Project description:CD4 T cell responses are characterized based on a limited number of molecular markers selected from exisiting knowledge. The goal of the experiment was to assess antigenic-peptide specific T-cell responses in vitro without bias using microarrays. PBMCs were isolated from 1 healthy donor. The cells were stimulated with peptides derived from influenza virus H1 and H5, human cytomegalovirus, and candida albicans for 24 hours. Unstimulated cells were cultured without the peptides for 24 hours.
Project description:Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections, but human anti-fungal immunity remains poorly defined. Expression profiling of Candida-stimulated human peripheral blood mononuclear cells (PBMCs) provides new insights into Candida-specific host defense mechanisms in humans. Total RNA was extracted from PBMCs from healthy human volunteers. PBMCs were stimulated with heat-killed Candida albicans (10^6/ml), non-fungal inflammatory stimuli or RPMI control for 4 or 24 hours. A large number of biological replicates (>20) were included per stimulation condition and duration.
Project description:Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections, but human anti-fungal immunity remains poorly defined. Expression profiling of Candida-stimulated human peripheral blood mononuclear cells (PBMCs) provides new insights into Candida-specific host defense mechanisms in humans.
Project description:Response of fresh or frozen peripheral blood mononuclear cells from 1 healthy donor to influenza virus derived peptide stimulation.
Project description:We have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii.
Project description:We have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii.
Project description:We have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii.
Project description:We have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii.
Project description:We have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii.
Project description:We have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii.
