
pmid: 16167889
GM-CSF was originally defined by its ability to generate in vitro granulocyte and macrophage colonies from bone marrow precursor cells. Apart from its physiological role in the control of alveolar macrophage development, it now appears more likely that its major role lies in its ability to govern the properties of the more mature myeloid cells of the granulocyte and macrophage lineages, particularly during host defence and inflammatory reactions. Recent evidence is summarized below for a key role for GM-CSF in inflammatory and autoimmune diseases, making it therefore worthy of consideration for targeting. Such evidence includes disease exacerbation following its administration and amelioration of disease in animal models by GM-CSF gene targeting or by anti-GM-CSF antibody blockade. This review summarizes the evidence supporting a major role for GM-CSF in inflammation and autoimmunity and its functions as major regulator governing granulocyte and macrophage lineage populations at all stages of maturation.
Macrophages, Animals, Granulocyte-Macrophage Colony-Stimulating Factor, Humans, Cell Lineage, Inflammation Mediators, Autoimmune Diseases, Granulocytes
Macrophages, Animals, Granulocyte-Macrophage Colony-Stimulating Factor, Humans, Cell Lineage, Inflammation Mediators, Autoimmune Diseases, Granulocytes
| citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 182 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
