Monocytes and Macrophages are widely distributed innate immune cells that play an indispensable role in a variety of physiologic and pathologic process, including the regulation of the initiation, development and resolution of many inflammatory disorders. They also actively participate in the development of autoimmune diseases as well as autoinflammatory diseases. These cells can secrete a wide range of cytokine and chemokines, leading to the recruitment of additional immune cells.
Abnormal regulation of monocytes and macrophages has been reported in several autoimmune and autoinflammatory diseases. An example of this is the significantly higher rate and absolute number of CD14+CD16+ monocytes seen in SLE patients. Macrophages from SLE patients overexpress ICAM-1 and this is reduced by corticosteroid treatment. Systemic Sclerosis (SSc) monocytes are reported to be more pro-fibrotic because they display increased differentiation potential towards type-1 collagen and increased TIMP-1 expression. Unusual expression of inflammatory and regulatory molecules, including PLAC8 in Adult-Onset Still’s Disease (AOSD) and miRNA-204-3p in Familial Mediterranean Fever (FMF), have also been described in autoinflammatory diseases.
Furthermore, macrophages can be phenotypically polarized by the surrounding microenvironmental stimuli and signals. Classically activated macrophages (M1) can produce toxic effector molecules such as reactive oxygen species and nitric monoxide, and inflammatory cytokines such as IL-1ß, TNF and IL-6. Alternatively activated macrophages (M2) drive immune regulation and tissue remodeling. In addition to this concept in macrophages, M1 monocytes and M2 monocytes, mirroring the M1/M2 macrophage polarization concept, have been suggested. It has been suggested that this macrophage and monocyte subset polarization contribute to autoimmune and autoinflammatory diseases, specifically in Rheumatoid Arthritis (RA) and Crohn’s Disease.
Interestingly, a recent investigation of immune profiling analysis linking to Genome Wide Association Studies (GWAS) also suggests the importance of monocyte-macrophage lineage cells for the development of autoimmune as well as autoinflammatory conditions. This Research Topic aims to provide an update on the role of monocyte and macrophage in autoimmune and autoinflammatory disease. We welcome Review, Mini Review and Original Research articles in this area with a clinical and/or experimental viewpoint focusing on, but not limited to:
· Imbalance of monocyte subset and dysregulation of monocyte function in autoimmune/autoinflammatory disease
· Macrophage regulation in autoimmune/autoinflammatory disease
· The dominant polarization of monocyte-macrophage (M1/M2) in each autoimmune/autoinflammatory disease
· Detailed role of imbalance of monocyte subsets and polarization in autoimmune/autoinflammatory disease
Monocytes and Macrophages are widely distributed innate immune cells that play an indispensable role in a variety of physiologic and pathologic process, including the regulation of the initiation, development and resolution of many inflammatory disorders. They also actively participate in the development of autoimmune diseases as well as autoinflammatory diseases. These cells can secrete a wide range of cytokine and chemokines, leading to the recruitment of additional immune cells.
Abnormal regulation of monocytes and macrophages has been reported in several autoimmune and autoinflammatory diseases. An example of this is the significantly higher rate and absolute number of CD14+CD16+ monocytes seen in SLE patients. Macrophages from SLE patients overexpress ICAM-1 and this is reduced by corticosteroid treatment. Systemic Sclerosis (SSc) monocytes are reported to be more pro-fibrotic because they display increased differentiation potential towards type-1 collagen and increased TIMP-1 expression. Unusual expression of inflammatory and regulatory molecules, including PLAC8 in Adult-Onset Still’s Disease (AOSD) and miRNA-204-3p in Familial Mediterranean Fever (FMF), have also been described in autoinflammatory diseases.
Furthermore, macrophages can be phenotypically polarized by the surrounding microenvironmental stimuli and signals. Classically activated macrophages (M1) can produce toxic effector molecules such as reactive oxygen species and nitric monoxide, and inflammatory cytokines such as IL-1ß, TNF and IL-6. Alternatively activated macrophages (M2) drive immune regulation and tissue remodeling. In addition to this concept in macrophages, M1 monocytes and M2 monocytes, mirroring the M1/M2 macrophage polarization concept, have been suggested. It has been suggested that this macrophage and monocyte subset polarization contribute to autoimmune and autoinflammatory diseases, specifically in Rheumatoid Arthritis (RA) and Crohn’s Disease.
Interestingly, a recent investigation of immune profiling analysis linking to Genome Wide Association Studies (GWAS) also suggests the importance of monocyte-macrophage lineage cells for the development of autoimmune as well as autoinflammatory conditions. This Research Topic aims to provide an update on the role of monocyte and macrophage in autoimmune and autoinflammatory disease. We welcome Review, Mini Review and Original Research articles in this area with a clinical and/or experimental viewpoint focusing on, but not limited to:
· Imbalance of monocyte subset and dysregulation of monocyte function in autoimmune/autoinflammatory disease
· Macrophage regulation in autoimmune/autoinflammatory disease
· The dominant polarization of monocyte-macrophage (M1/M2) in each autoimmune/autoinflammatory disease
· Detailed role of imbalance of monocyte subsets and polarization in autoimmune/autoinflammatory disease