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Critical Reviews™ in Immunology
IF: 1.352 5-Year IF: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Print: 1040-8401
ISSN Online: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v25.i5.50
pages 405-428

Functions of Granulocyte-Macrophage Colony-Stimulating Factor

Andrew J. Fleetwood
Arthritis and Inflammation Research Centre and Cooperative Research Centre for Chronic Inflammatory Diseases, Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville 3010, Victoria, Australia
Andrew D. Cook
Arthritis and Inflammation Research Centre and Cooperative Research Centre for Chronic Inflammatory Diseases, Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville 3010, Victoria, Australia
John A. Hamilton
Arthritis and Inflammation Research Centre and Cooperative Research Centre for Chronic Inflammatory Diseases, Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville 3010, Victoria, Australia

ABSTRACT

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.