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Cellular Immunity

Cellular Immunity: The immune response mediated by T lymphocytes and their secreted products.
This response is directed against foreign pathogens and may also be involved in autoimmune diseases and transplant rejection.
Cellular immunity is distinct from the humoral immunity mediated by antibodies.

Most cited protocols related to «Cellular Immunity»

1
Benchmarking quanTIseq immune cell profiler
To benchmark quanTIseq, we considered the expression data sets listed in Additional file 2: Table S1, using the options reported in Additional file 2: Table S3. Normalized microarray data were downloaded from the Gene Expression Omnibus (GEO) (https://www.ncbi.nlm.nih.gov/geo) with the GEOquery R package [34 (link)]. Probes were mapped to gene symbols with the biomaRt R package [35 (link)]. In case of multiple probes mapping to the same gene symbol, the probe with the highest average expression across all samples was selected. Immune cell fractions estimated with flow cytometry, Coulter Counter, or from images of stained tissue slides were used as ground truth to validate quanTIseq. Where necessary, different functional states of an immune cell type were aggregated by summing up the corresponding cell fractions (e.g., for the Newman’s data set [17 (link)], B cells were quantified summing up the fractions of naïve and memory B cells).
Finotello F., Mayer C., Plattner C., Laschober G., Rieder D., Hackl H., Krogsdam A., Loncova Z., Posch W., Wilflingseder D., Sopper S., Ijsselsteijn M., Brouwer T.P., Johnson D., Xu Y., Wang Y., Sanders M.E., Estrada M.V., Ericsson-Gonzalez P., Charoentong P., Balko J., de Miranda N.F, & Trajanoski Z. (2019). Molecular and pharmacological modulators of the tumor immune contexture revealed by deconvolution of RNA-seq data. Genome Medicine, 11, 34.
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Publication 2019
B-Lymphocytes Cells Cellular Immunity Flow Cytometry Gene Expression Memory B Cells Microarray Analysis Tissue Stains
2
Comprehensive Immune Profiling of COVID-19
Sample collection was designed to meet minimal risk guidelines for blood collection for hospitalized adults, and sample-sparing assays are used when feasible. Blood samples (10 ml per time point) and nasal swabs (mid-turbinate) are collected at each specified time point, and blood is processed within 6 hours of collection according to the IMPACC standardized operating procedure. Whole blood and peripheral blood mononuclear cells (PBMCs) are collected to identify distinct immune cell populations and quantify changes in cell populations, gene expression, and activation markers [e.g., cytometry by time-of-flight (CyTOF) and bulk RNA transcriptomics] over the course of COVID-19 and convalescence. DNA is collected from whole blood at a single time point for genetic analyses (e.g., whole-exome sequencing). Serum is used to characterize SARS-CoV-2–specific antibodies, including virus neutralization, both serum and plasma are used for proteomics and metabolomics, and plasma is used to measure soluble inflammatory mediators (e.g., cytokines and chemokines) using oligonucleotide-linked antibody detection (Olink). RNA from the nasal swab is used to assess SARS-CoV-2 viral load and genomic sequence and to evaluate changes in immune-related upper airway epithelial gene expression (i.e., bulk transcriptomics). In addition, EAs are collected from intubated patients and processed within 2 hours of collection according to the IMPACC standardized operating procedures. EA cells are assessed by CyTOF and bulk transcriptomics to identify and quantify changes in gene expression and activation state of distinct immune cell populations in the lower respiratory tract. Processed samples are barcoded and centrally tracked on a laboratory information management system (LDMS; Frontier Science). All supplies necessary for sample collection and sample processing are centrally procured and supplied to the participating sites. Sample collection, processing, and storage procedures (Fig. 3) are standardized across sites, and samples are transported to centralized core laboratories (Core Labs) in batches for testing and analysis. The complete sample processing manual of procedures is included as Supplementary Methods.
Rouphael N., Maecker H., Montgomery R.R., Diray-Arce J., Kleinstein S.H., Altman M.C., Bosinger S.E., Eckalbar W., Guan L., Hough C.L., Krammer F., Langelier C., Levy O., McEnaney K., Peters B., Rahman A., Rajan J.V., Sigelman S., Steen H., van Bakel H., Ward A., Wilson M.R., Woodruff P., Zamecnik C.R., Augustine A.D., Ozonoff A., Reed E.F., Becker P.M., Higuita N.A., Altman M.C., Atkinson M.A., Baden L.R., Becker P.M., Bime C., Brakenridge S.C., Calfee C.S., Cairns C.B., Corry D., Davis M.M., Augustine A.D., Ehrlich L.I., Haddad E.K., Erle D.J., Fernandez-Sesma A., Hafler D.A., Hough C.L., Kheradmand F., Kleinstein S.H., Kraft M., Levy O., McComsey G.A., Melamed E., Messer W., Metcalf J., Montgomery R.R., Nadeau K.C., Ozonoff A., Peters B., Pulendran B., Reed E.F., Rouphael N., Sarwal M., Schaenman J., Sekaly R., Shaw A.C, & Simon V. (2021). Immunophenotyping assessment in a COVID-19 cohort (IMPACC): A prospective longitudinal study. Science Immunology, 6(62), eabf3733.
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Publication 2021
Adult Antibodies Biological Assay BLOOD Cells Cellular Immunity Chemokine COVID 19 Cytokine Dietary Fiber Gene Expression Gene Expression Profiling Genome Immunoglobulins Inflammation Mediators Nose Oligonucleotides Patients PBMC Peripheral Blood Mononuclear Cells Plasma Population Group Reproduction Respiratory System SARS-CoV-2 Serum Specimen Collection Turbinates Virus
3
Quantifying Rubella-Specific Immune Responses

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Publication 2009
Antibodies, Anti-Idiotypic Biological Assay BLOOD Cells Cellular Immunity Cryopreservation Cytokine Enzyme-Linked Immunosorbent Assay Enzyme-Linked Immunospot Assay Glutamine Granulocyte-Macrophage Colony-Stimulating Factor Homo sapiens Infection Interferon Type II Interleukin-10 Interleukin-12 Subunit p40 PBMC Peripheral Blood Mononuclear Cells Penicillins Pharmaceutical Preparations Pyruvate Rubella Rubella virus secretion Sodium Sodium Citrate Strains Streptomycin Sulfoxide, Dimethyl T-Lymphocyte Tissues Tumor Necrosis Factor-alpha
4
Comprehensive Study of H1N1pdm Determinants
The main objective of this study was to identify individual and collective determinants of H1N1pdm infection; therefore we tried to collect comprehensive data about subjects and their environment, in addition to biological samples. Several household visits are carried on by nurses for this purpose (see Figure 3 for details).
· Inclusion visits During the inclusion visit, nurses collected from all subjects detailed data regarding medical history, vaccination and preventive measures against influenza, smoking habits, socioeconomic status, risk perception and beliefs, frequency and characteristics of meetings with other people and housing (personal room, house or apartment). As the households’ addresses were geocoded, we were able to get additional information from public databases regarding the immediate surrounding environment of households. An overview of data collected from questionnaires at entry in the cohort is shown in Figure 4. Blood samples were collected and centralized for serological analyses. For subjects over 10 years, a heparinated tube was also collected to study cellular immunity, as well as a blood sample dedicated to transcript analyses.
· Systematic yearly visits After the inclusion visit, systematic follow-up visits are carried on between influenza seasons. During a systematic visit, a nurse collects or updates individual and environmental data on questionnaires, completes previously missing data, and obtains blood samples from all members of the household. Two waves of systematic follow-up visits have already occurred (summer-fall 2010 and 2011). A third wave is expected by the end of the second year of follow-up (summer 2012).
· Influenza-like illness (ILI) visits During the influenza season (as defined by the French surveillance network [21 ]), we use an active surveillance system order to detect ILIs: all households are called by an interactive voice response system (IVRS) weekly and are asked if any subject has symptoms of ILI (fever ≥ 37.8°C associated with cough or sore throat, as defined by the CDC [22 ]). A free phone number is given to subjects to report symptoms spontaneously between two weekly calls. In case of reported ILI, symptoms are validated by the study team and then three “ILI visits” are organized: nurses visit the household within 48 h after the onset of symptoms, then 3–6 days and 8–12 days after the onset.
· During these visits, a detailed questionnaire collects data about the circumstances of possible exposure to influenza viruses and the chronology of symptoms (if any) in all subjects. Nasal swabs are collected from all subjects. A stool sample and a throat swab are also collected from subjects with ILI, as well as a blood sample from those over 10 years of age. Moreover, a self-swab procedure is previously sent to the households in order to collect virological samples when a visit by a nurse within the first 48 h is not possible. Nasal swabs are used to identify various respiratory viruses by PCR and biochips allowing for multiple diagnosis tests.
· This series of three visits can occur several times in the same household during an influenza season. There were 23 ILI alerts during the 2009–2010 season (as households were still being included) and 143 during the 2010-2011 season, all of which triggered up to three ILI visits.
· Vaccination visits In order to update serological information, a blood sample was collected from subjects who had an influenza vaccination, between 2 and 4 weeks following this vaccination. There was one vaccination visit following the inclusion visits; 29 vaccination visits were conducted following the first wave of follow-up visits and 69 following the second wave.
Lapidus N., de Lamballerie X., Salez N., Setbon M., Ferrari P., Delabre R.M., Gougeon M.L., Vely F., Leruez-Ville M., Andreoletti L., Cauchemez S., Boëlle P.Y., Vivier E., Abel L., Schwarzinger M., Legeas M., Le Cann P., Flahault A, & Carrat F. (2012). Integrative study of pandemic A/H1N1 influenza infections: design and methods of the CoPanFlu-France cohort. BMC Public Health, 12, 417.
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Publication 2012
Biopharmaceuticals BLOOD Cellular Immunity Cough Diagnosis Feces Fever Households Infection Nose Nurses Orthomyxoviridae Pharynx Respiratory Rate Sore Throat Vaccination Virus Virus Vaccine, Influenza Visiting Nurses
5
Measles Antibody and Cellular Immunity

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Publication 2011
Antibodies, Neutralizing Biological Assay Cellular Immunity Enzyme-Linked Immunospot Assay Gender Humoral Immunity Immunization Immunoglobulins Interferon Type II Measles Measles-Mumps-Rubella Vaccine Measles virus Secondary Immunization

Most recents protocols related to «Cellular Immunity»

1
Evaluation of MPV.10.34.d IRC Effectiveness
Not available on PMC !

Example 11

MPV.10.34.d IRC Effectiveness in Human Assays

While the in vitro functional test results of the above experiments were promising, the next desired step in the analysis was to perform similar experiments in human-based assays. To this end, the response of mock human cellular immune system components to tumor cells exposed to MPV.10.34.d IRC was examined in vitro. Human CMV (HCMV) was selected for this study since human CMV is highly prevalent (infecting 50-90% of the human population) and mostly asymptomatic in healthy individuals. (See, Longmate et al., Immunogenetics, 52(3-4):165-73, 2001; Pardieck et al., F1000Res, 7, 2018; and van den Berg et al., Med. Microbiol. Immunol., 208(3-4):365-373, 2019). Importantly, HCMV establishes a life-long persistent infection that requires long-lived cellular immunity to prevent disease. Hence, it is rational to hypothesize that a complex adaptive cell-mediated anti-viral immunity developed over many years to strongly control a viral infection in an aging person can be repurposed and harnessed to treat cancer.

In these experiments, CD8+ T cell responses to CMV peptides were tested in three different human tumor cell lines, including HCT116, OVCAR3, and MCF7. All three of these human tumor cell lines are HLA-A*0201 positive.

In vitro cytotoxicity assays. HTC112, human colon cancer cells, MCF7, human breast cancer cells, and OVCAR3, human ovarian cancer cells (all from ATCC, Manassas, VA, US) were seeded overnight at 0.01 to 0.2×106 per well per 100 μL per 96 well plate. The next day (about 20 to 22 hrs later), each cell line was incubated for one hour at 37° C. under the following conditions: (1) CMV peptide at a final concentration of 1 μg/mL (positive control), (2) MPV.10.34.d at a final concentration of 2.5 μg/mL (negative control), (3) CMV-conjugated MPV.10.34.d IRC at a final concentration of 2.5 μg/mL, (4) CMV-conjugated HPV16 IRC at a final concentration of 2.5 μg/mL, and (5) no antigen (negative control). After 1 hour, the cells were washed vigorously with 200 μL of media for three times to remove non-specific binding. Human patient donor CMV T cells (ASTARTE Biologics, Seattle, WA, US) were added at the E:T (effector cell:target cell) ratio of 10:1 and incubated in a tissue culture incubator for 24 hrs at 37 C, 5% CO2. The total final volume of each sample after co-culture was 200 μL. Cell viability was measured after co-culturing. Cell viability was measured with CELLTITER-GLO® (Promega, Madison, WI, US). This assay provides a luciferase-expressing chemical probe that detects and binds to ATP, a marker of cell viability. The amount of ATP generated from tumor cells was quantified according to manufacturer protocols. In these assays, reduced luciferase activity indicates cell death and suggests greater immune redirection and greater cytotoxicity.

The results are provided in FIG. 25. CMV-conjugated MPV.10.34.d IRC (“VERI-101” in FIGS. 25A, 25B, and 25C) was equally effective as CMV-conjugated HPV16 IRC (“CMV AIR-VLP” in FIGS. 25A, 25B, and 25C) in redirecting human healthy donor CMV pp65-specific CD8+ T-cells (Astarte Biologics, Inc., Bothell, WA, US) to kill immortalized HLA.A2 positive human colon cancer cells (HCT116), human ovarian cancer cells (OVCAR3), and human breast cancer cells (MCF7). The control samples (“No Ag” or “VERI-000” in FIGS. 25A, 25B, and 25C) showed no background tumor killing. Together, these data demonstrate that MPV.10.34.d IRC redirects mouse and human immune responses against tumor cells in vitro.

US11858964B2. Virus-inspired compositions and methods of redirecting preexisting immune responses using the same for treatment of cancer (2024-01-02). VerImmune Inc. [US]. Inventors: Joshua Weiyuan Wang [US], Ken Matsui [US], Philip Alan Storm [US], Kristin Marie Peters [US].
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Patent 2024
Acclimatization Antigens Antiviral Agents Biological Assay Biological Factors Cancer of Colon CD8-Positive T-Lymphocytes Cell Death Cell Line, Tumor Cell Lines Cells Cell Survival Cellular Immune Response Cellular Immunity Cytotoxin Figs HLA-A2 Antigen Homo sapiens Human papillomavirus 16 In Vitro Testing Luciferases Malignant Neoplasms Mammary Carcinoma, Human MCF-7 Cells Mus Neoplasms Ovarian Cancer Patients Peptides Persistent Infection Promega Response, Immune Response Elements System, Immune T-Lymphocyte Tissue Donors Tissues UL83 protein, Human herpesvirus 5 Virus Virus Diseases
2
Randomized Placebo-Controlled Trial of Ad5-nCoV Vaccine
The investigational vaccine, Ad5-nCoV, and the placebo were provided by NPO Petrovax Pharm LLC (Moscow, Russia). Both vaccine and placebo were developed by CanSino Biologics Inc. (Tianjin, China) and the Beijing Institute of Biotechnology (Beijing, China). The vaccine was administered with the optimal dose of 5 × 1010 viral particles per 0.5 mL dose, as determined in a previous study [9 (link),10 (link)]; placebo contained vaccine excipients only. The appearance of Ad5-nCoV and placebo syringes and packaging was identical.
Eligible participants were randomly allocated to the Ad5-nCoV group or the Placebo group, in a 3:1 ratio, by an independent statistician using a validated system including a pseudorandom number generator with a seed value; allocation used block randomisation and stratification by study site. Neither the investigators nor participants were aware of the group assignment. Investigators were trained to use the centralised interactive web response system that was used for randomisation. Randomisation codes were kept by authorised personnel from the responsible contracted organisation.
The Safety Analysis Set included all randomised participants who received a dose of the vaccine and was used to provide the disposition of study participants. Results for immunogenicity analyses are presented for the full analysis set ([FAS] for immunogenicity analysis), which included all eligible participants who received a dose of vaccine and provided at least one immunogenicity assessment result. The study design (S1 Protocol) also included the per-protocol sets ([PPS] for immunogenicity analysis and PPS efficacy analysis), which included members of the FAS for immunogenicity analysis and Safety Analysis Set, respectively, with no significant protocol deviations and who did not develop COVID-19 within the first 14 days post-vaccination. The population characteristics and results were similar between the FAS for immunogenicity analysis and both types of PPS (immunogenicity and efficacy analysis); therefore, only the FAS for immunogenicity analysis population was used to evaluate the immunogenicity endpoints in this study. Cellular immunity results were analysed in a subset of participants from the FAS for immunogenicity analysis population that attended the Moscow clinic site (n = 69). Details describing the sample sizes are provided in S1 Methods.
Lioznov D., Amosova I., Sheetikov S.A., Zornikova K.V., Serdyuk Y., Efimov G.A., Tsyferov M., Khmelevskii M., Afanasiev A., Khomyakova N., Zubkov D., Tikhonov A., Zhu T., Barreto L, & Dzutseva V. (2023). Immunogenicity and safety of a recombinant adenovirus type-5 COVID-19 vaccine in adults: Data from a randomised, double-blind, placebo-controlled, single-dose, phase 3 trial in Russia. PLOS ONE, 18(3), e0278878.
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Publication 2023
Antigens Biological Factors Cellular Immunity COVID 19 Placebos Safety SARS-CoV-2 Syringes Vaccination Vaccines Virion
3
Cellular Immunity to SARS-CoV-2 in Residents
Cellular immunity was determined in 24 of the initially recruited residents. Individuals were selected to include males (n = 8) and females (n = 16) and with and without prior infection. The selection covers the full range of anti-RBD antibody titers found in the study.
T-cell mediated immune response to SARS-CoV-2 was determined using the T-SPOT SARS-CoV-2 (Oxford Immunotec) according to the manufacturer´s instructions. Immune response to spike protein (S1 Questionnaire) and nucleocapsid after stimulation was measured. Since stimulation to both antigens occurs in separate wells, it should be possible to distinguish between infection and vaccinations. Nil and positive control were included in the assay. The test was considered positive if at least, one stimulation showed 8 or more spots.
Rodríguez-Avial I., García-Salguero C., Bermejo L., Teja J., Pérez-Cecilia E., Delgado-Iribarren A., Vigara M., Gil P, & Culebras E. (2023). Evolution of antibody titers after two doses of mRNA Pfizer-BioNTech vaccine and effect of the third dose in nursing home residents. PLOS ONE, 18(3), e0282388.
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Publication 2023
Antibodies, Anti-Idiotypic Antigens Biological Assay Cellular Immunity Exanthema Females Infection Males M protein, multiple myeloma Nucleocapsid Response, Immune SARS-CoV-2 T-Lymphocyte Vaccination
4
Trajectory Analysis of Tumor-Infiltrating Immune Cells
The status of the tumor-infiltrating immune cell subpopulations in the TME is dynamic and they may differentiate into different cellular states that exert different biological functions, e.g., cancer fighting or cancer tolerant. We performed the trajectory analysis using pseudo-time inferencing algorithm Monocle 210 (link),50 (link) to reconstruct the cell differentiation trajectory of different tumor-infiltrating immune cells. It uses a machine-learning technique called reversed graph embedding to describe multiple fate decisions in a fully unsupervised manner and derives a principal tree on a population of single cells that reveals the progression of cell and reconstruct their trajectory as a cell progresses through the biological process under study. Different branches in the cell trajectory likely distinguished molecularly distinct cell subpopulations (denoted by different cellular states) within a certain cell type.
Zhu G.Q., Tang Z., Huang R., Qu W.F., Fang Y., Yang R., Tao C.Y., Gao J., Wu X.L., Sun H.X., Zhou Y.F., Song S.S., Ding Z.B., Dai Z., Zhou J., Ye D., Wu D.J., Liu W.R., Fan J, & Shi Y.H. (2023). CD36+ cancer-associated fibroblasts provide immunosuppressive microenvironment for hepatocellular carcinoma via secretion of macrophage migration inhibitory factor. Cell Discovery, 9, 25.
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Publication 2023
Biological Processes Cells Cellular Immunity Disease Progression Malignant Neoplasms Neoplasms Population Group Somatostatin-Secreting Cells Trees
5
Pfizer/BioNTech Vaccine Immunogenicity in Nursing Homes

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Publication 2023
BNT162B2 Cellular Immunity Chaperone-Mediated Autophagy Comirnaty Hispanic or Latino Humoral Immunity Secondary Immunization Vaccines Workers

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More about "Cellular Immunity"

Cellular Immunity, also known as cell-mediated immunity, is a crucial component of the immune system that involves the activation and response of T lymphocytes, or T cells.
These specialized cells play a vital role in defending the body against foreign pathogens, including viruses, bacteria, and fungi.
T cells are produced in the thymus and can be further classified into different subtypes, such as CD4+ T helper cells and CD8+ cytotoxic T cells.
CD4+ T cells help coordinate the overall immune response, while CD8+ T cells directly attack and destroy infected or cancerous cells.
The process of Cellular Immunity involves the recognition of foreign antigens by T cells, which then proliferate and release various cytokines and other effector molecules.
These substances can activate other immune cells, such as macrophages and natural killer cells, to help eliminate the threat.
Cellular Immunity is distinct from Humoral Immunity, which is mediated by antibodies produced by B lymphocytes.
While Humoral Immunity focuses on neutralizing extracellular pathogens, Cellular Immunity is primarily responsible for targeting and destroying intracellular pathogens and abnormal cells.
Researchers often utilize tools and techniques like the Cytomics™ FC500 series instrument, Isotonic azide-free solution, Concanavalin A, QuantiFERON SARS-CoV-2, RPMI 1640 medium, Trucount tubes, Histopaque-1077, and Quan-T-Cell ELISA to study and analyze various aspects of Cellular Immunity, including T cell phenotyping, activation, and function.
Understanding the complex mechanisms of Cellular Immunity is crucial for the development of effective therapies and interventions for a wide range of diseases, including autoimmune disorders, transplant rejection, and cancer.
By harnessing the power of Cellular Immunity, researchers and clinicians can work towards improving patient outcomes and advancing the field of immunology.