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Humoral Immunity

Humoral Immunity: The immune response mediated by antibodies produced by B cells.
This includes the activation of B cells to produce immunoglobulins, which neutralize targets such as viruses and stimulate the removal of pathogens and cellular debris.
Humoral immunity is a key component of the adaptive immune system and plays a crucial role in protecting against infectious diseases.
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Most cited protocols related to «Humoral 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

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Publication 2019
Anticoagulants BLOOD Cell Proliferation Cells Centrifugation CFC1 protein, human Colon Formaldehyde Gastrointestinal Tract Humoral Immunity Ileum Immunoglobulin A Immunoglobulin G Inflammation Jejunum Jugular Vein Malondialdehyde Mucous Membrane Nitrogen Nutrients Oxidative Stress Phosphates Pigs Proteins Saline Solution Serum Specimen Collection Tissues Tumor Necrosis Factor-alpha Viscosity
Serological analysis was performed using a commercially available, CE-marked, IgGAM enzyme-linked immunosorbent assay (ELISA) that is optimized for seroprevalence studies and measures the total antibody response against the spike glycoprotein (product code: MK654; The Binding Site [TBS]). Briefly, this assay simultaneously measures any IgG, IgA, or IgM directed against the spike glycoprotein, facilitating detection of any antibody response against the antigen. Development of this assay was undertaken by the authors (AMS, SEF, AMC, MTD, AGR) at the University of Birmingham in collaboration with The Binding Site. Detailed descriptions of this assay, including its construction, validation, and verification, have been published previously (Cook et al. 2021 (link); Faustini et al. 2021 (link)). The assay demonstrates 98.3% (95% confidence interval [CI], 96.4%–99.4%) specificity and 98.6% sensitivity (95% CI, 92.6%–100%) in detecting serological responses to the SARS-CoV-2 spike glycoprotein following polymerase chain reaction (PCR)–positive, nonhospitalized, mild-to-moderate coronavirus disease 2019 (COVID-19). Internal quality control material demonstrates an interassay coefficient of variance of 7.2% at the cutoff. Samples are run at a standard dilution of 1/40.
To provide greater detail on the composition of the total serological response and insight into the correlates of protective humoral immunity (rather than seroprevalence), the IgG and IgA responses against the spike glycoprotein were measured individually. To do this, the IgGAM ELISA protocol was modified. The antigen coating layer, serum dilution, and washing steps were unchanged from the original IgGAM protocol (above), but the detection layer employed polyclonal sheep-anti-human horseradish peroxidase (HRP)–conjugated antibodies directed against IgG (1:16,000) or IgA (1:2,000) individually, rather than in combination. For these assays, a cutoff ratio of 1.0 relative to the existing TBS cutoff calibrators was determined by plotting the pre-2019 negatives (n = 90) in a frequency histogram chart. Once the ratio cutoff was determined from the pre-2019 negatives, a cutoff multiplier of 1.0 and 0.71 was established for IgG and IgA, respectively. Further comparison of the properties and comparative performance of these assays relative to the IgGAM assay and others has also been published (Shields, Faustini, Perez-Toledo, Jossi, Allen, et al. 2020 (link); Mohanraj et al. 2021 (link)).
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Publication 2021
Anti-Antibodies Antibody Formation Antigens Binding Sites Biological Assay COVID 19 Domestic Sheep Enzyme-Linked Immunosorbent Assay Homo sapiens Horseradish Peroxidase Humoral Immunity Hypersensitivity Polymerase Chain Reaction Serum spike protein, SARS-CoV-2 Technique, Dilution
B10.BR mice were immunized with 1×1010 particles of recombinant virus per mouse either by intramuscular injection (50 µl) in the right hindlimb, or by oral gavage (100 µl) using oral feeding needles (18G, 2.25 mm dia., Popper & Sons, Inc, New Hyde Park, NY). For nasal immunization, mice were anesthetized with isoflurane. Once anesthesia was achieved, 1×1010 particles of virus slowly delivered as a bolus into the nostrils using a standard micropipette (Gilson, Middleton, WI) as previously described [39] (link).
Pre-existing immunity to adenovirus serotype 5 was established by injecting 5×1010 particles of adenovirus expressing beta-galactosidase (AdlacZ) by intramuscular injection in the right hindlimb 30 days prior to vaccination with Ad5-ZGP. This protocol has been documented to activate T and B cells against virus capsid proteins and elicit humoral immunity [8] (link), [11] (link). At the time of vaccination, mice had an average anti-adenovirus circulating NAB titer of 1∶320, which falls within lower range of average values reported in humans after natural infection [11] (link). Mice were challenged by intraperitoneal injection of 200× LD50 of mouse-adapted Ebola virus, Zaire strain (MA-ZEBOV) in 200 µl sterile saline [40] (link). After challenge, the animals were weighed daily for 13 days and monitored for clinical signs of Ebola infection using an approved scoring sheet. All procedures and the scoring method were approved by the Institutional Animal Care Committee at the National Microbiology Laboratory (NML) of the Public Health Agency of Canada (PHAC) according to the guidelines of the Canadian Council on Animal Care. All infectious work was performed in the ‘Biosafety Level 4’ (BSL4) facility at NML, PHAC.
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Publication 2008
Adenovirus Vaccine Anesthesia Animal Care Committees Animals B-Lymphocytes Capsid Proteins Cells Ebolavirus GLB1 protein, human Hemorrhagic Fever, Ebola Herpesvirus 1, Cercopithecine Hindlimb Homo sapiens Humoral Immunity Infection Injections, Intraperitoneal Intramuscular Injection Isoflurane Mus Needles Nose Response, Immune Saline Solution Sons Sterility, Reproductive Strains Tube Feeding Vaccination Virion Virus

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Publication 2022
2019-nCoV Vaccine mRNA-1273 Adenovirus Vaccine Adult anti-IgG Antibodies, Blocking B-Lymphocytes BLOOD Cells Cellular Immunity ChAdOx1 nCoV-19 COVID 19 Cytokine Healthy Volunteers Humoral Immunity Immunization Schedule Immunoglobulin G Immunosuppression inhibitors Malignant Neoplasms Nurses Organ Transplantation Physicians Prednisolone Pregnancy RNA, Messenger Safety SARS-CoV-2 Secondary Immunization Serum Tumor Necrosis Factor Inhibitors Vaccination Vaccines

Most recents protocols related to «Humoral Immunity»

Supernatants from PBMCs culture systems after incubation with LPS or PHA, and plasma samples were used for cytokine detection. To explore the effects on the balance between immune response and tolerance, cellular and humoral immunity in AD, concentrations of PBMCs cytokines (IL-1α, IL-2, IL-6, IL-10, TNF-α, and IFN-γ) were determined by sandwich enzyme-linked immunosorbent assay using a commercially available kit (Beijing 4A Biotech Co., Ltd. China). All subjects were measured three times on the same day.
PBMCs pellets from peripheral blood were used to detect genome-wide methylation and hydroxymethylation with MethylFlash Methylated DNA Quantification Kit (Epigentek, Farmingdale, NY) and operated according to the instructions.
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Publication 2023
BLOOD Cells Cytokine Enzyme-Linked Immunosorbent Assay Genome Humoral Immunity IL10 protein, human Immune Tolerance Interferon Type II Pellets, Drug Plasma Response, Immune Tumor Necrosis Factor-alpha

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Publication 2023
BNT162B2 Cellular Immunity Chaperone-Mediated Autophagy Comirnaty Hispanic or Latino Humoral Immunity Secondary Immunization Vaccines Workers
As TFAM deletion resulted in enhanced maturation and activation of the DCs in vitro, we next investigated whether the humoral and cellular immune responses were promoted in Tfam-/- mice. To better model tumor responses, OVA was used as the model antigen to validate the activation of immune responses in vivo. Tfam-/- and control mice were immunized with OVA for three times and the sera were collected. The levels of total IgG and its subclasses were measured. The results showed that the antibody titers of IgG, IgG1, and IgG2c were all elevated in immunized Tfam-/- mice when compared with that of the control group (figure 4A), which suggested a potent activation of humoral immunity in mice Tfam-/- BMDCs. When it comes to the cellular immune response, we demonstrated that Tfam-/- deletion simulated more effective OVA-specific CD8+ T cell responses as evidenced by the increase in spleen lymphocytes from Tfam-/- and control mice after the stimulation with OVA257-264 peptides (figure 4B, C). In accordance, the ELISA results showed the increased production of IFN-γ by CD8+ T lymphocytes in Tfam-/- cells after OVA immunization when compared with the control (figure 4D). Furthermore, the immune-microenvironment and the critical cell populations in the spleen of Tfam-/- and control mice were characterized by FCM. The increased populations of DCs (CD11c+ DCs, figure 4E), CD8+ CD69+ T cells (figure 4F), CD8+ IFN-γ+ T cells, CD8+ GzmB+ T cells (figure 4G), CD4+ CD69+ T cells (figure 4H) and the decreased percentages of CD4+ FOXP3+ cells were also detected (figure 4H).
Next, we used the prophylactic model to identify the anti-cancer immunity activation in Tfam-/- and control group. Mice were challenged with subcutaneous injection of E.G7-OVA cells after three times of immunization. The tumor growth was significantly inhibited in Tfam-/- mice in the prophylactic tumor model with the OVA immunization when compared with that of the control mice (figure 4I), and this group of mice showed prolonged survival (figure 4J). To investigate whether such tumor inhibition effect was due to the activation of cellular immune response, the adoptive transfer study was carried out by isolating CD8+ T lymphocytes from the immunized mouse spleen. CD8+ T lymphocytes from immunized Tfam-/- mice or control mice were injected intravenously in WT mice on day 1 before E.G7-OVA cell inoculation and on day 1 and day 3 after E.G7-OVA cell inoculation. Interestingly, the tumor growth as detected by tumor weight and tumor volume was significantly inhibited in the group that received the adoptive transfer CD8+ T cells from Tfam-/- mice when compared with that received the control CD8+ T cells (figure 4K). To further figure out the myeloid cell subset responsible for the activation of antitumor immunity, we adopted control or Tfam-/- DCs/macrophages to WT LLC tumor-bearing mice. As expected, adoption of Tfam-/- DCs instead of Tfam-/- macrophages significantly inhibited tumor metastasis and tumor growth (online supplemental figure 5). In summary, TFAM deficiency not only caused DC activation, but also led to more efficient activation of antitumor humoral and cellular immunity in vivo.
Publication 2023
Adoptive Transfer Antigens Bears Cancer Vaccines CD4 Positive T Lymphocytes CD8-Positive T-Lymphocytes Cells Cellular Immune Response Cellular Immunity Condoms Deletion Mutation Enzyme-Linked Immunosorbent Assay GZMB protein, human Humoral Immunity IgG1 Immunoglobulin G Interferon Type II Lymphocyte Macrophage Malignant Neoplasms Mus Myeloid Progenitor Cells Neoplasm Metastasis Neoplasms Peptides Psychological Inhibition Response, Immune Serum Spleen Subcutaneous Injections T-Lymphocyte Vaccination
Peptide vaccines have weak ability to provoke host immune responses. The weak immunogenicity of the peptide vaccine can be handled with the technique of multi-epitopes peptide design [71 (link),72 (link)]. In multi-epitopes peptide-design phase, immunodominant epitopes were linked to each other [73 (link)]. All the selected screened epitopes were linked with the Gly-Pro-Gly-Pro-Gly (GPGPG) linkers to build an immunopotent multi-epitopes peptide vaccine. Furthermore, the vaccine was linked with the highly immunopotent cholera toxin B adjuvant (CTB) for the enhancement of the vaccine immunogenicity [74 (link),75 (link)]. The adjuvant binds to the monoganglioside GM1 receptor and is capable of stimulating cytokines, interferone, cellular and humoral immunity [75 (link)]. The adjuvant is used in vaccine design against cancer, tuberculosis and influenza [76 (link)].
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Publication 2023
Cells Choleragenoid Cytokine Debility Epitopes glycyl-prolyl-glycyl-glycine Humoral Immunity Immunodominant Epitopes Immunogenicity, Vaccine Malignant Neoplasms Peptides Pharmaceutical Adjuvants Response, Immune Tuberculosis Vaccines Vaccines, Peptide Virus Vaccine, Influenza
We use a new mathematical model to describe the dynamics of RNA viruses such as SARS-CoV-2 that incorporates two modes of transmission (virus-to-cell and cell-to-cell), two classes of infected cells, humoral immunity and antiviral treatment. The model is formulated by the following nonlinear system of ordinary differential equations (ODEs): dSdt=σμ1Sβ1SV1+q1Wβ2SI1+q2W+ρL,dLdt=β1SV1+q1W+β2SI1+q2W(μ2+δ+ρ)L,dIdt=δLμ3I,dVdt=k(1ϵ)Iμ4VpVW,dWdt=rVWμ5W,
where the uninfected cells (S) are generated at rate σ , die at rate μ1S and become infected either by free virus particles at rate β1SV or by direct contact with infected cells at rate β2SI . The two modes of transmission are inhibited by non-lytic humoral immune response at rate 1+q1W and 1+q2W , respectively. The latently infected cells (L) die at rate μ2L and become productively infected cells rate δL . Also, the latently infected cells are assumed to be cured at rate ρL , resulting from the clearance of virus through the non-cytolytic process as for HCV infection in [20 (link)] and HIV in [21 (link),22 (link)]. The cure of infected epithelial cells was also considered in a recent work of SARS-CoV-2 [23 (link)]. The productively infected cells (I) die at rate μ3I . Free viruses (V) are produced by infected cells at rate kI , cleared at rate μ4V and neutralized by antibodies at rate pVW . Antibodies develop in response to free virus at rate rVW and decay at rate μ5W . Here, the parameter ϵ represents the effectiveness of the antiviral treatment which blocks the production of viral particles. The flow diagram of the model is shown in Figure 1.
Most viruses can spread via two modes: by virus-to-cell infection and through direct cell-cell contact [24 (link),25 (link),26 (link)]. A recent study provided evidence that SARS-CoV-2 spreads through cell-cell contact in cultures, mediated by the spike glycoprotein [27 (link)]. Furthermore, it is known that antibodies neutralize free virus particles and inhibit the infection of susceptible cells [28 (link)]. They also contribute significantly to non-lytic antiviral activity [29 ]. For this reason, both modes of transmission with the lytic and non-lytic immune response are considered into the model.
On the other hand, it is very important to note that the SARS-CoV-2 model presented by system (1) includes many mathematical models for viral infection existing in the literature. For instance, we get the model of Rong et al. [21 (link)] when q1=0 , β2=0 and both treatment and humoral immunity are ignored. The global stability of the model [21 (link)] was investigated in [30 (link)]. In addition, the model of Baccam et al. [31 (link)] is a special case of system (1), it suffices to neglect immunity and take σ=0 , μ1=μ2=ρ=0 , β2=0 and ϵ=0 . The last model presented in [31 (link)] was recently used by Rodriguez and Dobrovolny [32 (link)] to determine viral kinetics parameters for young and aged SARS-CoV-2 infected macaques. In the case where latently infected cells not revert back to susceptible and when antibodies do not reduce cell-to-cell transmission, we have ρ=0 , q2=0 and system (1) reduces to the following model: dSdt=σμ1Sβ1SV1+q1Wβ2SI,dLdt=β1SV1+q1W+β2SI(μ2+δ)L,dIdt=δLμ3I,dVdt=k(1ϵ)Iμ4VpVW,dWdt=rVWμ5W,
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Publication 2023
Antibodies Antiviral Agents Cardiac Arrest Cells Epithelial Cells Hepatitis C Humoral Immunity Infection Kinetics Macaca Response, Immune RNA Viruses SARS-CoV-2 spike protein, SARS-CoV-2 Transmission, Communicable Disease Virion Virus Virus Diseases

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More about "Humoral Immunity"

Humoral immunity, the adaptive immune response mediated by antibodies, plays a crucial role in protecting against infectious diseases.
This process involves the activation of B cells to produce immunoglobulins, which neutralize targets like viruses and stimulate the removal of pathogens and cellular debris.
Optimizing humoral immunity can enhance research reproducibility and accuracy.
PubCompare.ai, an AI-driven platform, helps researchers easily locate the best protocols, products, and pre-prints from literature, patents, and more to support their humoral immunity studies.
The advanced AI-driven comparisons offered by PubCompare.ai can help identify the optimal solutions for your research, including the use of tools like the Elecsys Anti-SARS-CoV-2 S assay, TRIzol reagent, SPSS Statistics for Windows, Cobas analyzers, Synergy HT Multi-Mode Microplate Reader, THUNDERBIRD SYBR qPCR Mix, and the PET-28b expression vector.
Experiene the future of data-driven discovery today with PubCompare.ai and unlock the power of humoral immunity optimization for your research.