Abstract
Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) are well-recognized regulators of hematopoiesis and have an established role as growth factors in clinical practice. G-CSF and GM-CSF regulate myeloid cell production, differentiation and activation, and might also be important for driving inflammatory responses. Inappropriate engagement of this pathway could be a critical amplification mechanism when maladaptive immune responses predispose to autoimmunity and sterile tissue inflammation. We postulate that antagonism of G-CSF or GM-CSF could represent a novel therapeutic approach for a variety of autoimmune-mediated inflammatory diseases, including rheumatoid arthritis.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Antirheumatic Agents / therapeutic use*
-
Arthritis, Rheumatoid / drug therapy*
-
Arthritis, Rheumatoid / immunology
-
Arthritis, Rheumatoid / metabolism
-
Disease Models, Animal
-
Drug Design
-
Granulocyte Colony-Stimulating Factor / antagonists & inhibitors
-
Granulocyte Colony-Stimulating Factor / physiology*
-
Granulocyte-Macrophage Colony-Stimulating Factor / antagonists & inhibitors
-
Granulocyte-Macrophage Colony-Stimulating Factor / physiology*
-
Humans
-
Inflammation / drug therapy
-
Inflammation / physiopathology
-
Inflammation Mediators / therapeutic use
-
Neutrophils / physiology
Substances
-
Antirheumatic Agents
-
Inflammation Mediators
-
Granulocyte Colony-Stimulating Factor
-
Granulocyte-Macrophage Colony-Stimulating Factor