About this Research Topic
Uveitis is one of the leading causes of blindness worldwide and is comprised of a clinically heterogenous group of subtypes with diverse etiologies. A widely accepted hypothesis is that infectious agents and immunological abnormalities in genetically susceptible individuals may be responsible for the initiation and chronicity of uveitis. The majority of these uveitis subtypes are multifactorial, with the contribution of genetic inheritance, immune dysregulation and gut microbiota abnormalities all playing a part.
Both innate and adaptive immune responses are reported to be actively involved in the development of uveitis. Th1 cells were the first subtype of T cells shown to be involved, and Th17 cells, which typically produce IL-17 upon stimulation of IL-23, were later shown to play a vital role in the pathogenesis of uveitis. Quantitatively abnormal and functionally diminished Treg cells may also be an underlying reason. Further, γδT, macrophage and neutrophil abnormalities have also been recognized as contributing to the pathogenesis of uveitis.
Genes of the major histocompatibility complex in humans, known as human leukocyte antigens (HLA), play a pivotal role in uveitis susceptibility. HLA-B27 has been shown to be strongly associated with acute anterior uveitis and HLA-B51 with Behcet’s disease. Also, the non-HLA genetic background of uveitis has also been extensively explored through substantial candidate studies and genome wide association studies (GWAS). Nearly 1000 single nucleotide polymorphisms (SNPs) located in about 400 genes covering 14 uveitis entities and 40 populations have been identified as associated with various uveitis entities. These SNPs are mostly located in genes involved in innate and adaptive immunity mechanisms, including complement components, pattern recognition receptors, cytokines and chemokines.
In recent years, evidence is accumulating in favor of an important role of gut microbiota in uveitis pathogenesis. This has been confirmed in mouse models of experimental autoimmune uveitis (EAU). Dysbiosis of the patient gut microbiome has also been observed in several uveitis entities, such as Behcet’s disease and acute anterior uveitis. Fecal microbiota transplantation with feces from active BD patients significantly exacerbated EAU activity and increased the production of inflammatory cytokines including IL-17 and IFN-γ.
This Research Topic aims to bring together contributions covering various aspects related to the pathogenesis of uveitis. A more detailed and in-depth understanding of the mechanisms underlying disease initiation and chronicity could lead to an earlier and more precise diagnosis and also to the development of more appropriate and effective therapeutic approaches.
In this Research Topic, we welcome Original Research and Review articles that address, but are not limited to, the following themes:
• Immune and cellular mechanisms underlying uveitis pathogenesis
• Exploration on the genetic background of uveitis
• The role microbiota plays in the pathogenesis of uveitis
Both innate and adaptive immune responses are reported to be actively involved in the development of uveitis. Th1 cells were the first subtype of T cells shown to be involved, and Th17 cells, which typically produce IL-17 upon stimulation of IL-23, were later shown to play a vital role in the pathogenesis of uveitis. Quantitatively abnormal and functionally diminished Treg cells may also be an underlying reason. Further, γδT, macrophage and neutrophil abnormalities have also been recognized as contributing to the pathogenesis of uveitis.
Genes of the major histocompatibility complex in humans, known as human leukocyte antigens (HLA), play a pivotal role in uveitis susceptibility. HLA-B27 has been shown to be strongly associated with acute anterior uveitis and HLA-B51 with Behcet’s disease. Also, the non-HLA genetic background of uveitis has also been extensively explored through substantial candidate studies and genome wide association studies (GWAS). Nearly 1000 single nucleotide polymorphisms (SNPs) located in about 400 genes covering 14 uveitis entities and 40 populations have been identified as associated with various uveitis entities. These SNPs are mostly located in genes involved in innate and adaptive immunity mechanisms, including complement components, pattern recognition receptors, cytokines and chemokines.
In recent years, evidence is accumulating in favor of an important role of gut microbiota in uveitis pathogenesis. This has been confirmed in mouse models of experimental autoimmune uveitis (EAU). Dysbiosis of the patient gut microbiome has also been observed in several uveitis entities, such as Behcet’s disease and acute anterior uveitis. Fecal microbiota transplantation with feces from active BD patients significantly exacerbated EAU activity and increased the production of inflammatory cytokines including IL-17 and IFN-γ.
This Research Topic aims to bring together contributions covering various aspects related to the pathogenesis of uveitis. A more detailed and in-depth understanding of the mechanisms underlying disease initiation and chronicity could lead to an earlier and more precise diagnosis and also to the development of more appropriate and effective therapeutic approaches.
In this Research Topic, we welcome Original Research and Review articles that address, but are not limited to, the following themes:
• Immune and cellular mechanisms underlying uveitis pathogenesis
• Exploration on the genetic background of uveitis
• The role microbiota plays in the pathogenesis of uveitis
Keywords: uveitis, immunity, genes, microbes, EAU
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
