Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA245512 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This was a pilot study aimed at uncovering the role of myeloid-derived suppressor cells (myeloid-derived suppressor cell) in patients with Tuberculosis and differences between cells found in peripheral blood and in the lung. Fluidigm™ RT-PCR technology was used to quantify expression levels of 43 genes in monocytecytes and myeloid-derived suppressor cell from peripheral blood and monocytecytes and alveolar macrophages from bronchoalveolar lavage fluid taken from patients with Tuberculosis or other lung diseases.
2022-02-22 | GSE197113 | GEO
Project description:Myeloid-derived suppressor cells promote lung cancer metastasis
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Project description:We profiled lung tuberculosis granulomas and non-diseased lung tissue to understand myeloid dynamics in tuberculosis.
2023-05-31 | GSE211633 | GEO
Project description:This is a ODE-based mathematical model featuring equations describing the dynamics of tumor cells, cytotoxic T cells, natural killer cells, and myeloid-derived suppressor cells (MDSCs) that together describe the tumor-induced immunosuppression caused by MDSCs.
2019-09-09 | MODEL1909090003 | BioModels
Project description:The aim of the study is to evaluate whether the preoperative level of myeloid-derived suppressor cells is associated with postoperative complications classified by Clavien-Dindo categories. Levels of all MDSC, polymorphonuclear MDSC (PMNMDSC), monocytic MDSC (MMDSC), early-stage MDSC (EMDSC) and monocytic to polymorphonuclear MDSC ratio (M/PMN MDCS) were established and compared in patients with postoperative complications, severe postoperative complications (>= IIIA according to Clavien-Dindo) and severe septic complications.
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Project description:The critical role of type I IFN (IFN I ) in viral disease is thoroughly documented while their function in bacterial infection remains ambiguous. General interest in biological functions of IFN I in Mycobacterium tuberculosis (Mtb) infection was raised by the identification of a distinct IFN I gene expression signature in tuberculosis (TB) patients. Here we demonstrate that TB-susceptible mice lacking the receptor for IFN I (IFNAR1) were protected from death upon aerogenic infection with Mtb. Increased survival was accompanied by reduced bacterial burden and ameliorated lung pathology as well as diminished production of proinflammatory IL-1?, among other cytokines. IFNAR1 signaling did not affect T cell responses, but markedly altered migration of inflammatory monocytes and neutrophils to the lung during pulmonary TB. This process was orchestrated by presence of IFNAR1 in both immune and tissue-resident radioresistant cells. IFNAR1-driven TB susceptibility was initiated by CXCL5/CXCL1-driven accumulation of neutrophils into alveoli and subsequently a distinct compartmentalization of Mtb in lung phagocytes. We conclude that IFN I alters early innate events at the site of Mtb invasion leading to unleashed inflammation. Hence, our data furnish a mechanistic explanation for the detrimental role of IFN I in pulmonary TB. dual-color color-swap
2013-12-31 | E-GEOD-44848 | biostudies-arrayexpress
Project description:During tuberculosis, lung myeloid cells have two opposing roles: they are an intracellular niche occupied by Mycobacterium tuberculosis and they restrict bacterial replication. Lung myeloid cells from mice infected with yellow-fluorescent protein expressing M. tuberculosis mice were analyzed by flow cytometry and transcriptional profiling to identify the cell types infected and their response to infection. CD14, CD38, and Abca1 were expressed more highly by infected alveolar macrophages and CD11cHi monocyte-derived macrophages compared to uninfected cells. CD14, CD38, and Abca1 “triple positive” (TP) cells had incomparably high infection rates and bacterial loads, but also a strong interferon-γ signature and nitric oxide synthetase-2 production indicating recognition by T cells. Despite evidence of T cell recognition and appropriate activation, these TP+ macrophages became the dominant niche occupied by M. tuberculosis long-term. Defining this niche should help answer why M. tuberculosis resists elimination from activated macrophages even in the face of T cell immunity.
2020-02-29 | GSE146127 | GEO
Project description:Breast cancer cells display preferences for specific metastatic sites including the bone, lung and liver. Metastasis is a complex process that relies, in part, on interactions between disseminated cancer cells and resident/infiltrating stromal cells that constitute the metastatic microenvironment. Distinct immune infiltrates can either impair the metastatic process or conversely, assist in the seeding, colonization and growth of disseminated cancer cells. Using in vivo selection approaches, we previously isolated 4T1-derived breast cancer cells that preferentially metastasize to these organs and tissues. In this study, we examined whether the propensity of breast cancer cells to metastasize to the lung, liver or bone is associated with and dependent on distinct patterns of immune cell infiltration. Immunohistocytochemistry and immunohistofluorescence approaches were used to quantify granulocytic infiltrates within distinct metastases and depletion of Gr1+ cells was performed to functionally interrogate the role of myeloid/granulocytic infiltrates in promoting metastasis to these organs. We show that T lymphocytes (CD3+), myeloid-derived/granulocytic cells (Gr-1+) cells and neutrophils (NE+) exhibit the most pronounced recruitment in lung and liver metastases, with markedly less recruitment within bone metastatic lesions. Interestingly, these infiltrating cell populations display different patterns of localization within soft tissue metastases. T lymphocytes and neutrophils are localized around the periphery of liver metastases whereas they were dispersed throughout the lung metastases. Furthermore, Gr-1+ cell-depletion studies demonstrate that infiltrating myeloid-derived/granulocytic cells, including neutrophils, are essential for the formation of breast cancer liver metastases but dispensable for metastasis to the lung and bone. Finally, we demonstrate that neutrophils that infiltrate and surround the liver metastases are polarized towards an N2 phenotype, which have previously been shown to enhance tumor growth and metastasis. Our results demonstrate that the liver metastatic potential of breast cancer cells is heavily reliant on interactions with infiltrating myeloid/granulocytic cells in the liver microenvironment.
2015-03-20 | GSE62598 | GEO
Project description:Tuberculosis (TB) remains the leading cause of death by a single infectious agent worldwide. Despite decades of active research, host factors which underly susceptibility to Mycobacterium tuberculosis (Mtb), the etiologic agent of TB, are still ill defined. We investigated the role of platelets (PLTs) during primary TB in mice as these cells were recently assigned multiple immunological functions. PLTs were present at the site of infection, formed aggregates with different myeloid subsets during experimental TB and such aggregates were detected also in TB patients. PLTs were detrimental during the early phase of infection and this effect was uncoupled from their canonical activation. PLTs left lung cell dynamics and patterns of anti-mycobacterial T-cell responses unchanged. PLTs hampered cell autonomous defense by restricting production of reactive oxygen species (ROS) in lung residing myeloid cells. Thus, PLTs orchestrate immunity in TB by modulating innate immune responsiveness during primary lung infection and may be amenable to new interventions for this deadly disease.
2020-12-22 | GSE137421 | GEO