Interleukin-10 determines viral clearance or persistence in vivo
By D. Brooks, M. Trifilo, Kurt H. Edelmann, L. Teyton, D. McGavern, M. Oldstone. Nature Medicine, 2006
992 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology
View Paper: https://www.semanticscholar.org/paper/8cec13cbc36bb2e325c71ecb6cd1dd6135b4a95d
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Citations in the corpus
- Commensal Bacteria Calibrate the Activation Threshold of Innate Antiviral Immunity (2012, background): “The immunregulatory cytokine IL-10 has been demonstrated to influence the antiviral immune response (Brooks et al., 2006; McKinstry et al., 2009; Sun et al., 2009) and expression of this cytokine can be modulated by commensal bacteria (Amaral et al., 2008; Mazmanian et al., 2008).”
- T cell exhaustion (2011, background): “, and CD4 + T cells are probably an important source of increased IL-10 (ref”
- Effector T cells control lung inflammation during acute influenza virus infection by producing IL-10 (2009, background): “More recently, IL-10 has been found to mediate virus persistence during chronic viral infection”
- TH1 cells control themselves by producing interleukin-10 (2007, background): “More recently, the production of IL-10 was shown to maintain a chronic non-healing lymphocytic choriomeningitis virus infection, and the neutralization of IL-10 resulted in the clearance of this viru”
- CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer. (2019, background): “During chronic LCMV infection, blocking IL-10 in combination with PD-1 results in the maintenance of robust Teff responses, development of functional antiviral memory cells, and faster control of viral replication (143, 144, 151).”
- SARS-CoV-2 infection: The role of cytokines in COVID-19 disease (2020, positive): “Hence, the effective blocking of IL-10 signaling may be useful against resistant viral infections [129,130].”
- Redefining chronic viral infection. (2009, positive): “For example, when the IL-10 pathway was blocked, virus-specific CD8 T cell responses to chronic infection with LCMV were enhanced (Ejrnaes et al., 2006; Brooks et al., 2006).”
- Induction of a Striking Systemic Cytokine Cascade prior to Peak Viremia in Acute Human Immunodeficiency Virus Type 1 Infection, in Contrast to More Modest and Delayed Responses in Acute Hepatitis B and C Virus Infections (2009, background): “The late-peaking IL-10 response may not only be too late to subdue immunopathogenic levels of proinflammatory cytokine production but may also contribute to HIV persistence by driving the exhaustion of virus-specific CD8 T cells (8, 15).”
- Should we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions (2020, neutral): “lung macrophages or epithelial cells (first wave of hypercytokinemia), including TNF-α which causes T cell apoptosis [21], IL-10 which is known to prevent T cell proliferation [67], and type-I IFN which regulates lymphocyte recirculation [68].”
- Shaping and reshaping CD8+ T-cell memory (2008, background): “In addition, other recent studies suggest that IL-10 production during chronic infection limits memory CD8 + T-cell antiviral activit”