Roles of GM-CSF in the pathogenesis of autoimmune diseases: An update
- 1Isfahan University of Medical Sciences, Iran
- 2Thomas Jefferson University, United States
- 3Lorestan University of Medical Sciences, Iran
Granulocyte-macrophage colony-stimulating factor (GM-CSF) was first described as a growth factor that induces the differentiation and proliferation of myeloid progenitors in the bone marrow. GM-CSF also has an important cytokine effect in chronic inflammatory diseases by stimulating the activation and migration of myeloid cells to inflammation sites, promoting survival of target cells and stimulating the renewal of effector granulocytes and macrophages. Because of these pro-cellular effects, an imbalance in GM-CSF production/signaling may lead to harmful inflammatory conditions. In this context, GM-CSF has a pathogenic role in autoimmune diseases that are dependent on cellular immune responses such as multiple sclerosis (MS) and rheumatoid arthritis (RA). Conversely, a protective role has also been described in other autoimmune diseases where humoral responses are detrimental such as myasthenia graves (MG), Hashimoto’s thyroiditis, inflammatory bowel disease (IBD) and systemic lupus erythematosus (SLE). In this review, we aimed for a comprehensive analysis of literature data on the multiple roles of GM-CSF in autoimmue diseases and possible therapeutic strategies that target GM-CSF production.
Keywords: GM-CSF, Inflammation, tolerance, Immunomodulation, Autoimmune Diseases
Received: 12 Feb 2019;
Accepted: 17 May 2019.
Edited by:Silvano Sozzani, University of Brescia, Italy
Reviewed by:Vanessa Pinho, Federal University of Minas Gerais, Brazil
Tiziana Musso, University of Turin, Italy
Copyright: © 2019 Lotfi, Thome, Rezaei, zhang, Rezaei, Rostami and Esmaeil. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Prof. Abdolmohamad Rostami, Thomas Jefferson University, Philadelphia, 19107, Pennsylvania, United States, firstname.lastname@example.org
Dr. Nafiseh Esmaeil, Isfahan University of Medical Sciences, Isfahan, 81745, Isfahan, Iran, email@example.com