A20 (Tnfaip3) deficiency in myeloid cells protects against influenza A virus infection [PDF]
, 2012 The innate immune response provides the first line of defense against viruses and other pathogens by responding to specific microbial molecules. Influenza A virus (IAV) produces double-stranded RNA as an intermediate during the replication life cycle ...
Maelfait, Jonathan +8 more
core +2 more sources
CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3
Molecular Oncology, EarlyView.PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh +12 more
wiley +1 more source
Mapping of the Epstein-Barr virus and C3dg binding sites to a common domain on complement receptor type 2. [PDF]
, 1989 Complement receptor type 2 (CR2;CD21), a member of the superfamily of proteins containing short consensus repeats (SCRs), is the B cell receptor for both the gp350/220 envelope protein of Epstein-Barr virus (EBV), and for the C3dg protein of complement ...
Ahearn, JM +5 more
core
Antiviral treatment alters the frequency of activating and inhibitory receptor-expressing natural killer cells in chronic Hepatitis B virus infected patients [PDF]
, 2012 Natural killer (NK) cells play a critical role in innate antiviral immunity, but little is known about the impact of antiviral therapy on the frequency of NK cell subsets.
Chi, X. +12 more
core +3 more sources
E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer
Molecular Oncology, EarlyView.Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov +3 more
wiley +1 more source
Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer
Molecular Oncology, EarlyView.Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley +1 more source
Identifying the immune interactions underlying HLA class I disease associations
eLife, 2020 Variation in the risk and severity of many autoimmune diseases, malignancies and infections is strongly associated with polymorphisms at the HLA class I loci.
Bisrat J Debebe +10 more
doaj +1 more source
Cytokines of Birds: Conserved Functions [PDF]
, 2001 Targeted disruptions of the mouse genes for cytokines, cytokine receptors, or components of cytokine signaling cascades convincingly revealed the important roles of these molecules in immunologic processes. Cytokines are used at present as drugs to fight
Göbel, Thomas W. F. +4 more
core +1 more source
Virus-Receptor Interactions and Virus Neutralization: Insights for Oncolytic Virus Development.
Oncolytic virotherapy, 2020 Oncolytic viruses (OVs) are replication competent agents that selectively target cancer cells. After penetrating the tumor cell, viruses replicate and eventually trigger cell lysis, releasing the new viral progeny, which at their turn will attack and kill neighbouring cells. The ability of OVs to self-amplify within the tumor while sparing normal cells
Jayawardena, Nadishka +3 more
openaire +2 more sources
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
Molecular Oncology, EarlyView.IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source