Format

Send to

Choose Destination
Immunity. 2016 Nov 15;45(5):963-973. doi: 10.1016/j.immuni.2016.10.026.

GM-CSF: From Growth Factor to Central Mediator of Tissue Inflammation.

Author information

1
Institute of Experimental Immunology, University of Zurich Winterthurerstrasse 190, 8057 Zurich, Switzerland. Electronic address: becher@immunology.uzh.ch.
2
Institute of Experimental Immunology, University of Zurich Winterthurerstrasse 190, 8057 Zurich, Switzerland.

Abstract

The granulocyte-macrophage colony-stimulating factor (GM-CSF) was initially classified as a hematopoietic growth factor. However, unlike its close relatives macrophage CSF (M-CSF) and granulocyte CSF (G-CSF), the majority of myeloid cells do not require GM-CSF for steady-state myelopoiesis. Instead, in inflammation, GM-CSF serves as a communication conduit between tissue-invading lymphocytes and myeloid cells. Even though lymphocytes are in all likelihood the instigators of chronic inflammatory disease, GM-CSF-activated phagocytes are well equipped to cause tissue damage. The pivotal role of GM-CSF at the T cell:myeloid cell interface might shift our attention toward studying the function of the myeloid compartment in immunopathology. Targeting specifically the crosstalk between T cells and myeloid cells through GM-CSF holds promise for the development of therapeutics to combat chronic tissue inflammation. Here, we will review some of the major discoveries of the recent past, which indicate that GM-CSF is so much more than its name suggests.

PMID:
27851925
DOI:
10.1016/j.immuni.2016.10.026
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center