very large human populations infested with helminthic infections. We have tried to review the studies addressing the changes in the immune profiles and responses of hosts infected with either one of these two chronic infections. Not surprisingly, several of the immune derangements and impairments seen in HIV infection, and considered by many to be the "specific" effects of HIV, can be found in helminth-infected but HIV-noninfected individuals and can thus be accounted for by the chronic immune activation itself. A less appreciated element in chronic immune activation is the immune suppression and anergy which it may generate. Both HIV and helminth infections represent this aspect in a very wide and illustrative way. Different degrees of anergy and immune hyporesponsiveness are present in these infections and probably have far-reaching effects on the ability of the host to cope with these and other infections. Furthermore, they may have important practical implications, especially with regard to protective vaccinations against AIDS, for populations chronically infected with helminths and therefore widely anergic. The current knowledge of the mechanisms responsible for the generation of anergy by chronic immune activation is thoroughly reviewed.

AIDS-Related Opportunistic Infections↗

PubMed2004

Continuous antigenic stimulation system (CASS) as a new immunization strategy.

Protection against diseases is mediated by a sustained immune response. Here, we describe a new immunization strategy. Mice implanted with encapsulated C2C12 myoblasts secreting human factor IX (hFIX) elicited a strong humoral response against the transgene, as compared to mice immunized with complete Freund's adjuvant (FA). Mice also had increasing IgG2a antibody titer, indicating a switch to a Th1 profile immune response. Mice developed strong hFIX-specific cytotoxic T lymphocytes (CTL) that was detectable 213 days after implantation, demonstrating the sustained immunity elicited by encapsulated cells. Here, we propose continuous antigenic stimulation system (CASS) as a novel immunization strategy with potential application in the design of novel vaccines.

Animals↗

PubMed2005

Characterizing the symmetric equilibrium of multi-strain host-pathogen systems in the presence of cross immunity.

We investigate the population dynamics of host-pathogen systems in which the pathogen has a potentially arbitrary number of antigenically distinct strains interacting via cross-immunity. The interior equilibrium configuration of the symmetric multiple strain SIR model with cross-immunity is characterized. We develop an efficient iterative method for numerically solving the equilibrium equation together with a number of informative analytical approximations to the full solution. Equilibrium properties are studied as a function of the number of strains, reproduction number, infectious period, and cross immunity profile. We establish that the prevalence in the system increases monotonically with the number of strains and the reduction in cross immunity. Moreover, we demonstrate the existence of a phase transition separating high prevalence and low prevalence parameter regions, with the critical point being defined by sigmaR0 congruent with1, where sigma is the level of cross-immunity and R0 is the reproduction number. Above the threshold, prevalence saturates with increasing numbers of strains as a result of the inclusion of prohibition of co-infection in the model. Below the threshold, prevalence saturates much more rapidly as the number of strains increases--indicating that when cross-protection is sufficiently intense, the selective advantage for a pathogen to increase its diversity is substantially less than in the threshold region. Similarly, there is limited benefit to increased transmissibility (or decreased cross-immunity) both for the high and low diversity pathogen systems compared with systems at the threshold sigmaR0 congruent with1 where small increase in transmissibility can result in significant increase in prevalence.

Animals↗

PubMed2003

Induction of mosquitocidal activity in mice immunized with Anopheles gambiae midgut cDNA.

Vaccines that induce mosquito-killing (mosquitocidal) activity could substantially reduce the transmission of certain mosquito-borne diseases, especially vaccines against African malaria vectors, such as the mosquito Anopheles gambiae. To generate and characterize antimosquito immunity we immunized groups of mice with two individual A. gambiae midgut cDNAs, Ag-Aper1 (a secreted peritrophic matrix protein) and AgMuc1 (a midgut-bound mucin), and an A. gambiae midgut cDNA library from blood-fed mosquitoes. We observed significantly increased mortality among mosquitoes that fed on either the AgMuc1- or the cDNA library-immunized mice compared to that of controls, but no differences were observed among those fed on Ag-Aper1-immunized mice. Analysis of the humoral and cellular immune responses from mice showed that the induced mosquitocidal effect was associated with immune profiles characterized by elevated tumor necrosis factor alpha and gamma interferon cytokine levels and very low antibody titers. Furthermore, an additional immunization of cDNA library-immunized mice with midgut protein shifted immunity toward a Th2-type immune response, characterized by elevated antibody titers and high interleukin-5 and interleukin-10 cytokine levels; importantly, mosquitoes feeding on these mice exhibited no undue mortality. Finally, when immune sera was ingested by mosquitoes through a membrane feeder, no effect on mosquito mortality was observed, indicating that serum factors alone were not responsible for the mosquitocidal effect. Our results demonstrate that mosquitocidal immunity in mice can be consistently generated by midgut cDNA immunization and suggest this cDNA-induced mosquitocidal immunity is cell mediated.

Animals↗

PubMed2002

Identification of high caspase-3 mRNA expression as a unique signature profile for extremely old individuals.

Apoptosis, or programmed cell death, is important for maintaining tissue homeostasis, as it permits the elimination of damaged, functionless or unwanted cells. As we age, our immune system undergoes constant remodeling, during which age-associated changes in immune parameters, including decreased naïve and increased memory T cells, have been reported. However, excessive immune cell loss, rendering the elderly more vulnerable to infections, and inappropriate deletion of damaged or functionless lymphocytes, can contribute to the development of age-associated diseases. As such, we studied the mRNA expression of cell death (specifically caspase) genes in nonagenarians and centenarians, successful models of ageing who have survived or avoided age-associated diseases, as well as in their younger counterparts and found that population composed of extremely old individuals shows a unique pattern of caspase mRNA expression, characterized by high levels of caspase-1 and -3, and low levels of caspase-8, mRNA while those composed of old individuals are characterize by high level of caspase-8 mRNA expression. Furthermore, we show that the described changes in caspases mRNA do not appear to results from age-related changes in PBMC composition, such as decreases in CD24. Therefore, we suggest that unique patterns of caspase mRNA results from the regulation of message abundance on a per cell basis, via a putative regulation of caspase genes at the transcription or RNA processing level, rather than changes in immune profiles.

Adolescent↗

PubMed2004

Neurotoxic effects of postnatal thimerosal are mouse strain dependent.

The developing brain is uniquely susceptible to the neurotoxic hazard posed by mercurials. Host differences in maturation, metabolism, nutrition, sex, and autoimmunity influence outcomes. How population-based variability affects the safety of the ethylmercury-containing vaccine preservative, thimerosal, is unknown. Reported increases in the prevalence of autism, a highly heritable neuropsychiatric condition, are intensifying public focus on environmental exposures such as thimerosal. Immune profiles and family history in autism are frequently consistent with autoimmunity. We hypothesized that autoimmune propensity influences outcomes in mice following thimerosal challenges that mimic routine childhood immunizations. Autoimmune disease-sensitive SJL/J mice showed growth delay; reduced locomotion; exaggerated response to novelty; and densely packed, hyperchromic hippocampal neurons with altered glutamate receptors and transporters. Strains resistant to autoimmunity, C57BL/6J and BALB/cJ, were not susceptible. These findings implicate genetic influences and provide a model for investigating thimerosal-related neurotoxicity.

Animals↗

PubMed2025

An anti-androgen resistance-related gene signature acts as a prognostic marker and increases enzalutamide efficacy via PLK1 inhibition in prostate cancer.

BACKGROUND: Anti-androgen resistance remains a major clinical challenge in the treatment of prostate cancer (PCa), leading to disease progression and treatment failure. Despite extensive research on resistance mechanisms, a reliable prognostic model for predicting patient outcomes and guiding therapeutic strategies is still lacking. This study aimed to develop a novel gene signature related to anti-androgen resistance and evaluate its prognostic and therapeutic implications. METHODS: Anti-androgen resistance-related differentially expressed genes (ARRDEGs) were identified through transcriptomic analysis of enzalutamide- and dual enzalutamide abiraterone-resistant PCa cell lines from the GEO database. Functional enrichment analysis was performed to determine the biological roles of these genes. A prognostic gene signature was developed using univariate Cox regression, LASSO, and multivariate Cox regression models. The model was validated in independent PCa cohorts from The Cancer Genome Atlas (TCGA). Additionally, we assessed the correlation between the signature, immune infiltration, immune checkpoint expression, and drug sensitivity. The efficacy of PLK1 inhibition combined with enzalutamide was further explored using in vitro and in vivo experiments. RESULTS: We identified 304 ARRDEGs, from which three key genes (LMNB1, SSPO, and PLK1) were selected to construct a prognostic signature. This gene signature effectively stratified PCa patients into high- and low-risk groups, with the high-risk group exhibiting shorter recurrence-free survival and distinct immune characteristics. High-risk patients demonstrated elevated immune checkpoint expression (B7H3, CTLA-4, B7-1, and TIGIT), increased M2 macrophage infiltration, and enhanced sensitivity to chemotherapy and targeted therapy. Mechanistically, PLK1 inhibition potentiated the antitumor effect of enzalutamide by downregulating SLC7A11 and inducing ferroptosis, providing a potential therapeutic strategy to overcome anti-androgen resistance. CONCLUSION: We established a novel ARRDEGs-based prognostic signature that predicts PCa progression and response to chemotherapy and targeted therapy. The integration of this signature with immune profiling and drug sensitivity analysis provides a valuable tool for precision oncology in PCa. Our findings highlight the potential of PLK1 inhibition as a therapeutic strategy to enhance enzalutamide efficacy and overcome resistance.

Humans↗

PubMed1985

Ketotifen action upon the immunity state in bronchial asthma.

Alterations of the entire immunity profile of bronchial asthma patients have been studied following a half-year long Ketotifen treatment. It was observed that this drug leads to the normalization of the immunity state in a whole series of parameters and that it thus contributes on a large scale to the reestablishment of normal regulation. These findings may be utilized for expanding the possibilities of application of this preparation upon other immunopathological states that bronchial asthma and the atopic diseases.

Adolescent↗

PubMed2005

Armed CD4+ Th1 effector cells and activated macrophages participate in bile duct injury in murine biliary atresia.

Biliary atresia (BA) is an inflammatory cholangiopathy of infancy. A proposed mechanism regarding the pathogenesis of BA is that of a virus-induced, immune-mediated injury to bile ducts. The rotavirus (RRV)-induced murine model of BA was utilized to determine the hepatic inflammatory response related to ductal obstruction and if the immune response recapitulated human BA. One week after infection, there was a significant increase in liver CD4(+) T cells producing IFN-gamma and in macrophages producing TNF-alpha. The intrahepatic pattern of inflammation evolved rapidly from an initial predominant CD4(+) Th1 cellular response to a subsequent influx of activated macrophages producing TNF-alpha and iNOS. This immune response persisted despite viral clearance and was representative of the hepatic immune profile present in human BA. Utilization of the murine model of BA yielded mechanistic data that can provide much needed insight into the role played by different arms of the immune system related to the pathogenesis of human BA.

Animals↗

PubMed2023

Immunogenomics of cholangiocarcinoma.

The development of cholangiocarcinoma spans years, if not decades, during which the immune system becomes corrupted and permissive to primary tumor development and metastasis. This involves subversion of local immunity at tumor sites, as well as systemic immunity and the wider host response. While immune dysfunction is a hallmark of all cholangiocarcinoma, the specific steps of the cancer-immunity cycle that are perturbed differ between patients. Heterogeneous immune functionality impacts the evolutionary development, pathobiological behavior, and therapeutic response of these tumors. Integrative genomic analyses of thousands of primary tumors have supported a biological rationale for immune-based stratification of patients, encompassing immune cell composition and functionality. However, discerning immune alterations responsible for promoting tumor initiation, maintenance, and progression from those present as bystander events remains challenging. Functionally uncoupling the tumor-promoting or tumor-suppressing roles of immune profiles will be critical for identifying new immunomodulatory treatment strategies and associated biomarkers for patient stratification. This review will discuss the immunogenomics of cholangiocarcinoma, including the impact of genomic alterations on immune functionality, subversion of the cancer-immunity cycle, as well as clinical implications for existing and novel treatment strategies.

Humans↗

PubMed2003

Changes of percentages in immune cells phenotypes and cytokines production during two-year IFN-beta-1a treatment in multiple sclerosis patients.

OBJECTIVE: The aim of the study was to find out whether INF-beta-1a influences the immune profile of peripheral blood (PB) leukocytes in MS patients. METHOD: We have studied 20 patients with relapsing-remitting form of MS treated with INF-beta-1a using twocolor cytometry. We determined immune cells phenotypes and production of some cytokines: IL-4, IL-10, IL-12, IFN-gamma, before drug administration and after starting the treatment. RESULTS: In MS patients an increased percentage of CD14(+)CD86(+) cells and CD3(+)CD25(+) cells was noticed after 6, 9 and 12 months of INF-beta-1a therapy. Among cytokine-producing cells we noted an increased fraction of CD3(+)IL-4, CD14(+)IL-10 and CD14(+)IL-12 cells after 12 months, which decreased to the level observed before treatment after 24-month therapy. CONCLUSIONS: IFN-beta-1a treatment was associated with significant changes in immune response. This effect was mostly evident within the first year of treatment.

Adjuvants, Immunologic↗

PubMed1999

Ophthalmic manifestations of allergic fungal sinusitis.

PURPOSE: To highlight allergic fungal sinusitis as a cause of ophthalmic and sinus problems by identifying the profile of the patient with allergic fungal sinusitis and presenting a successful treatment approach. METHODS: Six consecutive cases of patients with ophthalmic manifestations of allergic fungal sinusitis were reviewed. Ophthalmic findings, sinus involvement, mycology, immune response, imaging studies, and treatment were examined. The characteristics of this patient group with ophthalmic manifestations of allergic fungal sinusitis were compared with those of the general group of patients with allergic fungal sinusitis. RESULTS: All six patients had proptosis. One had symptomatic diplopia and one had visual loss. Imaging studies, fungal characterization, and immune profiles were similar to the reported allergic fungal sinusitis population. After treatment there was no recurrence of ophthalmic or sinus symptoms at a mean follow-up of 34 months (range, 8 to 48 months). There were no complications of treatment. CONCLUSIONS: Initial diagnosis of allergic fungal sinusitis requires suspicion on the part of the ophthalmologist. Proptosis is the most common ophthalmic sign. Differentiation from invasive forms of fungal sinus disease is crucial, because systemic antifungal medication and extensive surgical tissue debridement are not required in allergic fungal sinusitis. Treatment consists of extirpation of the allergic mucin and fungus, sinus aeration, and systemic and topical corticosteroids.

Adolescent↗

PubMed2000

Known and plausible modulators of depressed immune functions following spinal cord injuries.

Recent evidence suggests that depression of immune function occurs early after spinal cord injury (SCI) and is maintained thereafter. Deviations from immune function observed in healthy persons with intact neuraxes include natural killer cell number and cytotoxicity, T cell function and activation, macrophage phagocytosis, levels of interleukins (IL)-2 and -6, the soluble IL-2R receptor, and intracellular adhesion molecules. While a single etiology explaining these abnormalities has not been identified, decentralization of the autonomic nervous system is the most likely cause. Otherwise, many persons with SCI, who sustain episodic autonomic overstimulation, are among the most physically deconditioned of all humans, and often select a diet rich in fat and low in protein. All of these are associated with suppressed immune function in persons without SCI. Those with SCI may also be (over)exposed to drugs and medications that suppress immune function, including methylprednisolone administered immediately after traumatic injury. No evidence suggests that the immune profiles of persons with SCI favor disease and illness resistance. As opportunistic infections of the urinary tract, lungs, and skin represent major causes of morbidity for those aging with SCI, attention to, or intervention on, immune suppressive states, traits, behaviors, diets, and medications may represent a means through which host defenses of persons with SCI can be fortified and their illness proclivities reduced.

Disease Susceptibility↗

PubMed2004

Airway peptidoglycan and immunostimulatory DNA exposures have divergent effects on the development of airway allergen hypersensitivities.

BACKGROUND: Environmental exposures to toll-like receptor (TLR) ligands have been suggested to provide immunologic protection against allergic diseases. However, some TLRs use unique intracellular signaling pathways, suggesting that ambient TLR ligand exposures might induce a range of host responses. OBJECTIVE: These investigations compared peptidoglycan (PGN; TLR2)-induced and immunostimulatory sequence DNA oligodeoxynucleotide (ISS-ODN; TLR9)-induced innate responses and determined how airway exposures to these TLR ligands affect adaptive immunity and the asthmatic phenotype. METHODS: In in vitro and in vivo studies innate responses to PGN and ISS-ODN were compared. Alternatively, mice were intranasally immunized with ovalbumin (OVA) alone or OVA plus PGN or ISS-ODN, and adaptive immune profiles and responses to airway OVA challenge were assessed. RESULTS: PGN and ISS-ODN induced divergent innate responses predictive of their having TH2- and TH1-biasing adjuvant potential, respectively. Consistent with these findings, mice intranasally immunized with OVA alone had relatively weak adaptive responses, whereas intranasal OVA/PGN- and OVA/ISS-ODN-coimmunized mice had much stronger humoral and cellular responses that were TH2 and TH1 biased, respectively. Finally, on airway allergen challenge, mice intranasally immunized with OVA alone had modest TH2-biased airway hypersensitivity responses, whereas airway responses were greatly exaggerated for intranasal OVA/PGN-immunized mice. In contrast, intranasal OVA/ISS-ODN-immunized mice had little evidence of airway hypersensitivity after airway allergen challenge. CONCLUSIONS: Considered in a larger context, these results suggest that inspired air is likely to contain TLR ligands capable of both preventing and precipitating the asthmatic phenotype.

Adjuvants, Immunologic↗

PubMed2006

H. pylori-infection and antibody immune response in a rural Tanzanian population.

BACKGROUND: Helicobacter pylori (H. pylori) infection is ubiquitous in sub-Saharan Africa, but paradoxically gastric cancer is rare. METHODS: Sera collected during a household-based survey in rural Tanzania in 1985 were tested for anti-H. pylori IgG and IgG subclass antibodies by enzyme immunoassay. Odds ratios (OR) and confidence intervals (CI) of association of seropositivity with demographic variables were computed by logistic regression models. RESULTS: Of 788 participants, 513 were aged < or = 17 years. H. pylori seropositivity increased from 76% at 0-4 years to 99% by > or = 18 years of age. Seropositivity was associated with age (OR 11.5, 95% CI 4.2-31.4 for 10-17 vs. 0-4 years), higher birth-order (11.1; 3.6-34.1 for > or = 3rd vs. 1st born), and having a seropositive next-older sibling (2.7; 0.9-8.3). Median values of IgG subclass were 7.2 for IgG1 and 2.0 for IgG2. The median IgG1/IgG2 ratio was 3.1 (IQR: 1.7-5.6), consistent with a Th2-dominant immune profile. Th2-dominant response was more frequent in children than adults (OR 2.4, 95% CI 1.3-4.4). CONCLUSION: H. pylori seropositivity was highly prevalent in Tanzania and the immunological response was Th2-dominant. Th2-dominant immune response, possibly caused by concurrent bacterial or parasitic infections, could explain, in part, the lower risk of H. pylori-associated gastric cancer in Africa.

Journal Article↗

PubMed1993

[Comparative study of immunologic consequences of autotransfusion and homologous transfusion in lung cancer surgery].

A study was carried out to determine the effects of transfusion with either autologous or homologous blood in 35 patients with lung cancer undergoing lung surgery. The patients were randomly allocated to two groups, "allo" receiving homologous blood (n = 10), and "auto" receiving autologous blood only (n = 13). A third control group included the patients (n = 12) who had not required any blood. In patients of "auto" group, two blood removals of 7 ml.kg-1 each were performed, provided their haemoglobin concentration was over 110 g.l-1 and their haematocrit over 34%. The following parameters were studied at t-1 (the day of inclusion), t0 (just before surgery and transfusion), t1 (one week after surgery), and t2 (one month later): haematocrit and haemoglobin concentration; IgG, IgA and IgM concentrations; polymorphonuclear and neutrophil leucocyte and lymphocyte numbers, lymphocyte subpopulations (CD4/CD8), activated natural killers (NK), polymorphonuclear leukocyte chemotaxis and chemoluminescence. Anaesthesia and surgery initiated initiated an early decrease in immunity in all three groups. The immune profile, and its time course in patients who received autologous blood only was similar to that of those who were not transfused at all. On the other hand, homologous blood transfusion seems to modify the recipient's non specific immune system. In group "allo", a decrease occurred in the number of auxiliary lymphocytes CD4, an increase in suppressor lymphocyte numbers CD8, with an increase in the CD4/CD8 ratio, and no increase in NK activity. These data suggest that autologous transfusion is well tolerated in cancer patients undergoing surgery.

Adult↗

PubMed2026

Paired genomic profiling of primary tumor and lymph-node metastases identifies candidate prognostic features in penile squamous cell carcinoma.

BACKGROUND: Penile squamous cell carcinoma (PSCC) is a rare malignancy with limited genomic data in Asian populations. Lymph node metastasis heavily dictates prognosis, yet molecular determinants of progression remain poorly understood. We aimed to characterize the genomic landscape and explore candidate prognostic genomic features using paired primary and metastatic PSCC tumors. PATIENTS AND METHODS: Targeted next-generation sequencing (437 cancer-related genes) was performed on primary tumors and matched lymph node metastases from 20 Chinese patients. Somatic alterations, intralesional heterogeneity, and tumor mutation burden (TMB) were analyzed and correlated with disease-free survival (DFS) and overall survival (OS). RESULTS: The most frequent primary tumor mutations included TP53 (45%) and TERT (40%). Notably, CCND1/FGF19 co-amplification (20% of cases) was associated with inferior DFS (P = .027) and showed a trend toward shorter OS (P = .050). Conversely, T-cell receptor (TCR) pathway alterations correlated with markedly improved survival. Comparing paired lesions revealed 59.8% shared alterations. Elevated TMB in metastases relative to matched primary tumors was significantly associated with poorer DFS (P = .008), while higher intralesional heterogeneity showed a trend toward worse OS. CONCLUSION: Paired profiling revealed broadly conserved genomic features together with lesion-specific divergence in PSCC. Recurrent CCND1/FGF19-containing 11q13 amplification, TCR pathway alterations, and elevated metastatic TMB warrant evaluation as potential prognostic features in larger, independently validated cohorts with integrated HPV and immune profiling.

Humans↗

PubMed1979

An in vivo model for assessing effects of drugs and toxicants on immunocompetence.

An in vivo assessment of the capacity of exposed animals to respond to antigenic challenge is recommended as the first screening phase for detecting potential immunotoxicants, with subsequent in vitro functional tests utilized to pinpoint the site of induced cellular alteration. Risk assessment of a candidate toxicant is based on a comparison of immune profiles of exposed animals with those of animals treated with prototype immunotoxicants. Extrapolation to man is facilitated by the use of licensed vaccines for antigenic challenge and the selection of clinically useful pharmaceutical drugs as prototype immunotoxicants. Three chemically induced alterations in immune responses are presented: 1) Immunosuppression characterized by impaired capacity to produce IgG and IgM classes of antibody on stimulation, 2) chronic high levels of IgE antibody in response to commonly encountered antigens, 3) modification of the capacity to mount an inflammatory response to antigenic material.

Animals↗