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    1. Neuroscience

    Accelerating with FlyBrainLab the discovery of the functional logic of the Drosophila brain in the connectomic and synaptomic era

    Aurel A Lazar, Tingkai Liu ... Yiyin Zhou
    FlyBrainLab is an open-source computing platform that integrates 3D exploration and visualization of diverse Drosophila connectomic/synaptomic datasets with interactive exploration of the functional logic of modeled executable brain circuits.
    1. Immunology and Inflammation
    2. Microbiology and Infectious Disease

    NK cells inhibit Plasmodium falciparum growth in red blood cells via antibody-dependent cellular cytotoxicity

    Gunjan Arora, Geoffrey T Hart ... Eric O Long
    Red blood cells infected by the malaria parasite Plasmodium falciparum are destroyed by human natural killer cells in the presence of antibodies from people who have acquired clinical immunity to malaria.
    1. Cancer Biology
    2. Stem Cells and Regenerative Medicine

    Reprogramming and redifferentiation of mucosal-associated invariant T cells reveal tumor inhibitory activity

    Chie Sugimoto, Yukie Murakami ... Hiroshi Wakao
    Mucosal-associated invariant T cells, an emerging member of the innate-like T cells abundant in humans bridging the innate and the adaptive immunity, could be exploited as a novel tool for cancer immunotherapy through cell reprogramming.
    1. Stem Cells and Regenerative Medicine
    2. Immunology and Inflammation

    The basic leucine zipper transcription factor NFIL3 directs the development of a common innate lymphoid cell precursor

    Xiaofei Yu, Yuhao Wang ... Lora V Hooper
    The transcription factor NFIL3 is essential for the development of a committed bone marrow precursor that gives rise to all known innate lymphoid cell lineages in mice.
    1. Immunology and Inflammation

    A population of innate myelolymphoblastoid effector cell expanded by inactivation of mTOR complex 1 in mice

    Fei Tang, Peng Zhang ... Pan Zheng
    A novel population of hematopoietic cells unmasked by mTORC1 inactivation reveals a new mechanism of innate immune tolerance and a new consequence of defective hematopoiesis.
    1. Cell Biology
    2. Immunology and Inflammation

    Metabolic but not transcriptional regulation by PKM2 is important for natural killer cell responses

    Jessica F Walls, Jeff J Subleski ... David K Finlay
    Pharmacological activation of the metabolic activities of PKM2 in murine NK cells disrupts cellular redox balance and inhibits optimal NK cell effector functions.
    1. Immunology and Inflammation

    Resting natural killer cells promote the progress of colon cancer liver metastasis by elevating tumor-derived stem cell factor

    Chenchen Mao, Yanyu Chen ... Xiangyang Xue
    Resting natural killer cells promote the progress of colon cancer liver metastasis (CCLM), which may be exploited for novel strategies to improve therapeutic outcomes for patients with CCLM.
    1. Cancer Biology
    2. Cell Biology

    CXCL10/CXCR3 signaling contributes to an inflammatory microenvironment and its blockade enhances progression of murine pancreatic precancerous lesions

    Veethika Pandey, Alicia Fleming-Martinez ... Peter Storz
    Blockage of CXCL10/CXCR3 signaling between murine pancreatic precancerous lesion cells and inflammatory macrophages generates a tumor-promoting microenvironment.
    1. Immunology and Inflammation

    Prdm1 positively regulates liver Group 1 ILCs cancer immune surveillance and preserves functional heterogeneity

    Jitian He, Le Gao ... Youwei Wang
    Prdm1 (BLIMP1) promotes liver Group 1 ILCs cancer surveillance and preserves functional heterogeneity.
    1. Immunology and Inflammation

    Cytomegalovirus restricts ICOSL expression on antigen-presenting cells disabling T cell co-stimulation and contributing to immune evasion

    Guillem Angulo, Jelena Zeleznjak ... Ana Angulo
    ICOSL-dependent T-cell co-stimulation contributes to the host defense against herpesvirus infections, and accordingly, these pathogens have developed immune evasion mechanisms to interrupt the ICOSL:ICOS signaling pathway.