So, I take the view that antigen presentation is a function, not a cell type, and prefer to restrict the use of the term DC to APCs that depend up Flt3L. The mononuclear phagocyte system of the pig as a model for understanding human innate immunity and disease. Systems biology approaches identify ATF3 as a negative regulator of toll-like receptor 4. An expression atlas of human primary cells: Remodeling of the enhancer landscape during macrophage activation is coupled to enhancer transcription. Genetic programs expressed in resting and IL-4 alternatively activated mouse and human macrophages: Nat Immunol 4:
The underlying principal of guilt-by-association was recently extended to RNAseq data including long non-coding RNAs in the networks Interestingly, the LPS target genes differ in their dose-responsiveness, so even the response to a single agent cannot be classified. To identify those genes, we can compare the expression profiles of macrophages with cells that are not phagocytic. BioGPS is one example of a new era of emerging user-friendly portals see text footnote 1 that enable the analysis of complex transcriptomic data. They also initiate acquired immunity by processing and presenting antigens and provide the downstream effector functions. Mol Cell The function of myb, in particular, correlates with its known downregulation as progenitor cells differentiate and exit the cell cycle 1 , and its ability to repress macrophage differentiation and to directly repress csf1r transcription
In mRNA from the wall of the gut, macrophage-specific transcripts derived from the abundant lamina propria macrophage population were easily detected, but the C-type lectins were undetectable. For example, microglia, the macrophages of the brain, are quite different from blood monocytes and tissue macrophages isolated from other locations For example, the promoters of these phagocyte-restricted genes contain purine-rich motifs binding sites for the macrophage-specific transcription factor, PU.
A lineage of myeloid cells independent of Myb and hematopoietic stem cells. On this basis, the variation in IFN-response genes between patient samples in many large datasets probably reflects the underlying genetic predisposition rather than the disease state.
The impact of breed and tissue compartment on the response of pig macrophages to lipopolysaccharide. In essence, when dealing with an ever-changing pathogen landscape, it is desirable not to have all the macrophage eggs in one basket.
However, this did not appear in any co-expression clusters from large mouse or human datasets. IFITM3 restricts the morbidity and mortality associated with influenza. Meta-analysis of lineage-specific gene expression signatures in mouse leukocyte populations. busineds
The web site, www. The expanded genomic view above links the TSS to the expression profile. These inducible feedback regulators act at every level of llan TLR signaling cascade.
Monocyte and macrophage heterogeneity. Interestingly, the LPS target genes differ in their dose-responsiveness, so even the response to a single agent cannot be classified.
Trophic macrophages in development and disease.
Treatment of mice with monoclonal antibody against CSF1R depletes most tissue macrophage populations in adult mice Annu Rev Immunol 2: Latent enhancers activated by stimulation in differentiated cells. At top right, we see that three of the distal promoters were induced by LPS in human monocyte-derived macrophages, starting around 3—4 h after stimulation.
The activation states in recruited macrophages have since been classified as M1 and M2, or classically activated and alternatively activated 346 — Kawai T, Akira S. The motifs over-represented in the promoters, and their relative over-representation, was conserved suggesting that in both species the promoters sample a common transcriptional milieu. The mononuclear phagocyte system.
BMC Biol Transcriptional control of the inflammatory response. There is also considerable divergence in the sets of target genes between mouse strains, between individuals, and in other species such as pigs.
BMC Immunol 4: The quite different response to macrophages to toll-like receptor agonists such as LPS 54 — 59 has also been called an M1 response. The MPS has been viewed as a linear sequence from pluripotent progenitors, through committed myeloid progenitors shared with granulocytes, to promonocytes and blood monocytes, finally giving rise to tissue macrophages 2 — 7.
Frontiers | The Many Alternative Faces of Macrophage Activation | Immunology
J Leukoc Biol Monoallelic expression of the murine gene encoding toll-like receptor 4. Even these modules are clearly a simplification based upon synchronous stimulation with individual agents or combinations. Macrophage plasticity and polarization: The Cells of the Mononuclear Phagocyte System The mononuclear phagocyte system MPS 1 is a family of professional phagocytes derived from hematopoietic progenitor cells under the influence of specific growth factors.