scholarly journals Peste des Petits Ruminants Virus-Like Particles Induce a Potent Humoral and Cellular Immune Response in Goats

Viruses ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 918 ◽  
Author(s):  
Yan ◽  
Banadyga ◽  
Zhao ◽  
Zhao ◽  
Schiffman ◽  
...  
Keyword(s):  
Immune Response ◽  
Cellular Immune Response ◽  
Vaccine Development ◽  
Expression System ◽  
Small Ruminants ◽  
Economic Losses ◽  
Potential Candidate ◽  
Peste Des Petits Ruminants ◽  
Ifn Γ ◽  
Cellular Immune

Peste des petits ruminants is a highly contagious acute or subacute disease of small ruminants caused by the peste des petits ruminants virus (PPRV), and it is responsible for significant economic losses in animal husbandry. Vaccination represents the most effective means of controlling this disease, with virus-like particle (VLP) vaccines offering promising vaccine candidates. In this study, a PPRV VLP-based vaccine was developed using a baculovirus expression system, allowing for the simultaneous expression of the PPRV matrix (M), hemagglutinin (H), fusion (F) and nucleocapsid (N) proteins in insect cells. Immunization of mice and goats with PPRV VLPs elicited a robust neutralization response and a potent cellular immune response. Mouse studies demonstrated that VLPs induced a more robust IFN-γ response in CD4+ and CD8+ T cells than PPRV Nigeria 75/1 and recruited and/or activated more B cells and dendritic cells in inguinal lymph nodes. In addition, PPRV VLPs induced a strong Th1 class response in mice, as indicated by a high IgG2a to IgG1 ratio. Goat studies demonstrated that PPRV VLPs can induce the production of antibodies specific for F and H proteins and can also stimulate the production of virus neutralizing antibodies to the same magnitude as the PPRV Nigeria 75/1 vaccine. Higher amounts of IFN-γ in VLP-immunized animal serum suggested that VLPs also elicited a cellular immune response in goats. These results demonstrated that VLPs elicit a potent immune response against PPRV infection in small ruminants, making PPRV VLPs a potential candidate for PPRV vaccine development.

scholarly journals Induction of Cellular Immune Response by DNA Vaccine CoexpressingE. acervulina3-1E Gene and Mature CHIl-15 Gene

2012 ◽  
Vol 2012 ◽  
pp. 1-7
Author(s):  
Dexing Ma ◽  
Chunli Ma ◽  
Mingyang Gao ◽  
Guangxing Li ◽  
Ze Niu ◽  
...  
Keyword(s):  
Immune Response ◽  
Dna Vaccine ◽  
Cellular Immune Response ◽  
Lymphocyte Proliferation ◽  
Vaccine Development ◽  
Flow Cytometric Analysis ◽  
Potential Candidate ◽  
Spleen Lymphocyte ◽  
Cellular Immune ◽  
And Control

We previously reported that the chimeric DNA vaccine pcDNA-3-1E-linker-mChIL-15, fused through linkingEimeria acervulina3-1E encoding gene and mature chicken IL-15 (mChIL-15) gene with four flexible amino acid SPGS, could significantly offer protection against homologous challenge. In the present study, the induction of cellular immune response induced by the chimeric DNA vaccine pcDNA-3-1E-linker-mChIL-15 was investigated. Spleen lymphocyte subpopulations were characterized by flow cytometric analysis. The spleen lymphocyte proliferation assays were measured by 3-[4,5-dimethylthiazol-2-y1]-2,5-diphenyltetrazolium bromide (MTT) method. The mRNA profiles of ChIL-2 and ChIFN-γ in spleen were characterized by means of real-time PCR. Chickens immunized with pcDNA-3-1E-linker-mChIL-15 exhibited significant upregulated level of ChIL-2 and ChIFN-γ transcripts in spleen following two immunizations compared with chickens in other groups (P<0.01). In comparison with pcDNA3.1-immunized and control groups, lymphocyte proliferation, percentage of CD8α+cell, and levels of ChIL-2 and ChIFN-γ transcripts in the group immunized with pcDNA-3-1E-linker-mChIL-15 were significantly increased on day 6 following challenge (P<0.05,P<0.01, andP<0.01, resp.). Our data suggested that the fusion antigen 3-1E-linker-mChIL-15 could be a potential candidate forE. acervulinavaccine development.

scholarly journals Regional Differences in the Cellular Immune Response to Experimental Cutaneous or Visceral Infection withLeishmania donovani

1998 ◽  
Vol 66 (1) ◽  
pp. 18-27 ◽  
Author(s):  
Peter C. Melby ◽  
Yan-Zhu Yang ◽  
Jun Cheng ◽  
Weiguo Zhao
Keyword(s):  
Immune Response ◽  
Cellular Immune Response ◽  
Parasite Burden ◽  
Systemic Infection ◽  
Inos Mrna ◽  
Cutaneous Infection ◽  
Spleen Cells ◽  
Ifn Γ ◽  
Cellular Immune ◽  
Visceral Infection

ABSTRACT Infection with the protozoan Leishmania donovani can cause serious visceral disease or subclinical infection in humans. To better understand the pathogenesis of this dichotomy, we have investigated the host cellular immune response to cutaneous or visceral infection in a murine model. Mice infected in the skin developed no detectable visceral parasitism, whereas intravenous inoculation resulted in hepatosplenomegaly and an increasing visceral parasite burden. Spleen cells from mice with locally controlled cutaneous infection showed strong parasite-specific proliferative and gamma interferon (IFN-γ) responses, but spleen cells from systemically infected mice were unresponsive to parasite antigens. The in situ expression of IFN-γ, interleukin-4 (IL-4), IL-10, IL-12, and inducible nitric oxide synthase (iNOS) mRNAs was determined in the spleen, draining lymph node (LN), and cutaneous site of inoculation. There was considerably greater expression of IFN-γ and IL-12 p40 mRNAs in the LN draining a locally controlled cutaneous infection than in the spleen following systemic infection. Similarly, there was a high level of IFN-γ production by LN cells following subcutaneous infection but no IFN-γ production by spleen cells following systemic infection. Splenic IL-4 expression was transiently increased early after systemic infection, but splenic IL-10 transcripts increased throughout the course of visceral infection. IL-4 and IL-10 mRNAs were also increased in the LN following cutaneous infection. iNOS mRNA was detected earlier in the LN draining a cutaneous site of infection compared to the spleen following systemic challenge. Thus, locally controlled cutaneous infection was associated with antigen-specific spleen cell responsiveness and markedly increased levels of IFN-γ, IL-12, and iNOS mRNA in the draining LN. Progressive splenic parasitism was associated with an early IL-4 response, markedly increased IL-10 but minimal IL-12 expression, and delayed expression of iNOS.

scholarly journals Highly functional virus-specific cellular immune response in asymptomatic SARS-CoV-2 infection

2020 ◽  
Author(s):  
Nina Le Bert ◽  
Hannah E Clapham ◽  
Anthony T Tan ◽  
Wan Ni Chia ◽  
Christine YL Tham ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Inflammatory Cytokines ◽  
T Cell Activation ◽  
Cellular Immune Response ◽  
Cell Activation ◽  
Tnf Α ◽  
Specific Cellular Immune Response ◽  
Ifn Γ ◽  
Cellular Immune

AbstractThe efficacy of virus-specific T cells in clearing pathogens involves a fine balance between their antiviral and inflammatory features. SARS-CoV-2-specific T cells in individuals who clear SARS-CoV-2 infection without symptoms or disease could reveal non-pathological yet protective characteristics. We therefore compared the quantity and function of SARS-CoV-2-specific T cells in a cohort of asymptomatic individuals (n=85) with that of symptomatic COVID-19 patients (n=76), at different time points after antibody seroconversion. We quantified T cells reactive to structural proteins (M, NP and Spike) using ELISpot assays, and measured the magnitude of cytokine secretion (IL-2, IFN-γ, IL-4, IL-6, IL-1β, TNF-α and IL-10) in whole blood following T cell activation with SARS-CoV-2 peptide pools as a functional readout. Frequencies of T cells specific for the different SARS-CoV-2 proteins in the early phases of recovery were similar between asymptomatic and symptomatic individuals. However, we detected an increased IFN-γ and IL-2 production in asymptomatic compared to symptomatic individuals after activation of SARS-CoV-2-specific T cells in blood. This was associated with a proportional secretion of IL-10 and pro-inflammatory cytokines (IL-6, TNF-α and IL-1β) only in asymptomatic infection, while a disproportionate secretion of inflammatory cytokines was triggered by SARS-CoV-2-specific T cell activation in symptomatic individuals. Thus, asymptomatic SARS-CoV-2 infected individuals are not characterized by a weak antiviral immunity; on the contrary, they mount a robust and highly functional virus-specific cellular immune response. Their ability to induce a proportionate production of IL-10 might help to reduce inflammatory events during viral clearance.

Detection of long term cellular immune response to Japanese encephalitis vaccination using IFN-γ ELIspot assay

2017 ◽  
Vol 89 (12) ◽  
pp. 2235-2238
Author(s):  
Amreen Zia ◽  
Dharamveer Singh ◽  
Swati Saxena ◽  
Jyoti Umrao ◽  
Manjari Baluni ◽  
...  
Keyword(s):  
Immune Response ◽  
Japanese Encephalitis ◽  
Cellular Immune Response ◽  
Elispot Assay ◽  
Ifn Γ ◽  
Cellular Immune

scholarly journals Evidence of Long-Lasting Humoral and Cellular Immunity against SARS-CoV-2 Even in Elderly COVID-19 Convalescents Showing a Mild to Moderate Disease Progression

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 805
Author(s):  
Bastian Fischer ◽  
Christopher Lindenkamp ◽  
Christoph Lichtenberg ◽  
Ingvild Birschmann ◽  
Cornelius Knabbe ◽  
...  
Keyword(s):  
Immune Response ◽  
Cellular Immune Response ◽  
Nucleocapsid Protein ◽  
Interferon Γ ◽  
Special Equipment ◽  
Humoral And Cellular Immunity ◽  
Moderate Disease ◽  
Ifn Γ ◽  
Blood Specimens ◽  
Cellular Immune

We here evaluate the humoral and cellular immune response against SARS-CoV-2 in 41 COVID-19 convalescents. As previous studies mostly included younger individuals, one advantage of our study is the comparatively high mean age of the convalescents included in the cohort considered (54 ± 8.4 years). While anti-SARS-CoV-2 antibodies were still detectable in 95% of convalescents up to 8 months post infection, an antibody-decay over time was generally observed in most donors. Using a multiplex assay, our data additionally reveal that most convalescents exhibit a broad humoral immunity against different viral epitopes. We demonstrate by flow cytometry that convalescent donors show a significantly elevated number of natural killer cells when compared to healthy controls, while no differences were found concerning other leucocyte subpopulations. We detected a specific long-lasting cellular immune response in convalescents by stimulating immune cells with SARS-CoV-2-specific peptides, covering domains of the viral spike, membrane and nucleocapsid protein, and measuring interferon-γ (IFN-γ) release thereafter. We modified a commercially available ELISA assay for IFN-γ determination in whole-blood specimens of COVID-19 convalescents. One advantage of this assay is that it does not require special equipment and can, thus, be performed in any standard laboratory. In conclusion, our study adds knowledge regarding the persistence of immunity of convalescents suffering from mild to moderate COVID-19. Moreover, our study provides a set of simple methods to characterize and confirm experienced COVID-19.

scholarly journals Induction of a Specific Strong Polyantigenic Cellular Immune Response after Short-Term Chemotherapy Controls Bacillary Reactivation in Murine and Guinea Pig Experimental Models of Tuberculosis

2008 ◽  
Vol 15 (8) ◽  
pp. 1229-1237 ◽  
Author(s):  
Evelyn Guirado ◽  
Olga Gil ◽  
Neus Cáceres ◽  
Mahavir Singh ◽  
Cristina Vilaplana ◽  
...  
Keyword(s):  
Immune Response ◽  
Guinea Pig ◽  
Cellular Immune Response ◽  
Therapeutic Vaccine ◽  
Experimental Models ◽  
Interleukin 12 ◽  
Short Term ◽  
Ifn Γ ◽  
Cellular Immune ◽  
Therapeutic Administration

ABSTRACT RUTI is a therapeutic vaccine that is generated from detoxified and liposomed Mycobacterium tuberculosis cell fragments that has demonstrated its efficacy in the control of bacillus reactivation after short-term chemotherapy. The aim of this study was to characterize the cellular immune response generated after the therapeutic administration of RUTI and to corroborate the lack of toxicity of the vaccine. Mouse and guinea pig experimental models were infected with a low-dose M. tuberculosis aerosol. RUTI-treated animals showed the lowest bacillary load in both experimental models. RUTI also decreased the percentage of pulmonary granulomatous infiltration in the mouse and guinea pig models. This was not the case after Mycobacterium bovis BCG treatment. Cellular immunity was studied through the characterization of the intracellular gamma interferon (IFN-γ)-producing cells after the splenocytes' stimulation with M. tuberculosis-specific structural and growth-related antigens. Our data show that the difference between the therapeutic administration of BCG and RUTI resides mainly in the stronger activation of IFN-γ + CD4+ cells and CD8+ cells against tuberculin purified protein derivative, ESAT-6, and Ag85B that RUTI generates. Both vaccines also triggered a specific immune response against the M. tuberculosis structural antigens Ag16kDa and Ag38kDa and a marked mRNA expression of IFN-γ, tumor necrosis factor, interleukin-12, inducible nitric oxide synthase, and RANTES in the lung. The results show that RUTI's therapeutic effect is linked not only to the induction of a Th1 response but also to the stimulation of a quicker and stronger specific immunity against structural and growth-related antigens that reduces both the bacillary load and the pulmonary pathology.

A sequential interferon gamma directed chemotactic cellular immune response determines survival and cardiac function post-myocardial infarction

2019 ◽  
Vol 115 (13) ◽  
pp. 1907-1917 ◽  
Author(s):  
Stefanie Finger ◽  
Maike Knorr ◽  
Michael Molitor ◽  
Rebecca Schüler ◽  
Venkata Garlapati ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Immune Response ◽  
Inflammatory Response ◽  
Cardiac Function ◽  
Interferon Gamma ◽  
Cellular Immune Response ◽  
Post Myocardial Infarction ◽  
Ifn Γ ◽  
Cellular Immune

Abstract Aims Myelomonocytic cells are critical in injury and healing post-myocardial infarction (MI). Mechanisms of regulation, however, are incompletely understood. The aim of the study was to elucidate the role of interferon gamma (IFN-γ) in the orchestrated inflammatory response in a murine model of MI. Methods and results MI was induced in 8- to 12-week-old male mice (C57BL/6 background) by permanent ligation of the left anterior descending (LAD) coronary artery. Lysozyme M (LysM)+ cell-depleted LysMiDTR transgenic mice displayed a reduced influx of CD45.2+/CD3−/CD11b+/Gr-1high neutrophils into infarcted myocardium 1 day post-MI compared with infarcted controls, paralleled by decreased cardiac mRNA levels of IFN-γ and tumour necrosis factor alpha (TNF-α). Mortality after MI was significantly increased in LysM+ cell-depleted mice within 28 days post-MI. To more specifically address the role of neutrophils, we depleted C57BL/6 mice with a monoclonal anti-Gr-1 antibody and found increased mortality, deteriorated cardiac function as well as decreased cardiac IFN-γ mRNA expression early after MI. Ccl2, Cxcl1, Cx3cl1, and Il12b mRNA were reduced 3 days after MI, as was the amount of CD11b+/Ly-6G−/Ly-6Chigh inflammatory monocytes. LAD-ligated Cramp−/− mice lacking cathelicidin important in neutrophil-dependent monocyte chemotaxis as well as IFNγ−/− and TNFα−/− mice phenocopied Gr-1+ cell-depleted mice, supporting a regulatory role of IFN-γ impacting on both the sequence of inflammatory cell invasion and cardiac outcome early after MI. The use of conditional IFN-γ receptor deficient mice indicated a direct effect of IFN-γ on LysM+ cells in cardiac injury post-MI. Using IFN-γ reporter mice and flow cytometry, we identified cardiac lymphoid cells (CD4+ and CD8+ T cells and natural killer cells) as primary source of this cytokine in the cardiac inflammatory response post-MI. Conclusion IFN-γ directs a sequential chemotactic cellular immune response and determines survival and cardiac function post-MI.

IL-35 inhibits HBV antigen-specific IFN-γ-producing CTLs in vitro

2015 ◽  
Vol 129 (5) ◽  
pp. 395-404 ◽  
Author(s):  
Xuefen Li ◽  
Li Tian ◽  
Yuejiao Dong ◽  
Qiaoyun Zhu ◽  
Yiyin Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Cellular Immune Response ◽  
Cd4 T Cells ◽  
Ifn Γ ◽  
Cellular Immune

Inhibitory cytokine, interleukin-35 (IL-35), is highly expressed in CD4+ T-cells from CHB patients and plays an important role in the inhibition of the cellular immune response, which contribute to the development and progression of chronic hepatitis B.

scholarly journals Highly functional virus-specific cellular immune response in asymptomatic SARS-CoV-2 infection

2021 ◽  
Vol 218 (5) ◽  
Author(s):  
Nina Le Bert ◽  
Hannah E. Clapham ◽  
Anthony T. Tan ◽  
Wan Ni Chia ◽  
Christine Y.L. Tham ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Cell Activation ◽  
Cellular Immune Response ◽  
Cell Activation ◽  
Asymptomatic Infection ◽  
Tnf Α ◽  
Specific Cellular Immune Response ◽  
Ifn Γ ◽  
Cellular Immune

The efficacy of virus-specific T cells in clearing pathogens involves a fine balance between antiviral and inflammatory features. SARS-CoV-2–specific T cells in individuals who clear SARS-CoV-2 without symptoms could reveal nonpathological yet protective characteristics. We longitudinally studied SARS-CoV-2–specific T cells in a cohort of asymptomatic (n = 85) and symptomatic (n = 75) COVID-19 patients after seroconversion. We quantified T cells reactive to structural proteins (M, NP, and Spike) using ELISpot and cytokine secretion in whole blood. Frequencies of SARS-CoV-2–specific T cells were similar between asymptomatic and symptomatic individuals, but the former showed an increased IFN-γ and IL-2 production. This was associated with a proportional secretion of IL-10 and proinflammatory cytokines (IL-6, TNF-α, and IL-1β) only in asymptomatic infection, while a disproportionate secretion of inflammatory cytokines was triggered by SARS-CoV-2–specific T cell activation in symptomatic individuals. Thus, asymptomatic SARS-CoV-2–infected individuals are not characterized by weak antiviral immunity; on the contrary, they mount a highly functional virus-specific cellular immune response.

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