Monocyte-mediated defense against microbial pathogens.
By N. Serbina, Ting Jia, T. Hohl, Eric G. Pamer. Annual Review of Immunology, 2008
1,205 citations recorded by the source corpus.
Subfields: Immunology, Parasitology
View Paper: https://www.semanticscholar.org/paper/8f4bef0624e00a8a1276049945931789a5feaba8
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
In Parasitology
Citations in the corpus
- Human CD14dim Monocytes Patrol and Sense Nucleic Acids and Viruses via TLR7 and TLR8 Receptors (2010, neutral): “Blood monocytes are bone marrow-derived phagocytes involved in the innate response to bacterial, fungal, parasitic, and viral infection (Barbalat et al., 2009; Gupta et al., 2001; Im Serbina et al., 2009; Serbina et al., 2008; Ströher et al., 2001).”
- Protective and pathogenic functions of macrophage subsets (2011, background): “Tissue stress, including acute and chronic infection, as well as sterile inflammation , drives the production of monocytes and neutrophils in a process that is dependent on cytokines such as granulocyte colony stimulating factor (G-CSF) and chemokines including CC-chemokine ligand 2 (CCL2) and CCL5”
- Monocyte and macrophage differentiation: circulation inflammatory monocyte as biomarker for inflammatory diseases (2014, background): “Functional properties of mouse monocyte subsets As shown in Figure 1, mouse Ly6C monocytes have a high antimicrobial capability due to their potent capacity for phagocytosis, secrete ROS, TNFα, nitric oxide, IL-1β, little IL-10 upon bacterial infection [17] and large amount of type 1 interferon (IFN”
- CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages (2015, background): “Furthermore, loss of CCL2 signaling in mouse models severely depresses the numbers of circulating monocytes and increases susceptibility to infection (Serbina et al., 2008).”
- Chemokine nitration prevents intratumoral infiltration of antigen-specific T cells (2011, background): “In addition to CD8+ T cells, CCL2 attracts monocytes and macrophages to sites of inflammation (Serbina et al., 2008) and cancer (Sozzani et al., 1995).”
- From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “In some circumstances, monocytes can trigger and polarize T-cell responses (27, 28) and may also contribute to angiogenesis and atherogenesis (29).”
- Innate Immune Activity Conditions the Effect of Regulatory Variants upon Monocyte Gene Expression (2014, background): “Upon stimulation, monocytes exhibit large-scale gene transcription with concomitant cytokine production, enhanced antigen processing, and migration (11, 12).”
- Nr4a1-Dependent Ly6Clow Monocytes Monitor Endothelial Cells and Orchestrate Their Disposal (2013, background): “…and infected tissues in order to recruit neutrophils 362 Cell 153, 362–375, April 11, 2013 ª2013 Elsevier Inc. within a few hours and ‘‘inflammatory’’ lymphocyte antigen 6c (Ly6C)+ monocytes 1 day later, herein initiating a cellular immune response (Auffray et al., 2009b; Serbina et al., 2008).”
- Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis (2012, neutral): “, 2010) and poised to traffic to sites of infection and inflammation (Geissmann et al., 2003; Serbina et al., 2008).”
- Origin of monocytes and macrophages in a committed progenitor (2013, background): “Analysis of fractalkine receptor CX(3)CR1 function by targeted deletion and green fluorescent protein reporter gene insertion.”
- Blood monocytes: development, heterogeneity, and relationship with dendritic cells. (2009, background): “Murine Ly6C+ (Gr1+) monocytes are selectively recruited to inflamed tissues and lymph nodes in vivo, produce high levels of TNF-α and IL-1 during infection or tissue damage, and were termed inflammatory monocytes (8, 10, 16, 69, 104, 128).”
- The microRNA miR-29 controls innate and adaptive immune responses to intracellular bacterial infection by targeting interferon-γ (2011, background): “tuberculosis relies on T cells, and the main resistance to infection is attributed to the production of IFN-γ by CD8 + T cells and T H 1 effector cell”
- The transcription factor NR4A1 (Nur77) controls bone marrow differentiation and survival of Ly6C− monocytes (2011, neutral): “and can differentiate into antigen-presenting cells that produce tumor necrosis factor, nitric oxide and reactive oxygen specie”