Granulocyte colony ‐stimulating factor is not pathogenic in lupus nephritis

Graphical abstractLupus nephritis is perpetuated by unrestrained inflammation, potentially driven by the hematopoietic growth factor granulocyte colony-stimulating factor (G-CSF). Lupus-prone Lyn-deficient mice lacking G-CSF were not protected from the development of autoimmunity and, in fact, exhibited exacerbated indices of kidney pathology. Furthermore, G-CSF levels in human serum were not elevated in systemic lupus erythematosus patients or in correlation with renal disease, overall indicating that G-CSF is not a major pathogenic factor in lupus nephritis. AbstractSystemic lupus erythematosus (lupus) is an autoimmune disease characterized by autoantibodies that form immune complexes with self-antigens, which deposit in various tissues, leading to inflammation and disease. The etiology of disease is complex and still not completely elucidated. Dysregulated inflammation is an important disease feature, and the mainstay of lupus treatment still utilizes nonspecific anti-inflammatory drugs. Granulocyte colony-stimulating factor (G-CSF) is a growth, survival, and activation factor for neutrophils and a mobilizer of hematopoietic stem cells, both of which underlie inflammatory responses in lupus. To determine whether G-CSF has a causal role in lupus, we genetically deleted G-CSF from Lyn-deficient mice, an experimental model of lupus nephritis. Lyn−/−G-CSF−/− mice displayed many of the inflammatory features of Lyn-deficient mice; however, they had reduced bone marrow an...
Source: Immunity, Inflammation and Disease - Category: Allergy & Immunology Authors: Tags: ORIGINAL ARTICLE Source Type: research